DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Status of the Claims
Claims 1, 5-17, 20-23, 25, and 31 are pending.
Claims 1, 7, 16, and 20 are newly amended.
Claims 9-11 and 14-15 are withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to nonelected species, there being no allowable generic or linking claim. Applicant timely traversed the restriction (election) requirement in the reply filed on 09/11/2025.
Claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31 have been examined on their merits.
Withdrawn Objections & Rejections
The objections and rejections presented herein represent the full set of objections and rejections currently pending in the application. Any objections or rejections not specifically reiterated are hereby withdrawn.
The rejection of claims 1, 5-8, 12-13, 16-17, 21-23, 25, and 31 under 35 U.S.C. 103 as being unpatentable over Nelson et al. (WO2018075591A1, published 04/26/2018, on IDS 08/12/2022, previously cited) in view of Fielding et al. (PLOS ONE, 2014) and Leviton et al. (Clinical and Developmental Immunology, 2013) is withdrawn upon further consideration and in order to incorporate Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022).
The rejection of claim 20 under 35 U.S.C. 103 as being unpatentable over Nelson et al. (WO2018075591A1, published 04/26/2018, on IDS 08/12/2022) Fielding et al. (PLOS ONE, 2014) and Leviton et al. (Clinical and Developmental Immunology, 2013) as applied to claims 1 and 16 above, and further in view of Becerra et al. (FEBS Letters, 1990) is withdrawn upon further consideration and in order to incorporate Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022).
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 1, 5-8, 12-13, 16-17, 21-23, 25, and 31 are rejected under 35 U.S.C. 103 as being unpatentable over Nelson et al. (WO2018075591A1, published 04/26/2018, on IDS 08/12/2022, previously cited) in view of Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022).
In regards to claim 1, Nelson teaches a recombinant HCMV vector comprising a nucleic acid sequence encoding heterologous antigen, wherein the recombinant HCMV vector does not express UL128 and UL130 (Claims 1 and 7; Fig. 4).
Nelson does not explicitly teach that the vector does not comprise UL18.
However, Browne teaches a HCMV with a deleted UL18 genes (Title, Abstract, p6784). Browne also teaches that UL18 is dispensable, not required for HCMV growth in culture, and is a useful site for insertion of other genes in the HCMV genome (Abstract, p6784; p6785 right column).
Therefore, a person of ordinary skill in the art would have been motivated to modify the HCMV of Nelson and knock-out the UL18 gene in order to take advantage of this site and insert other genes. Furthermore, because Browne teaches that it is dispensable and teaches that UL18 can be knocked out of the HCMV genome, it could have been done with predictable results and a reasonable expectation of success.
In regards to claim 5, Nelson also teaches that that the vector also lacks UL146 and UL147 (claim 1; Fig. 4).
In regards to claim 6, Nelson also teaches that vectors do not express an active UL128, UL130, U146, UL147 protein due to the presence of a mutation in the nucleic acid sequence encoding UL128, UL130, UL146, or UL147 (paragraph [0080]).
In regards to claim 7, Nelson teaches that vectors do not express an active ULs can be introduced by frameshift mutations in the nucleic acid sequence encoding at least UL128, UL130, UL146, or UL147 (paragraph [0080]).
In regards to claim 8, Nelson teaches that the vector comprises UL40 (paragraphs [0070, 0084]).
In regards to claims 12-13, Nelson teaches that the vector comprises nucleic acids encoding miRNA recognition elements targeting endothelial cells including miR126-3p (paragraphs [0046-0048, 0071-0071]).
In regards to claims 16, Nelson teaches that the heterologous antigen can be any of a pathogen-specific antigen, a tumor antigen or a host self-antigen (claim 33).
In regards to claim 17, Nelson teaches that the pathogen-specific antigen can be derived from HIV (claim 35).
In regards to claim 21, Nelson teaches that the pathogen-specific antigen is related to acute myelogenous leukemia (claim 36).
In regards to claim 22, Nelson teaches that the host-self antigen is an antigen derived from the variable region of a TCR (claim 34).
In regards to claim 23, Nelson teaches that the vector may be used as a composition with a pharmaceutically acceptable carrier (paragraph [0095]).
In regards to claim 25, Nelson teaches a method of generating an immune response in a subject to the at least one heterologous antigen, comprising administering to the subject the recombinant HCMV vector as in claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 25).
In regards to claim 31, Nelson teaches a method of treating or preventing a pathogenic infection in a subject, comprising administering to the subject the recombinant HCMV vector of claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 31).
Therefore, the combined teachings of Nelson, Fielding, and Leviton renders the invention unpatentable as claimed.
Claim 20 is rejected under 35 U.S.C. 103 as being unpatentable over Nelson et al. (WO2018075591A1, published 04/26/2018, on IDS 08/12/2022) in view of Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022) as applied to claims 1 and 16 above, and further in view of Becerra et al. (FEBS Letters, 1990).
In regards to claim 20, as discussed above, Nelson teaches that heterologous antigen can be either a pathogen-specific antigen derived from HIV (claims 33 and 34). Since the vectors, are used to target T cells (claim 13), a person of ordinary skill in the art would have recognized that the antigen derived from HIV also comprises an HIV epitope (which is required for T cell receptor recognition).
While Nelson is silent on the sequences of the HIV epitope, Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
In the instant case, a person of ordinary skill in the art would have been motivated to clone the cDNA corresponding to the HIV epitope corresponding to SEQ ID NO: 13 as in claim 29 because Becerra teaches that sequences with 100% hit identity with the claimed sequences (Fig. 1, p77; see also 20251031_101237_us-17-636-506-13.rpr, Result 1 S11523), encodes the HIV RNase H protein which can be used for biological studies (Abstract, Introduction, p76).
Furthermore, because, Becerra teaches constructs with amino acids sequences that are identical to the claimed sequence (Fig. 1, p77) and because Becerra teaches that it results in sufficient amounts for generation of HIV RNase H protein (Abstract, Introduction, p76), it could have been done with predictable results and a reasonable expectation of success.
Therefore, the combined teachings of Nelson, Fielding, Leviton, and Becerra renders the invention unpatentable as claimed.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 1, 5-6, 16-17 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6, 8, 12, 15, 19, 20, 25-26, 28, 30, 57, 83, 109, 135, and 143 copending Application No. 19/111,143.
Claims 8, 12-13, 21-23, 25, and 31 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6, 8, 12, 15, 19, 20, 25-26, 28, 30, 57, 83, 109, 135, and 143 copending Application No. 19/111,143 as applied claims 1 and 16 above, and further in view of Nelson et al. (WO2018075591A1, published 04/26/2018, on IDS 08/12/2022, previously cited).
Claim 20 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6, 8, 12, 15, 19, 20, 25-26, 28, 30, 57, 83, 109, 135, and 143 copending Application No. 19/111,143 as applied claims 1 and 16 above, and further in view of Becerra et al. (FEBS Letters, 1990).
Although the conflicting claims of the co-pending application are not identical to the currently prosecuted claims, they are not patently distinct from each other because said claims of both inventions are drawn to a HCMV vector and uses of that vector that does not express UL18, UL128, UL130, UL146, and UL147, and with overlapping embodiments.
In regards to the various embodiments, these were all known in prior art before the effective filing date.
As discussed above, Nelson also teaches that that the vector also lacks UL146 and UL147 (claim 1; Fig. 4); teaches that vectors do not express an active UL128, UL130, U146, UL147 protein due to the presence of a mutation in the nucleic acid sequence encoding UL128, UL130, UL146, or UL147 (paragraph [0080]); teaches that vectors do not express an active ULs can be introduced by frameshift mutations in the nucleic acid sequence encoding at least UL128, UL130, UL146, or UL147 (paragraph [0080]); teaches that the vector comprises UL40 (paragraphs [0070, 0084]); teaches that the vector comprises nucleic acids encoding miRNA recognition elements targeting endothelial cells including miR126-3p (paragraphs [0046-0048, 0071-0071]); teaches that the heterologous antigen can be any of a pathogen-specific antigen, a tumor antigen or a host self-antigen (claim 33); teaches that the pathogen-specific antigen can be derived from HIV (claim 35); teaches that the pathogen-specific antigen is related to acute myelogenous leukemia (claim 36); teaches that the host-self antigen is an antigen derived from the variable region of a TCR (claim 34); teaches that the vector may be used as a composition with a pharmaceutically acceptable carrier (paragraph [0095]); teaches a method of generating an immune response in a subject to the at least one heterologous antigen, comprising administering to the subject the recombinant HCMV vector as in claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 25); and teaches a method of treating or preventing a pathogenic infection in a subject, comprising administering to the subject the recombinant HCMV vector of claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 31).
A person or ordinary skill in the art would have been motivated to incorporate these embodiments because Nelson teaches that HCMV vectors with these embodiments are useful for immunizations (paragraph [0002]). Furthermore, because these are all known HCMV vector embodiments, it could have been done with predictable results and a reasonable expectation of success.
In regards to the sequences in claim 20, Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
In the instant case, a person of ordinary skill in the art would have been motivated to clone the cDNA corresponding to the HIV epitope corresponding to SEQ ID NO: 13 as in claim 29 because Becerra teaches that sequences with 100% hit identity with the claimed sequences (Fig. 1, p77; see also 20251031_101237_us-17-636-506-13.rpr, Result 1 S11523), encodes the HIV RNase H protein which can be used for biological studies (Abstract, Introduction, p76).
Furthermore, because, Becerra teaches constructs with amino acids sequences that are identical to the claimed sequence (Fig. 1, p77) and because Becerra teaches that it results in sufficient amounts for generation of HIV RNase H protein (Abstract, Introduction, p76), it could have been done with predictable results and a reasonable expectation of success.
This is a provisional nonstatutory double patenting rejection.
Claims 1, 5-6, and 16-17 provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-2, 4-10, 16, 18, 88-89, 96, 101-103, 114-115, and 165 of copending Application No. 17/786,186.
Claims 8, 12-13, 21-23, 25, and 31 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 11-2, 4-10, 16, 18, 88-89, 96, 101-103, 114-115, and 165 of copending Application No. 17/786,186 as applied claims 1 and 16 above, and further in view of Nelson et al. (WO2018075591A1, published 04/26/2018, on IDS 08/12/2022, previously cited).
Claim 20 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-2, 4-10, 16, 18, 88-89, 96, 101-103, 114-115, and 165 of copending Application No. 17/786,186 as applied claims 1 and 16 above, and further in view of Becerra et al. (FEBS Letters, 1990).
Although the conflicting claims of the co-pending application are not identical to the currently prosecuted claims, they are not patently distinct from each other because said claims of both inventions are drawn to a CMV vector and uses of that vector that does not express UL18, UL128, UL130, UL146, and UL147, and with overlapping embodiments.
In regards to the various embodiments, these were all known in prior art before the effective filing date.
As discussed above, Nelson teaches that vectors do not express an active ULs can be introduced by frameshift mutations in the nucleic acid sequence encoding at least UL128, UL130, UL146, or UL147 (paragraph [0080]); teaches that the vector comprises UL40 (paragraphs [0070, 0084]); teaches that the vector comprises nucleic acids encoding miRNA recognition elements targeting endothelial cells including miR126-3p (paragraphs [0046-0048, 0071-0071]); teaches that the pathogen-specific antigen is related to acute myelogenous leukemia (claim 36); teaches that the host-self antigen is an antigen derived from the variable region of a TCR (claim 34); teaches that the vector may be used as a composition with a pharmaceutically acceptable carrier (paragraph [0095]); teaches a method of generating an immune response in a subject to the at least one heterologous antigen, comprising administering to the subject the recombinant HCMV vector as in claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 25); and teaches a method of treating or preventing a pathogenic infection in a subject, comprising administering to the subject the recombinant HCMV vector of claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 31).
A person or ordinary skill in the art would have been motivated to incorporate these embodiments because Nelson teaches that HCMV vectors with these embodiments are useful for immunizations (paragraph [0002]). Furthermore, because these are all known HCMV vector embodiments, it could have been done with predictable results and a reasonable expectation of success.
In regards to the sequences in claim 20, Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
In the instant case, a person of ordinary skill in the art would have been motivated to clone the cDNA corresponding to the HIV epitope corresponding to SEQ ID NO: 13 as in claim 29 because Becerra teaches that sequences with 100% hit identity with the claimed sequences (Fig. 1, p77; see also 20251031_101237_us-17-636-506-13.rpr, Result 1 S11523), encodes the HIV RNase H protein which can be used for biological studies (Abstract, Introduction, p76).
Furthermore, because, Becerra teaches constructs with amino acids sequences that are identical to the claimed sequence (Fig. 1, p77) and because Becerra teaches that it results in sufficient amounts for generation of HIV RNase H protein (Abstract, Introduction, p76), it could have been done with predictable results and a reasonable expectation of success.
This is a provisional nonstatutory double patenting rejection.
Claims 1, 5-6, 16-17 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6 of U.S. Patent No. 12/599,658B2 in view of Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022).
Claims 8, 12-13, 21-23, 25, and 31 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6 of U.S. Patent No. 12/599,658B2 in view of Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022) as applied claims 1 and 16 above, and further in view of Nelson et al. (WO2018075591A1, published 04/26/2018, on IDS 08/12/2022, previously cited).
Claim 20 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6, 8, 12, 15, 19, 20, 25-26, 28, 30, 57, 83, 109, 135, and 143 copending Application No. 19/111,143 as applied claims 1 and 16 above, and further in view of Becerra et al. (FEBS Letters, 1990).
Although the conflicting claims of the patent are not identical to the currently prosecuted claims, they are not patently distinct from each other because said claims of both inventions are drawn to a CMV vector and uses of that vector that does not express UL128, UL130, UL146, and UL147, and with overlapping embodiments.
The patent not explicitly require that the vector does not comprise UL18.
However, Browne teaches a HCMV with a deleted UL18 genes (Title, Abstract, p6784). Browne also teaches that UL18 is dispensable, not required for HCMV growth in culture, and is a useful site for insertion of other genes in the HCMV genome (Abstract, p6784; p6785 right column).
Therefore, a person of ordinary skill in the art would have been motivated to modify the HCMV of Nelson and knock-out the UL18 gene in order to take advantage of this site and insert other genes. Furthermore, because Browne teaches that it is dispensable and teaches that UL18 can be knocked out of the HCMV genome, it could have been done with predictable results and a reasonable expectation of success.
In regards to the various embodiments, these were all known in prior art before the effective filing date.
As discussed above, Nelson teaches that vectors do not express an active ULs can be introduced by frameshift mutations in the nucleic acid sequence encoding at least UL128, UL130, UL146, or UL147 (paragraph [0080]); teaches that the vector comprises UL40 (paragraphs [0070, 0084]); teaches that the vector comprises nucleic acids encoding miRNA recognition elements targeting endothelial cells including miR126-3p (paragraphs [0046-0048, 0071-0071]); teaches that the pathogen-specific antigen is related to acute myelogenous leukemia (claim 36); teaches that the host-self antigen is an antigen derived from the variable region of a TCR (claim 34); teaches that the vector may be used as a composition with a pharmaceutically acceptable carrier (paragraph [0095]); teaches a method of generating an immune response in a subject to the at least one heterologous antigen, comprising administering to the subject the recombinant HCMV vector as in claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 25); and teaches a method of treating or preventing a pathogenic infection in a subject, comprising administering to the subject the recombinant HCMV vector of claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 31).
A person or ordinary skill in the art would have been motivated to incorporate these embodiments because Nelson teaches that HCMV vectors with these embodiments are useful for immunizations (paragraph [0002]). Furthermore, because these are all known HCMV vector embodiments, it could have been done with predictable results and a reasonable expectation of success.
In regards to the sequences in claim 20, Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
In the instant case, a person of ordinary skill in the art would have been motivated to clone the cDNA corresponding to the HIV epitope corresponding to SEQ ID NO: 13 as in claim 29 because Becerra teaches that sequences with 100% hit identity with the claimed sequences (Fig. 1, p77; see also 20251031_101237_us-17-636-506-13.rpr, Result 1 S11523), encodes the HIV RNase H protein which can be used for biological studies (Abstract, Introduction, p76).
Furthermore, because, Becerra teaches constructs with amino acids sequences that are identical to the claimed sequence (Fig. 1, p77) and because Becerra teaches that it results in sufficient amounts for generation of HIV RNase H protein (Abstract, Introduction, p76), it could have been done with predictable results and a reasonable expectation of success.
Claim 1 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 12-13 of U.S. Patent No. 10,995,121 in view of Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022).
Claims 5-8, 12-13, 16-17, 20-23, 25, and 31 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 12-13 of U.S. Patent No. 10,995,121 in view of Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022) as applied claim 1 above, and further in view of Nelson et al. (WO2018075591A1, published 04/26/2018, on IDS 08/12/2022, previously cited).
Claim 20 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6, 8, 12, 15, 19, 20, 25-26, 28, 30, 57, 83, 109, 135, and 143 copending Application No. 19/111,143 as applied claims 1 and 16 above, and further in view of Becerra et al. (FEBS Letters, 1990).
Although the conflicting claims of the patent are not identical to the currently prosecuted claims, they are not patently distinct from each other because said claims of both inventions are drawn to a CMV vector that does not express UL128 and UL130.
The patent not explicitly require that the vector does not comprise UL18.
However, Browne teaches a HCMV with a deleted UL18 genes (Title, Abstract, p6784). Browne also teaches that UL18 is dispensable, not required for HCMV growth in culture, and is a useful site for insertion of other genes in the HCMV genome (Abstract, p6784; p6785 right column).
Therefore, a person of ordinary skill in the art would have been motivated to modify the HCMV of Nelson and knock-out the UL18 gene in order to take advantage of this site and insert other genes. Furthermore, because Browne teaches that it is dispensable and teaches that UL18 can be knocked out of the HCMV genome, it could have been done with predictable results and a reasonable expectation of success.
In regards to the various embodiments, these were all known in prior art before the effective filing date.
As discussed above, Nelson also teaches that that the vector also lacks UL146 and UL147 (claim 1; Fig. 4); teaches that vectors do not express an active UL128, UL130, U146, UL147 protein due to the presence of a mutation in the nucleic acid sequence encoding UL128, UL130, UL146, or UL147 (paragraph [0080]); teaches that vectors do not express an active ULs can be introduced by frameshift mutations in the nucleic acid sequence encoding at least UL128, UL130, UL146, or UL147 (paragraph [0080]); teaches that the vector comprises UL40 (paragraphs [0070, 0084]); teaches that the vector comprises nucleic acids encoding miRNA recognition elements targeting endothelial cells including miR126-3p (paragraphs [0046-0048, 0071-0071]); teaches that the heterologous antigen can be any of a pathogen-specific antigen, a tumor antigen or a host self-antigen (claim 33); teaches that the pathogen-specific antigen can be derived from HIV (claim 35); teaches that the pathogen-specific antigen is related to acute myelogenous leukemia (claim 36); teaches that the host-self antigen is an antigen derived from the variable region of a TCR (claim 34); teaches that the vector may be used as a composition with a pharmaceutically acceptable carrier (paragraph [0095]); teaches a method of generating an immune response in a subject to the at least one heterologous antigen, comprising administering to the subject the recombinant HCMV vector as in claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 25); and teaches a method of treating or preventing a pathogenic infection in a subject, comprising administering to the subject the recombinant HCMV vector of claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 31).
A person or ordinary skill in the art would have been motivated to incorporate these embodiments because Nelson teaches that HCMV vectors with these embodiments are useful for immunizations (paragraph [0002]). Furthermore, because these are all known HCMV vector embodiments, it could have been done with predictable results and a reasonable expectation of success.
In regards to the sequences in claim 20, Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
In the instant case, a person of ordinary skill in the art would have been motivated to clone the cDNA corresponding to the HIV epitope corresponding to SEQ ID NO: 13 as in claim 29 because Becerra teaches that sequences with 100% hit identity with the claimed sequences (Fig. 1, p77; see also 20251031_101237_us-17-636-506-13.rpr, Result 1 S11523), encodes the HIV RNase H protein which can be used for biological studies (Abstract, Introduction, p76).
Furthermore, because, Becerra teaches constructs with amino acids sequences that are identical to the claimed sequence (Fig. 1, p77) and because Becerra teaches that it results in sufficient amounts for generation of HIV RNase H protein (Abstract, Introduction, p76), it could have been done with predictable results and a reasonable expectation of success.
Claim 1 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 14-15 of U.S. Patent No. 11,692,012 in view of Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022).
Claims 5-8, 12-13, 16-17, 20-23, 25, and 31 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 14-15 of U.S. Patent No. 11,692,012 in view of Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022) as applied claim 1 above, and further in view of Nelson et al. (WO2018075591A1, published 04/26/2018, on IDS 08/12/2022, previously cited).
Claim 20 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6, 8, 12, 15, 19, 20, 25-26, 28, 30, 57, 83, 109, 135, and 143 copending Application No. 19/111,143 as applied claims 1 and 16 above, and further in view of Becerra et al. (FEBS Letters, 1990).
Although the conflicting claims of the patent are not identical to the currently prosecuted claims, they are not patently distinct from each other because said claims of both inventions are drawn to a CMV vector that does not express UL128 and UL130.
The patent not explicitly require that the vector does not comprise UL18.
However, Browne teaches a HCMV with a deleted UL18 genes (Title, Abstract, p6784). Browne also teaches that UL18 is dispensable, not required for HCMV growth in culture, and is a useful site for insertion of other genes in the HCMV genome (Abstract, p6784; p6785 right column).
Therefore, a person of ordinary skill in the art would have been motivated to modify the HCMV of Nelson and knock-out the UL18 gene in order to take advantage of this site and insert other genes. Furthermore, because Browne teaches that it is dispensable and teaches that UL18 can be knocked out of the HCMV genome, it could have been done with predictable results and a reasonable expectation of success.
In regards to the various embodiments, these were all known in prior art before the effective filing date.
As discussed above, Nelson also teaches that that the vector also lacks UL146 and UL147 (claim 1; Fig. 4); teaches that vectors do not express an active UL128, UL130, U146, UL147 protein due to the presence of a mutation in the nucleic acid sequence encoding UL128, UL130, UL146, or UL147 (paragraph [0080]); teaches that vectors do not express an active ULs can be introduced by frameshift mutations in the nucleic acid sequence encoding at least UL128, UL130, UL146, or UL147 (paragraph [0080]); teaches that the vector comprises UL40 (paragraphs [0070, 0084]); teaches that the vector comprises nucleic acids encoding miRNA recognition elements targeting endothelial cells including miR126-3p (paragraphs [0046-0048, 0071-0071]); teaches that the heterologous antigen can be any of a pathogen-specific antigen, a tumor antigen or a host self-antigen (claim 33); teaches that the pathogen-specific antigen can be derived from HIV (claim 35); teaches that the pathogen-specific antigen is related to acute myelogenous leukemia (claim 36); teaches that the host-self antigen is an antigen derived from the variable region of a TCR (claim 34); teaches that the vector may be used as a composition with a pharmaceutically acceptable carrier (paragraph [0095]); teaches a method of generating an immune response in a subject to the at least one heterologous antigen, comprising administering to the subject the recombinant HCMV vector as in claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 25); and teaches a method of treating or preventing a pathogenic infection in a subject, comprising administering to the subject the recombinant HCMV vector of claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 31).
A person or ordinary skill in the art would have been motivated to incorporate these embodiments because Nelson teaches that HCMV vectors with these embodiments are useful for immunizations (paragraph [0002]). Furthermore, because these are all known HCMV vector embodiments, it could have been done with predictable results and a reasonable expectation of success.
In regards to the sequences in claim 20, Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
In the instant case, a person of ordinary skill in the art would have been motivated to clone the cDNA corresponding to the HIV epitope corresponding to SEQ ID NO: 13 as in claim 29 because Becerra teaches that sequences with 100% hit identity with the claimed sequences (Fig. 1, p77; see also 20251031_101237_us-17-636-506-13.rpr, Result 1 S11523), encodes the HIV RNase H protein which can be used for biological studies (Abstract, Introduction, p76).
Furthermore, because, Becerra teaches constructs with amino acids sequences that are identical to the claimed sequence (Fig. 1, p77) and because Becerra teaches that it results in sufficient amounts for generation of HIV RNase H protein (Abstract, Introduction, p76), it could have been done with predictable results and a reasonable expectation of success.
Claims 1, 5-6, 16-17 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-10 of U.S. Patent No. 11,266,732 in view of Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022).
Claims 8, 12-13, 21-23, 25, and 31 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-10 of U.S. Patent No. 11,266,732 in view of Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022) as applied claims 1 and 16 above, and further in view of Nelson et al. (WO2018075591A1, published 04/26/2018, on IDS 08/12/2022, previously cited).
Claim 20 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6, 8, 12, 15, 19, 20, 25-26, 28, 30, 57, 83, 109, 135, and 143 copending Application No. 19/111,143 as applied claims 1 and 16 above, and further in view of Becerra et al. (FEBS Letters, 1990).
Although the conflicting claims of the patent are not identical to the currently prosecuted claims, they are not patently distinct from each other because said claims of both inventions are drawn to a CMV vector and uses of that vector that does not express UL128, UL130, UL146, and UL147, and with overlapping embodiments.
The patent not explicitly require that the vector does not comprise UL18.
However, Browne teaches a HCMV with a deleted UL18 genes (Title, Abstract, p6784). Browne also teaches that UL18 is dispensable, not required for HCMV growth in culture, and is a useful site for insertion of other genes in the HCMV genome (Abstract, p6784; p6785 right column).
Therefore, a person of ordinary skill in the art would have been motivated to modify the HCMV of Nelson and knock-out the UL18 gene in order to take advantage of this site and insert other genes. Furthermore, because Browne teaches that it is dispensable and teaches that UL18 can be knocked out of the HCMV genome, it could have been done with predictable results and a reasonable expectation of success.
In regards to the various embodiments, these were all known in prior art before the effective filing date.
As discussed above, Nelson teaches that vectors do not express an active ULs can be introduced by frameshift mutations in the nucleic acid sequence encoding at least UL128, UL130, UL146, or UL147 (paragraph [0080]); teaches that the vector comprises UL40 (paragraphs [0070, 0084]); teaches that the vector comprises nucleic acids encoding miRNA recognition elements targeting endothelial cells including miR126-3p (paragraphs [0046-0048, 0071-0071]); teaches that the pathogen-specific antigen is related to acute myelogenous leukemia (claim 36); teaches that the host-self antigen is an antigen derived from the variable region of a TCR (claim 34); teaches that the vector may be used as a composition with a pharmaceutically acceptable carrier (paragraph [0095]); teaches a method of generating an immune response in a subject to the at least one heterologous antigen, comprising administering to the subject the recombinant HCMV vector as in claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 25); and teaches a method of treating or preventing a pathogenic infection in a subject, comprising administering to the subject the recombinant HCMV vector of claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 31).
A person or ordinary skill in the art would have been motivated to incorporate these embodiments because Nelson teaches that HCMV vectors with these embodiments are useful for immunizations (paragraph [0002]). Furthermore, because these are all known HCMV vector embodiments, it could have been done with predictable results and a reasonable expectation of success.
In regards to the sequences in claim 20, Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
In the instant case, a person of ordinary skill in the art would have been motivated to clone the cDNA corresponding to the HIV epitope corresponding to SEQ ID NO: 13 as in claim 29 because Becerra teaches that sequences with 100% hit identity with the claimed sequences (Fig. 1, p77; see also 20251031_101237_us-17-636-506-13.rpr, Result 1 S11523), encodes the HIV RNase H protein which can be used for biological studies (Abstract, Introduction, p76).
Furthermore, because, Becerra teaches constructs with amino acids sequences that are identical to the claimed sequence (Fig. 1, p77) and because Becerra teaches that it results in sufficient amounts for generation of HIV RNase H protein (Abstract, Introduction, p76), it could have been done with predictable results and a reasonable expectation of success.
Claim 1 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of U.S. Patent No. 11,091,779 in view of Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022).
Claims 5-8, 12-13, 16-17, 20-23, 25, and 31 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-20 of U.S. Patent No. 11,091,779 in view of Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022) as applied claim 1 above, and further in view of Nelson et al. (WO2018075591A1, published 04/26/2018, on IDS 08/12/2022, previously cited).
Claim 20 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6, 8, 12, 15, 19, 20, 25-26, 28, 30, 57, 83, 109, 135, and 143 copending Application No. 19/111,143 as applied claims 1 and 16 above, and further in view of Becerra et al. (FEBS Letters, 1990).
Although the conflicting claims of the patent are not identical to the currently prosecuted claims, they are not patently distinct from each other because said claims of both inventions are drawn to a CMV vector that does not express UL128 and UL130.
The patent not explicitly require that the vector does not comprise UL18.
However, Browne teaches a HCMV with a deleted UL18 genes (Title, Abstract, p6784). Browne also teaches that UL18 is dispensable, not required for HCMV growth in culture, and is a useful site for insertion of other genes in the HCMV genome (Abstract, p6784; p6785 right column).
Therefore, a person of ordinary skill in the art would have been motivated to modify the HCMV of Nelson and knock-out the UL18 gene in order to take advantage of this site and insert other genes. Furthermore, because Browne teaches that it is dispensable and teaches that UL18 can be knocked out of the HCMV genome, it could have been done with predictable results and a reasonable expectation of success.
In regards to the various embodiments, these were all known in prior art before the effective filing date.
As discussed above, Nelson also teaches that that the vector also lacks UL146 and UL147 (claim 1; Fig. 4); teaches that vectors do not express an active UL128, UL130, U146, UL147 protein due to the presence of a mutation in the nucleic acid sequence encoding UL128, UL130, UL146, or UL147 (paragraph [0080]); teaches that vectors do not express an active ULs can be introduced by frameshift mutations in the nucleic acid sequence encoding at least UL128, UL130, UL146, or UL147 (paragraph [0080]); teaches that the vector comprises UL40 (paragraphs [0070, 0084]); teaches that the vector comprises nucleic acids encoding miRNA recognition elements targeting endothelial cells including miR126-3p (paragraphs [0046-0048, 0071-0071]); teaches that the heterologous antigen can be any of a pathogen-specific antigen, a tumor antigen or a host self-antigen (claim 33); teaches that the pathogen-specific antigen can be derived from HIV (claim 35); teaches that the pathogen-specific antigen is related to acute myelogenous leukemia (claim 36); teaches that the host-self antigen is an antigen derived from the variable region of a TCR (claim 34); teaches that the vector may be used as a composition with a pharmaceutically acceptable carrier (paragraph [0095]); teaches a method of generating an immune response in a subject to the at least one heterologous antigen, comprising administering to the subject the recombinant HCMV vector as in claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 25); and teaches a method of treating or preventing a pathogenic infection in a subject, comprising administering to the subject the recombinant HCMV vector of claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 31).
A person or ordinary skill in the art would have been motivated to incorporate these embodiments because Nelson teaches that HCMV vectors with these embodiments are useful for immunizations (paragraph [0002]). Furthermore, because these are all known HCMV vector embodiments, it could have been done with predictable results and a reasonable expectation of success.
In regards to the sequences in claim 20, Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
In the instant case, a person of ordinary skill in the art would have been motivated to clone the cDNA corresponding to the HIV epitope corresponding to SEQ ID NO: 13 as in claim 29 because Becerra teaches that sequences with 100% hit identity with the claimed sequences (Fig. 1, p77; see also 20251031_101237_us-17-636-506-13.rpr, Result 1 S11523), encodes the HIV RNase H protein which can be used for biological studies (Abstract, Introduction, p76).
Furthermore, because, Becerra teaches constructs with amino acids sequences that are identical to the claimed sequence (Fig. 1, p77) and because Becerra teaches that it results in sufficient amounts for generation of HIV RNase H protein (Abstract, Introduction, p76), it could have been done with predictable results and a reasonable expectation of success.
Claims 1, 5-6, 16-17 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-64 of U.S. Patent No. 10,532,099 in view of Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022).
Claims 8, 12-13, 21-23, 25, and 31 are rejected on the ground of nonstatutory double patenting as being unpatentable over 1-64 of U.S. Patent No. 10,532,099 in view of Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022) as applied claims 1 and 16 above, and further in view of Nelson et al. (WO2018075591A1, published 04/26/2018, on IDS 08/12/2022, previously cited).
Claim 20 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6, 8, 12, 15, 19, 20, 25-26, 28, 30, 57, 83, 109, 135, and 143 copending Application No. 19/111,143 as applied claims 1 and 16 above, and further in view of Becerra et al. (FEBS Letters, 1990).
Although the conflicting claims of the patent are not identical to the currently prosecuted claims, they are not patently distinct from each other because said claims of both inventions are drawn to a CMV vector and uses of that vector that does not express UL128, UL130, UL146, and UL147, and with overlapping embodiments.
The patent not explicitly require that the vector does not comprise UL18.
However, Browne teaches a HCMV with a deleted UL18 genes (Title, Abstract, p6784). Browne also teaches that UL18 is dispensable, not required for HCMV growth in culture, and is a useful site for insertion of other genes in the HCMV genome (Abstract, p6784; p6785 right column).
Therefore, a person of ordinary skill in the art would have been motivated to modify the HCMV of Nelson and knock-out the UL18 gene in order to take advantage of this site and insert other genes. Furthermore, because Browne teaches that it is dispensable and teaches that UL18 can be knocked out of the HCMV genome, it could have been done with predictable results and a reasonable expectation of success.
In regards to the various embodiments, these were all known in prior art before the effective filing date.
As discussed above, Nelson teaches that vectors do not express an active ULs can be introduced by frameshift mutations in the nucleic acid sequence encoding at least UL128, UL130, UL146, or UL147 (paragraph [0080]); teaches that the vector comprises UL40 (paragraphs [0070, 0084]); teaches that the vector comprises nucleic acids encoding miRNA recognition elements targeting endothelial cells including miR126-3p (paragraphs [0046-0048, 0071-0071]); teaches that the pathogen-specific antigen is related to acute myelogenous leukemia (claim 36); teaches that the host-self antigen is an antigen derived from the variable region of a TCR (claim 34); teaches that the vector may be used as a composition with a pharmaceutically acceptable carrier (paragraph [0095]); teaches a method of generating an immune response in a subject to the at least one heterologous antigen, comprising administering to the subject the recombinant HCMV vector as in claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 25); and teaches a method of treating or preventing a pathogenic infection in a subject, comprising administering to the subject the recombinant HCMV vector of claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 31).
A person or ordinary skill in the art would have been motivated to incorporate these embodiments because Nelson teaches that HCMV vectors with these embodiments are useful for immunizations (paragraph [0002]). Furthermore, because these are all known HCMV vector embodiments, it could have been done with predictable results and a reasonable expectation of success.
In regards to the sequences in claim 20, Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
In the instant case, a person of ordinary skill in the art would have been motivated to clone the cDNA corresponding to the HIV epitope corresponding to SEQ ID NO: 13 as in claim 29 because Becerra teaches that sequences with 100% hit identity with the claimed sequences (Fig. 1, p77; see also 20251031_101237_us-17-636-506-13.rpr, Result 1 S11523), encodes the HIV RNase H protein which can be used for biological studies (Abstract, Introduction, p76).
Furthermore, because, Becerra teaches constructs with amino acids sequences that are identical to the claimed sequence (Fig. 1, p77) and because Becerra teaches that it results in sufficient amounts for generation of HIV RNase H protein (Abstract, Introduction, p76), it could have been done with predictable results and a reasonable expectation of success.
Claims 1, 5-6, 8, 12-13, 16-17, 21-23, 25, and 31 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 20 of U.S. Patent No. 11,091,775 in view of Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022) and Nelson et al. (WO2018075591A1, published 04/26/2018, on IDS 08/12/2022, previously cited).
Claim 20 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6, 8, 12, 15, 19, 20, 25-26, 28, 30, 57, 83, 109, 135, and 143 copending Application No. 19/111,143 as applied claims 1 and 16 above, and further in view of Becerra et al. (FEBS Letters, 1990).
Although the conflicting claims of the patent are not identical to the currently prosecuted claims, they are not patently distinct from each other because said claims of both inventions are drawn to a CMV vector and uses of that vector that does not express UL130.
The patent not explicitly require that the vector does not comprise UL18.
However, Browne teaches a HCMV with a deleted UL18 genes (Title, Abstract, p6784). Browne also teaches that UL18 is dispensable, not required for HCMV growth in culture, and is a useful site for insertion of other genes in the HCMV genome (Abstract, p6784; p6785 right column).
Therefore, a person of ordinary skill in the art would have been motivated to modify the HCMV of Nelson and knock-out the UL18 gene in order to take advantage of this site and insert other genes. Furthermore, because Browne teaches that it is dispensable and teaches that UL18 can be knocked out of the HCMV genome, it could have been done with predictable results and a reasonable expectation of success.
In regards to the various embodiments, these were all known in prior art before the effective filing date.
As discussed above, Nelson also teaches that that the vector also lacks UL146 and UL147 (claim 1; Fig. 4); teaches that vectors do not express an active UL128, UL130, U146, UL147 protein due to the presence of a mutation in the nucleic acid sequence encoding UL128, UL130, UL146, or UL147 (paragraph [0080]); teaches that vectors do not express an active ULs can be introduced by frameshift mutations in the nucleic acid sequence encoding at least UL128, UL130, UL146, or UL147 (paragraph [0080]); teaches that the vector comprises UL40 (paragraphs [0070, 0084]); teaches that the vector comprises nucleic acids encoding miRNA recognition elements targeting endothelial cells including miR126-3p (paragraphs [0046-0048, 0071-0071]); teaches that the heterologous antigen can be any of a pathogen-specific antigen, a tumor antigen or a host self-antigen (claim 33); teaches that the pathogen-specific antigen can be derived from HIV (claim 35); teaches that the pathogen-specific antigen is related to acute myelogenous leukemia (claim 36); teaches that the host-self antigen is an antigen derived from the variable region of a TCR (claim 34); teaches that the vector may be used as a composition with a pharmaceutically acceptable carrier (paragraph [0095]); teaches a method of generating an immune response in a subject to the at least one heterologous antigen, comprising administering to the subject the recombinant HCMV vector as in claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 25); and teaches a method of treating or preventing a pathogenic infection in a subject, comprising administering to the subject the recombinant HCMV vector of claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 31).
A person or ordinary skill in the art would have been motivated to incorporate these embodiments because Nelson teaches that HCMV vectors with these embodiments are useful for immunizations (paragraph [0002]). Furthermore, because these are all known HCMV vector embodiments, it could have been done with predictable results and a reasonable expectation of success.
In regards to the sequences in claim 20, Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
In the instant case, a person of ordinary skill in the art would have been motivated to clone the cDNA corresponding to the HIV epitope corresponding to SEQ ID NO: 13 as in claim 29 because Becerra teaches that sequences with 100% hit identity with the claimed sequences (Fig. 1, p77; see also 20251031_101237_us-17-636-506-13.rpr, Result 1 S11523), encodes the HIV RNase H protein which can be used for biological studies (Abstract, Introduction, p76).
Furthermore, because, Becerra teaches constructs with amino acids sequences that are identical to the claimed sequence (Fig. 1, p77) and because Becerra teaches that it results in sufficient amounts for generation of HIV RNase H protein (Abstract, Introduction, p76), it could have been done with predictable results and a reasonable expectation of success.
Claims 1, 5-6, 8, 12-13, 16-17, 21-23, 25, and 31 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 18 of U.S. Patent No. 11,834,669 in view of Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022) and Nelson et al. (WO2018075591A1, published 04/26/2018, on IDS 08/12/2022, previously cited).
Claim 20 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6, 8, 12, 15, 19, 20, 25-26, 28, 30, 57, 83, 109, 135, and 143 copending Application No. 19/111,143 as applied claims 1 and 16 above, and further in view of Becerra et al. (FEBS Letters, 1990).
Although the conflicting claims of the patent are not identical to the currently prosecuted claims, they are not patently distinct from each other because said claims of both inventions are drawn to a CMV vector and uses of that vector that does not express UL130.
The patent not explicitly require that the vector does not comprise UL18.
However, Browne teaches a HCMV with a deleted UL18 genes (Title, Abstract, p6784). Browne also teaches that UL18 is dispensable, not required for HCMV growth in culture, and is a useful site for insertion of other genes in the HCMV genome (Abstract, p6784; p6785 right column).
Therefore, a person of ordinary skill in the art would have been motivated to modify the HCMV of Nelson and knock-out the UL18 gene in order to take advantage of this site and insert other genes. Furthermore, because Browne teaches that it is dispensable and teaches that UL18 can be knocked out of the HCMV genome, it could have been done with predictable results and a reasonable expectation of success.
In regards to the various embodiments, these were all known in prior art before the effective filing date.
As discussed above, Nelson also teaches that that the vector also lacks UL146 and UL147 (claim 1; Fig. 4); teaches that vectors do not express an active UL128, UL130, U146, UL147 protein due to the presence of a mutation in the nucleic acid sequence encoding UL128, UL130, UL146, or UL147 (paragraph [0080]); teaches that vectors do not express an active ULs can be introduced by frameshift mutations in the nucleic acid sequence encoding at least UL128, UL130, UL146, or UL147 (paragraph [0080]); teaches that the vector comprises UL40 (paragraphs [0070, 0084]); teaches that the vector comprises nucleic acids encoding miRNA recognition elements targeting endothelial cells including miR126-3p (paragraphs [0046-0048, 0071-0071]); teaches that the heterologous antigen can be any of a pathogen-specific antigen, a tumor antigen or a host self-antigen (claim 33); teaches that the pathogen-specific antigen can be derived from HIV (claim 35); teaches that the pathogen-specific antigen is related to acute myelogenous leukemia (claim 36); teaches that the host-self antigen is an antigen derived from the variable region of a TCR (claim 34); teaches that the vector may be used as a composition with a pharmaceutically acceptable carrier (paragraph [0095]); teaches a method of generating an immune response in a subject to the at least one heterologous antigen, comprising administering to the subject the recombinant HCMV vector as in claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 25); and teaches a method of treating or preventing a pathogenic infection in a subject, comprising administering to the subject the recombinant HCMV vector of claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 31).
A person or ordinary skill in the art would have been motivated to incorporate these embodiments because Nelson teaches that HCMV vectors with these embodiments are useful for immunizations (paragraph [0002]). Furthermore, because these are all known HCMV vector embodiments, it could have been done with predictable results and a reasonable expectation of success.
In regards to the sequences in claim 20, Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
In the instant case, a person of ordinary skill in the art would have been motivated to clone the cDNA corresponding to the HIV epitope corresponding to SEQ ID NO: 13 as in claim 29 because Becerra teaches that sequences with 100% hit identity with the claimed sequences (Fig. 1, p77; see also 20251031_101237_us-17-636-506-13.rpr, Result 1 S11523), encodes the HIV RNase H protein which can be used for biological studies (Abstract, Introduction, p76).
Furthermore, because, Becerra teaches constructs with amino acids sequences that are identical to the claimed sequence (Fig. 1, p77) and because Becerra teaches that it results in sufficient amounts for generation of HIV RNase H protein (Abstract, Introduction, p76), it could have been done with predictable results and a reasonable expectation of success.
Claim 1 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-26 of U.S. Patent No. 10,894,078 in view of Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022).
Claims 5-8, 12-13, 16-17, 20-23, 25, and 31 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-26 of U.S. Patent No. 10,894,078 in view of Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022) as applied claim 1 above, and further in view of Nelson et al. (WO2018075591A1, published 04/26/2018, on IDS 08/12/2022, previously cited).
Claim 20 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6, 8, 12, 15, 19, 20, 25-26, 28, 30, 57, 83, 109, 135, and 143 copending Application No. 19/111,143 as applied claims 1 and 16 above, and further in view of Becerra et al. (FEBS Letters, 1990).
Although the conflicting claims of the patent are not identical to the currently prosecuted claims, they are not patently distinct from each other because said claims of both inventions are drawn to a CMV vector that does not express UL128 and UL130.
The patent not explicitly require that the vector does not comprise UL18.
However, Browne teaches a HCMV with a deleted UL18 genes (Title, Abstract, p6784). Browne also teaches that UL18 is dispensable, not required for HCMV growth in culture, and is a useful site for insertion of other genes in the HCMV genome (Abstract, p6784; p6785 right column).
Therefore, a person of ordinary skill in the art would have been motivated to modify the HCMV of Nelson and knock-out the UL18 gene in order to take advantage of this site and insert other genes. Furthermore, because Browne teaches that it is dispensable and teaches that UL18 can be knocked out of the HCMV genome, it could have been done with predictable results and a reasonable expectation of success.
In regards to the various embodiments, these were all known in prior art before the effective filing date.
As discussed above, Nelson also teaches that that the vector also lacks UL146 and UL147 (claim 1; Fig. 4); teaches that vectors do not express an active UL128, UL130, U146, UL147 protein due to the presence of a mutation in the nucleic acid sequence encoding UL128, UL130, UL146, or UL147 (paragraph [0080]); teaches that vectors do not express an active ULs can be introduced by frameshift mutations in the nucleic acid sequence encoding at least UL128, UL130, UL146, or UL147 (paragraph [0080]); teaches that the vector comprises UL40 (paragraphs [0070, 0084]); teaches that the vector comprises nucleic acids encoding miRNA recognition elements targeting endothelial cells including miR126-3p (paragraphs [0046-0048, 0071-0071]); teaches that the heterologous antigen can be any of a pathogen-specific antigen, a tumor antigen or a host self-antigen (claim 33); teaches that the pathogen-specific antigen can be derived from HIV (claim 35); teaches that the pathogen-specific antigen is related to acute myelogenous leukemia (claim 36); teaches that the host-self antigen is an antigen derived from the variable region of a TCR (claim 34); teaches that the vector may be used as a composition with a pharmaceutically acceptable carrier (paragraph [0095]); teaches a method of generating an immune response in a subject to the at least one heterologous antigen, comprising administering to the subject the recombinant HCMV vector as in claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 25); and teaches a method of treating or preventing a pathogenic infection in a subject, comprising administering to the subject the recombinant HCMV vector of claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 31).
A person or ordinary skill in the art would have been motivated to incorporate these embodiments because Nelson teaches that HCMV vectors with these embodiments are useful for immunizations (paragraph [0002]). Furthermore, because these are all known HCMV vector embodiments, it could have been done with predictable results and a reasonable expectation of success.
In regards to the sequences in claim 20, Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
In the instant case, a person of ordinary skill in the art would have been motivated to clone the cDNA corresponding to the HIV epitope corresponding to SEQ ID NO: 13 as in claim 29 because Becerra teaches that sequences with 100% hit identity with the claimed sequences (Fig. 1, p77; see also 20251031_101237_us-17-636-506-13.rpr, Result 1 S11523), encodes the HIV RNase H protein which can be used for biological studies (Abstract, Introduction, p76).
Furthermore, because, Becerra teaches constructs with amino acids sequences that are identical to the claimed sequence (Fig. 1, p77) and because Becerra teaches that it results in sufficient amounts for generation of HIV RNase H protein (Abstract, Introduction, p76), it could have been done with predictable results and a reasonable expectation of success.
Claim 1 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-24 of U.S. Patent No. 11,554,168 in view of Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022).
Claims 5-8, 12-13, 16-17, 20-23, 25, and 31 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-24 of U.S. Patent No. 11,554,168 in view of Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022) as applied claim 1 above, and further in view of Nelson et al. (WO2018075591A1, published 04/26/2018, on IDS 08/12/2022, previously cited).
Claim 20 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6, 8, 12, 15, 19, 20, 25-26, 28, 30, 57, 83, 109, 135, and 143 copending Application No. 19/111,143 as applied claims 1 and 16 above, and further in view of Becerra et al. (FEBS Letters, 1990).
Although the conflicting claims of the patent are not identical to the currently prosecuted claims, they are not patently distinct from each other because said claims of both inventions are drawn to a CMV vector that does not express UL128 and UL130.
The patent not explicitly require that the vector does not comprise UL18.
However, Browne teaches a HCMV with a deleted UL18 genes (Title, Abstract, p6784). Browne also teaches that UL18 is dispensable, not required for HCMV growth in culture, and is a useful site for insertion of other genes in the HCMV genome (Abstract, p6784; p6785 right column).
Therefore, a person of ordinary skill in the art would have been motivated to modify the HCMV of Nelson and knock-out the UL18 gene in order to take advantage of this site and insert other genes. Furthermore, because Browne teaches that it is dispensable and teaches that UL18 can be knocked out of the HCMV genome, it could have been done with predictable results and a reasonable expectation of success.
In regards to the various embodiments, these were all known in prior art before the effective filing date.
As discussed above, Nelson also teaches that that the vector also lacks UL146 and UL147 (claim 1; Fig. 4); teaches that vectors do not express an active UL128, UL130, U146, UL147 protein due to the presence of a mutation in the nucleic acid sequence encoding UL128, UL130, UL146, or UL147 (paragraph [0080]); teaches that vectors do not express an active ULs can be introduced by frameshift mutations in the nucleic acid sequence encoding at least UL128, UL130, UL146, or UL147 (paragraph [0080]); teaches that the vector comprises UL40 (paragraphs [0070, 0084]); teaches that the vector comprises nucleic acids encoding miRNA recognition elements targeting endothelial cells including miR126-3p (paragraphs [0046-0048, 0071-0071]); teaches that the heterologous antigen can be any of a pathogen-specific antigen, a tumor antigen or a host self-antigen (claim 33); teaches that the pathogen-specific antigen can be derived from HIV (claim 35); teaches that the pathogen-specific antigen is related to acute myelogenous leukemia (claim 36); teaches that the host-self antigen is an antigen derived from the variable region of a TCR (claim 34); teaches that the vector may be used as a composition with a pharmaceutically acceptable carrier (paragraph [0095]); teaches a method of generating an immune response in a subject to the at least one heterologous antigen, comprising administering to the subject the recombinant HCMV vector as in claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 25); and teaches a method of treating or preventing a pathogenic infection in a subject, comprising administering to the subject the recombinant HCMV vector of claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 31).
A person or ordinary skill in the art would have been motivated to incorporate these embodiments because Nelson teaches that HCMV vectors with these embodiments are useful for immunizations (paragraph [0002]). Furthermore, because these are all known HCMV vector embodiments, it could have been done with predictable results and a reasonable expectation of success.
In regards to the sequences in claim 20, Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
In the instant case, a person of ordinary skill in the art would have been motivated to clone the cDNA corresponding to the HIV epitope corresponding to SEQ ID NO: 13 as in claim 29 because Becerra teaches that sequences with 100% hit identity with the claimed sequences (Fig. 1, p77; see also 20251031_101237_us-17-636-506-13.rpr, Result 1 S11523), encodes the HIV RNase H protein which can be used for biological studies (Abstract, Introduction, p76).
Furthermore, because, Becerra teaches constructs with amino acids sequences that are identical to the claimed sequence (Fig. 1, p77) and because Becerra teaches that it results in sufficient amounts for generation of HIV RNase H protein (Abstract, Introduction, p76), it could have been done with predictable results and a reasonable expectation of success.
Claim 1 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-28 of U.S. Patent No. 9,783,823 in view of Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022).
Claims 5-8, 12-13, 16-17, 20-23, 25, and 31 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-28 of U.S. Patent No. 9,783,823 in view of Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022) as applied claim 1 above, and further in view of Nelson et al. (WO2018075591A1, published 04/26/2018, on IDS 08/12/2022, previously cited).
Claim 20 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6, 8, 12, 15, 19, 20, 25-26, 28, 30, 57, 83, 109, 135, and 143 copending Application No. 19/111,143 as applied claims 1 and 16 above, and further in view of Becerra et al. (FEBS Letters, 1990).
Although the conflicting claims of the patent are not identical to the currently prosecuted claims, they are not patently distinct from each other because said claims of both inventions are drawn to a CMV vector that does not express UL128 and UL130.
The patent not explicitly require that the vector does not comprise UL18.
However, Browne teaches a HCMV with a deleted UL18 genes (Title, Abstract, p6784). Browne also teaches that UL18 is dispensable, not required for HCMV growth in culture, and is a useful site for insertion of other genes in the HCMV genome (Abstract, p6784; p6785 right column).
Therefore, a person of ordinary skill in the art would have been motivated to modify the HCMV of Nelson and knock-out the UL18 gene in order to take advantage of this site and insert other genes. Furthermore, because Browne teaches that it is dispensable and teaches that UL18 can be knocked out of the HCMV genome, it could have been done with predictable results and a reasonable expectation of success.
In regards to the various embodiments, these were all known in prior art before the effective filing date.
As discussed above, Nelson also teaches that that the vector also lacks UL146 and UL147 (claim 1; Fig. 4); teaches that vectors do not express an active UL128, UL130, U146, UL147 protein due to the presence of a mutation in the nucleic acid sequence encoding UL128, UL130, UL146, or UL147 (paragraph [0080]); teaches that vectors do not express an active ULs can be introduced by frameshift mutations in the nucleic acid sequence encoding at least UL128, UL130, UL146, or UL147 (paragraph [0080]); teaches that the vector comprises UL40 (paragraphs [0070, 0084]); teaches that the vector comprises nucleic acids encoding miRNA recognition elements targeting endothelial cells including miR126-3p (paragraphs [0046-0048, 0071-0071]); teaches that the heterologous antigen can be any of a pathogen-specific antigen, a tumor antigen or a host self-antigen (claim 33); teaches that the pathogen-specific antigen can be derived from HIV (claim 35); teaches that the pathogen-specific antigen is related to acute myelogenous leukemia (claim 36); teaches that the host-self antigen is an antigen derived from the variable region of a TCR (claim 34); teaches that the vector may be used as a composition with a pharmaceutically acceptable carrier (paragraph [0095]); teaches a method of generating an immune response in a subject to the at least one heterologous antigen, comprising administering to the subject the recombinant HCMV vector as in claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 25); and teaches a method of treating or preventing a pathogenic infection in a subject, comprising administering to the subject the recombinant HCMV vector of claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 31).
A person or ordinary skill in the art would have been motivated to incorporate these embodiments because Nelson teaches that HCMV vectors with these embodiments are useful for immunizations (paragraph [0002]). Furthermore, because these are all known HCMV vector embodiments, it could have been done with predictable results and a reasonable expectation of success.
In regards to the sequences in claim 20, Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
In the instant case, a person of ordinary skill in the art would have been motivated to clone the cDNA corresponding to the HIV epitope corresponding to SEQ ID NO: 13 as in claim 29 because Becerra teaches that sequences with 100% hit identity with the claimed sequences (Fig. 1, p77; see also 20251031_101237_us-17-636-506-13.rpr, Result 1 S11523), encodes the HIV RNase H protein which can be used for biological studies (Abstract, Introduction, p76).
Furthermore, because, Becerra teaches constructs with amino acids sequences that are identical to the claimed sequence (Fig. 1, p77) and because Becerra teaches that it results in sufficient amounts for generation of HIV RNase H protein (Abstract, Introduction, p76), it could have been done with predictable results and a reasonable expectation of success.
Claim 1 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-23 of U.S. Patent No. 10,316,334 in view of Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022).
Claims 5-8, 12-13, 16-17, 20-23, 25, and 31 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-23 of U.S. Patent No. 10,316,334 in view of Browne et al. (Journal of Virology, 1992, on IDS 08/12/2022) as applied claim 1 above, and further in view of Nelson et al. (WO2018075591A1, published 04/26/2018, on IDS 08/12/2022, previously cited).
Claim 20 is rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-6, 8, 12, 15, 19, 20, 25-26, 28, 30, 57, 83, 109, 135, and 143 copending Application No. 19/111,143 as applied claims 1 and 16 above, and further in view of Becerra et al. (FEBS Letters, 1990).
Although the conflicting claims of the patent are not identical to the currently prosecuted claims, they are not patently distinct from each other because said claims of both inventions are drawn to a CMV vector that does not express UL128 and UL130.
The patent not explicitly require that the vector does not comprise UL18.
However, Browne teaches a HCMV with a deleted UL18 genes (Title, Abstract, p6784). Browne also teaches that UL18 is dispensable, not required for HCMV growth in culture, and is a useful site for insertion of other genes in the HCMV genome (Abstract, p6784; p6785 right column).
Therefore, a person of ordinary skill in the art would have been motivated to modify the HCMV of Nelson and knock-out the UL18 gene in order to take advantage of this site and insert other genes. Furthermore, because Browne teaches that it is dispensable and teaches that UL18 can be knocked out of the HCMV genome, it could have been done with predictable results and a reasonable expectation of success.
In regards to the various embodiments, these were all known in prior art before the effective filing date.
As discussed above, Nelson also teaches that that the vector also lacks UL146 and UL147 (claim 1; Fig. 4); teaches that vectors do not express an active UL128, UL130, U146, UL147 protein due to the presence of a mutation in the nucleic acid sequence encoding UL128, UL130, UL146, or UL147 (paragraph [0080]); teaches that vectors do not express an active ULs can be introduced by frameshift mutations in the nucleic acid sequence encoding at least UL128, UL130, UL146, or UL147 (paragraph [0080]); teaches that the vector comprises UL40 (paragraphs [0070, 0084]); teaches that the vector comprises nucleic acids encoding miRNA recognition elements targeting endothelial cells including miR126-3p (paragraphs [0046-0048, 0071-0071]); teaches that the heterologous antigen can be any of a pathogen-specific antigen, a tumor antigen or a host self-antigen (claim 33); teaches that the pathogen-specific antigen can be derived from HIV (claim 35); teaches that the pathogen-specific antigen is related to acute myelogenous leukemia (claim 36); teaches that the host-self antigen is an antigen derived from the variable region of a TCR (claim 34); teaches that the vector may be used as a composition with a pharmaceutically acceptable carrier (paragraph [0095]); teaches a method of generating an immune response in a subject to the at least one heterologous antigen, comprising administering to the subject the recombinant HCMV vector as in claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 25); and teaches a method of treating or preventing a pathogenic infection in a subject, comprising administering to the subject the recombinant HCMV vector of claim 1 in an amount effective to elicit a CD8+ T cell response to the at least one heterologous antigen (claim 31).
A person or ordinary skill in the art would have been motivated to incorporate these embodiments because Nelson teaches that HCMV vectors with these embodiments are useful for immunizations (paragraph [0002]). Furthermore, because these are all known HCMV vector embodiments, it could have been done with predictable results and a reasonable expectation of success.
In regards to the sequences in claim 20, Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
In the instant case, a person of ordinary skill in the art would have been motivated to clone the cDNA corresponding to the HIV epitope corresponding to SEQ ID NO: 13 as in claim 29 because Becerra teaches that sequences with 100% hit identity with the claimed sequences (Fig. 1, p77; see also 20251031_101237_us-17-636-506-13.rpr, Result 1 S11523), encodes the HIV RNase H protein which can be used for biological studies (Abstract, Introduction, p76).
Furthermore, because, Becerra teaches constructs with amino acids sequences that are identical to the claimed sequence (Fig. 1, p77) and because Becerra teaches that it results in sufficient amounts for generation of HIV RNase H protein (Abstract, Introduction, p76), it could have been done with predictable results and a reasonable expectation of success.
Response to Arguments
Applicant argues that Fielding and Leviton are deficient (Remarks, p8-9).
Applicant’s arguments with respect to the claims in regards to the teachings of Fielding and Leviton have been considered but are moot because the new ground of rejection does not rely on Fielding or Leviton for any teaching or matter specifically challenged in the argument.
Instead, as above, a person of ordinary skill in the art would have been motivated to modify the HCMV of Nelson and knock-out the UL18 gene in order to take advantage of this site and insert other genes as taught by Browne. Furthermore, because Browne teaches that it is dispensable and teaches that UL18 can be knocked out of the HCMV genome, it could have been done with predictable results and a reasonable expectation of success.
Applicant argues that Becerra relates to HIV antigens, not CMV vectors (Remarks, p9-10).
Applicant’s arguments filed 05/04/2026 has been fully considered but is not persuasive.
Nelson teaches that heterologous antigen can be either a pathogen-specific antigen derived from HIV (claims 33 and 34). Since the vectors, are used to target T cells (claim 13), a person of ordinary skill in the art would have recognized that the antigen derived from HIV also comprises an HIV epitope (which is required for T cell receptor recognition).
While Nelson is silent on the sequences of the HIV epitope, Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
Applicant should note that that the successful cloning and sequencing of the cDNA encoding a known protein is obvious, and thus unpatentable, if (1) there was some suggestion or motivation in the prior art to clone the cDNA, and (2) there was a “reasonable expectation of success,” based on "detailed enabling methodology" in the prior art. Ex parte Kubin, 83 U.S.P.Q.2d (BNA) 1410 (B.P.A.I. 2007), aff'd, 561 F.3d 1351 (Fed. Cir. 2009).
In the instant case, a person of ordinary skill in the art would have been motivated to clone the cDNA corresponding to the HIV epitope corresponding to SEQ ID NO: 13 as in claim 29 because Becerra teaches that sequences with 100% hit identity with the claimed sequences (Fig. 1, p77; see also 20251031_101237_us-17-636-506-13.rpr, Result 1 S11523), encodes the HIV RNase H protein which can be used for biological studies (Abstract, Introduction, p76).
Furthermore, because, Becerra teaches constructs with amino acids sequences that are identical to the claimed sequence (Fig. 1, p77) and because Becerra teaches that it results in sufficient amounts for generation of HIV RNase H protein (Abstract, Introduction, p76), it could have been done with predictable results and a reasonable expectation of success.
In regards to the double-patenting rejections over Co-Pending Application no. 17/786,186, Applicant argues that the instant Application is the earlier filed application, and therefore, the provisional rejection is inappropriate (citing Allergan or Ex Parte Baurin; Remarks, p10-11).
Applicant’s arguments filed 05/04/2026 has been fully considered but is not persuasive.
The MPEP does not cite or provide guidance in reference to Allergan USA, Inc. v MSC Laboratories or Ex Parte Baurin.
Indeed, since MPEP 804(I)(B)(1)(b)(iii)) directs that if a provisional non-statutory double-patenting rejection is the only remaining in an application with an earlier patent term date, the provisional double-patenting rejection would be withdrawn, it suggests that provisional non-statutory double-patenting rejections should be made over co-pending applications with a later patent term date when appropriate (as it is here).
Indeed, the Federal Circuit has sustained non-statutory double patenting rejections where the reference patent has a later priority and patent-term filing date than the application under examination. For example, In re Fallaux, 564 F.3d 1313 (Fed. Cir. 2009), where the Federal Circuit affirmed the Board's ODP rejection based on these later-priority reference patents. Id. at 1319. The court acknowledged that “the unjustified patent term extension justification for obviousness-type double patenting has limited force in this case,” but it identified a “second justification for obviousness-type double patenting-harassment by multiple assignees.” Id. at 1318-19 (citing In re Van Ornum, 686 F.2d 937, 944-48 (C.C.P.A. 1982)).
Therefore, the provisional non-statutory double patenting rejection over the co-pending Application is maintained as discussed above.
In regards to the remaining double-patenting rejections, Applicant argues that the instant claims are distinct, for the reasons discussed above (Remarks, p11-14).
Applicant’s arguments filed 05/04/2026 has been fully considered but is not persuasive.
The claims are prima facie obvious as discussed above, and therefore, the non-statutory double patenting rejections are maintained as discussed above.
Specifically, it is noted that the difference between the independent claim of the instant application and the patents is that the instant claims require the absence of UL18.
However, as discussed above, Browne teaches a HCMV with a deleted UL18 genes (Title, Abstract, p6784). Browne also teaches that UL18 is dispensable, not required for HCMV growth in culture, and is a useful site for insertion of other genes in the HCMV genome (Abstract, p6784; p6785 right column).
Therefore, a person of ordinary skill in the art would have been motivated to modify the HCMV and knock-out the UL18 gene in order to take advantage of this site and insert other genes. Furthermore, because Browne teaches that it is dispensable and teaches that UL18 can be knocked out of the HCMV genome, it could have been done with predictable results and a reasonable expectation of success.
Conclusion
No claims are allowed.
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/JOSEPH PAUL MIANO/Examiner, Art Unit 1631
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