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 .
Election/Restrictions
Claims 1, 5-17, 20-23, 25, and 31 are pending.
Applicant's election with traverse of Group I, corresponding to claim 1, 5-17, and 20-22 in the reply filed 09/11/20255 is acknowledged.
Applicant’s election without traverse of the species of: (A) the species of recombinant vectors corresponding to the genes in claims 5-7; (B) the species of recombinant vectors that explicitly express specific CMV genes in claim 8 (UL40); and (C) the species of cells that express miRNA in claims 12-13 (endothelial, miR126) without traverse in the reply filed 09/11/20255 is acknowledged.
In regards to the traversal of Group I, the traversal is on the grounds that according to 37 CFR 1.475(a), a product and a process of use of said product in an improper grounds for lack of unity (Remarks, p9). Therefore, Applicant requests withdrawal of the restriction between Groups I and III.
It is noted that the claims of Groups IV, V, and VI (corresponding to claims 52, 76, 90, and 116-117) are newly cancelled, and the only remaining groups are Group I (a vector), Group II (a pharmaceutical composition), and group III (methods for treating a patient).
In regards to the restriction of Groups I and II, because there is a genus/species relationship between the vector in claim 1 and the pharmaceutical composition in claim 23 (Group II), upon further consideration, the restriction requirement between Group I and Group II is withdrawn.
In regards to the restriction of Groups I and III, because the claims are now drawn only to a product and a process of use of said product, as persuasively argued by Applicant, upon further consideration, the restriction requirement between Group I and Group III is withdrawn.
Claims 9-11 and 14-15 are withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to nonelected species, there being no allowable generic or linking claim.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.
Specification
The disclosure is objected to because it contains an embedded hyperlink and/or other form of browser-executable code. Applicant is required to delete the embedded hyperlink and/or other form of browser-executable code; references to websites should be limited to the top-level domain name without any prefix such as http:// or other browser-executable code. See MPEP § 608.01. Specifically, paragraph [0137] contains reference to a website that is a browser-executable code.
Claim Objections
Claim 1 is objected for the following informalities: claim 1 recites the abbreviation “HCMV.” Abbreviated terms should be spelled out in their first instance. Amending the claim to “human cytomegalovirus (HCMV)” would be ameliorative.
Claim 16 is objected to for the following informalities: claim 16 recites “tissue- specific” which should be “tissue-specific.”
Claim 20 is objected to for the following informalities: claim 20 recites “pathogen- specific” which should be “pathogen-specific.”
Claim Rejections - 35 USC § 112(b)
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claim 7 is rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claim 7 recites the limitation “the mutations” in lines 1-2. There is insufficient antecedent basis for this limitation in the claim as claim 6 from which it depends establishes “one or more mutations”. Amending the claim to “the one or more mutations” would be ameliorative.
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 Fielding et al. (PLOS ONE, 2014) and Leviton et al. (Clinical and Developmental Immunology, 2013).
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, Fielding teaches that UL18 helps HCMV evade NK cells (Introduction, p2), but that CMV vectors lacking UL18 replicate less efficiently and exhibit increased surface levels of MICA (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4) which can more easily be targeted by NK cells (Abstract, p1; Author Summary, p2).
Furthermore, as taught by Leviton, development of vaccines against CMV is a public health priority, that CMVs encode immune evasion genes that complicate live virus vaccine design, but that deletion of genes can result in an attenuated CMV vaccine (Title, Abstract, p1).
Therefore, a person of ordinary skill in the art would have been motivated to delete UL18 because it would decrease HCMV replicability in cells, would reduce the ability of the vector to evade the immune cell, and would allow production of an attenuated vaccine.
Furthermore, because Fielding teaches that there are known CMV vectors that lack UL18 (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4), 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) 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).
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, 5-8, 12-13, 16-17, 20-23, 25, and 31 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 in view of Fielding et al. (PLOS ONE, 2014) and Leviton et al. (Clinical and Developmental Immunology, 2013).
Although the conflicting claims 1-2, 4-10, 16, 18, 88-89, 96, 101-103, 114-115, and 165 of copending Application No. 17/786,186 are not identical to the currently prosecuted claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31, 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.
The co-pending application not explicitly require that the vector does not comprise UL18.
However, Fielding teaches that UL18 helps HCMV evade NK cells (Introduction, p2), but that CMV vectors lacking UL18 replicate less efficiently and exhibit increased surface levels of MICA (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4) which can more easily be targeted by NK cells (Abstract, p1; Author Summary, p2).
Furthermore, as taught by Leviton, development of vaccines against CMV is a public health priority, that CMVs encode immune evasion genes that complicate live virus vaccine design, but that deletion of genes can result in an attenuated CMV vaccine (Title, Abstract, p1).
Therefore, a person of ordinary skill in the art would have been motivated to delete UL18 because it would decrease HCMV replicability in cells, would reduce the ability of the vector to evade the immune cell, and would allow production of an attenuated vaccine.
Furthermore, because Fielding teaches that there are known CMV vectors that lack UL18 (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4), it could have been done with predictable results and a reasonable expectation of success.
This is a provisional nonstatutory double patenting rejection.
Claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31 provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-2, 9-11, 17-18, 20-21, 34-44 of copending Application No. 17/616,939 in view of Fielding et al. (PLOS ONE, 2014) and Leviton et al. (Clinical and Developmental Immunology, 2013).
Although the conflicting claims 1-2, 9-11, 17-18, 20-21, 34-44 of copending Application No. 17/616,939 are not identical to the currently prosecuted claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31, 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, UL130, UL146, and UL147.
The co-pending application not explicitly require that the vector does not comprise UL18.
However, Fielding teaches that UL18 helps HCMV evade NK cells (Introduction, p2), but that CMV vectors lacking UL18 replicate less efficiently and exhibit increased surface levels of MICA (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4) which can more easily be targeted by NK cells (Abstract, p1; Author Summary, p2).
Furthermore, as taught by Leviton, development of vaccines against CMV is a public health priority, that CMVs encode immune evasion genes that complicate live virus vaccine design, but that deletion of genes can result in an attenuated CMV vaccine (Title, Abstract, p1).
Therefore, a person of ordinary skill in the art would have been motivated to delete UL18 because it would decrease HCMV replicability in cells, would reduce the ability of the vector to evade the immune cell, and would allow production of an attenuated vaccine.
Furthermore, because Fielding teaches that there are known CMV vectors that lack UL18 (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4), it could have been done with predictable results and a reasonable expectation of success.
This is a provisional nonstatutory double patenting rejection.
Claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31 provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 11-24, 43-44, 89, and 144 of copending Application No. 17/616,941 in view of Fielding et al. (PLOS ONE, 2014) and Leviton et al. (Clinical and Developmental Immunology, 2013).
Although the conflicting claims 1, 11-24, 43-44, 89, and 144 of copending Application No. 17/616,941 are not identical to the currently prosecuted claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31, 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, UL130, UL146, and UL147.
The co-pending application not explicitly require that the vector does not comprise UL18.
However, Fielding teaches that UL18 helps HCMV evade NK cells (Introduction, p2), but that CMV vectors lacking UL18 replicate less efficiently and exhibit increased surface levels of MICA (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4) which can more easily be targeted by NK cells (Abstract, p1; Author Summary, p2).
Furthermore, as taught by Leviton, development of vaccines against CMV is a public health priority, that CMVs encode immune evasion genes that complicate live virus vaccine design, but that deletion of genes can result in an attenuated CMV vaccine (Title, Abstract, p1).
Therefore, a person of ordinary skill in the art would have been motivated to delete UL18 because it would decrease HCMV replicability in cells, would reduce the ability of the vector to evade the immune cell, and would allow production of an attenuated vaccine.
Furthermore, because Fielding teaches that there are known CMV vectors that lack UL18 (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4), it could have been done with predictable results and a reasonable expectation of success.
This is a provisional nonstatutory double patenting rejection.
Claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31 provisionally 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 Fielding et al. (PLOS ONE, 2014) and Leviton et al. (Clinical and Developmental Immunology, 2013).
Although the conflicting claims 12-13 of U.S. Patent No. 10,995,121 are not identical to the currently prosecuted claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31, 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 does explicitly require that the vector does not comprise UL18.
However, Fielding teaches that UL18 helps HCMV evade NK cells (Introduction, p2), but that CMV vectors lacking UL18 replicate less efficiently and exhibit increased surface levels of MICA (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4) which can more easily be targeted by NK cells (Abstract, p1; Author Summary, p2).
Furthermore, as taught by Leviton, development of vaccines against CMV is a public health priority, that CMVs encode immune evasion genes that complicate live virus vaccine design, but that deletion of genes can result in an attenuated CMV vaccine (Title, Abstract, p1).
Therefore, a person of ordinary skill in the art would have been motivated to delete UL18 because it would decrease HCMV replicability in cells, would reduce the ability of the vector to evade the immune cell, and would allow production of an attenuated vaccine.
Furthermore, because Fielding teaches that there are known CMV vectors that lack UL18 (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4), it could have been done with predictable results and a reasonable expectation of success.
Claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31 provisionally 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 Fielding et al. (PLOS ONE, 2014) and Leviton et al. (Clinical and Developmental Immunology, 2013).
Although the conflicting claims 12-13 of U.S. Patent No. 11,692,012 are not identical to the currently prosecuted claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31, 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 does explicitly require that the vector does not comprise UL18.
However, Fielding teaches that UL18 helps HCMV evade NK cells (Introduction, p2), but that CMV vectors lacking UL18 replicate less efficiently and exhibit increased surface levels of MICA (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4) which can more easily be targeted by NK cells (Abstract, p1; Author Summary, p2).
Furthermore, as taught by Leviton, development of vaccines against CMV is a public health priority, that CMVs encode immune evasion genes that complicate live virus vaccine design, but that deletion of genes can result in an attenuated CMV vaccine (Title, Abstract, p1).
Therefore, a person of ordinary skill in the art would have been motivated to delete UL18 because it would decrease HCMV replicability in cells, would reduce the ability of the vector to evade the immune cell, and would allow production of an attenuated vaccine.
Furthermore, because Fielding teaches that there are known CMV vectors that lack UL18 (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4), it could have been done with predictable results and a reasonable expectation of success.
Claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31 provisionally 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 Fielding et al. (PLOS ONE, 2014) and Leviton et al. (Clinical and Developmental Immunology, 2013).
Although the conflicting claims 1-10 of U.S. Patent No. 11,266,732 are not identical to the currently prosecuted claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31, 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 does explicitly require that the vector does not comprise UL18.
However, Fielding teaches that UL18 helps HCMV evade NK cells (Introduction, p2), but that CMV vectors lacking UL18 replicate less efficiently and exhibit increased surface levels of MICA (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4) which can more easily be targeted by NK cells (Abstract, p1; Author Summary, p2).
Furthermore, as taught by Leviton, development of vaccines against CMV is a public health priority, that CMVs encode immune evasion genes that complicate live virus vaccine design, but that deletion of genes can result in an attenuated CMV vaccine (Title, Abstract, p1).
Therefore, a person of ordinary skill in the art would have been motivated to delete UL18 because it would decrease HCMV replicability in cells, would reduce the ability of the vector to evade the immune cell, and would allow production of an attenuated vaccine.
Furthermore, because Fielding teaches that there are known CMV vectors that lack UL18 (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4), it could have been done with predictable results and a reasonable expectation of success.
Claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31 provisionally 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 Fielding et al. (PLOS ONE, 2014) and Leviton et al. (Clinical and Developmental Immunology, 2013).
Although the conflicting claims 1-10 of U.S. Patent No. 11,091,779 are not identical to the currently prosecuted claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31, 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 does explicitly require that the vector does not comprise UL18.
However, Fielding teaches that UL18 helps HCMV evade NK cells (Introduction, p2), but that CMV vectors lacking UL18 replicate less efficiently and exhibit increased surface levels of MICA (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4) which can more easily be targeted by NK cells (Abstract, p1; Author Summary, p2).
Furthermore, as taught by Leviton, development of vaccines against CMV is a public health priority, that CMVs encode immune evasion genes that complicate live virus vaccine design, but that deletion of genes can result in an attenuated CMV vaccine (Title, Abstract, p1).
Therefore, a person of ordinary skill in the art would have been motivated to delete UL18 because it would decrease HCMV replicability in cells, would reduce the ability of the vector to evade the immune cell, and would allow production of an attenuated vaccine.
Furthermore, because Fielding teaches that there are known CMV vectors that lack UL18 (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4), it could have been done with predictable results and a reasonable expectation of success.
Claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31 provisionally 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 Fielding et al. (PLOS ONE, 2014) and Leviton et al. (Clinical and Developmental Immunology, 2013).
Although the conflicting claims 1-64 of U.S. Patent No. 10,532,099 are not identical to the currently prosecuted claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31, 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 does explicitly require that the vector does not comprise UL18.
However, Fielding teaches that UL18 helps HCMV evade NK cells (Introduction, p2), but that CMV vectors lacking UL18 replicate less efficiently and exhibit increased surface levels of MICA (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4) which can more easily be targeted by NK cells (Abstract, p1; Author Summary, p2).
Furthermore, as taught by Leviton, development of vaccines against CMV is a public health priority, that CMVs encode immune evasion genes that complicate live virus vaccine design, but that deletion of genes can result in an attenuated CMV vaccine (Title, Abstract, p1).
Therefore, a person of ordinary skill in the art would have been motivated to delete UL18 because it would decrease HCMV replicability in cells, would reduce the ability of the vector to evade the immune cell, and would allow production of an attenuated vaccine.
Furthermore, because Fielding teaches that there are known CMV vectors that lack UL18 (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4), it could have been done with predictable results and a reasonable expectation of success.
Claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31 provisionally 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 Fielding et al. (PLOS ONE, 2014) and Leviton et al. (Clinical and Developmental Biology, 2013).
Although the conflicting claim 20 of U.S. Patent No. 10,532,099 is not identical to the currently prosecuted claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31, they are not patently distinct from each other because said claims of both inventions are drawn to a CMV vector that does express UL130.
The patent does explicitly require that the vector does not comprise UL18.
However, Fielding teaches that UL18 helps HCMV evade NK cells (Introduction, p2), but that CMV vectors lacking UL18 replicate less efficiently and exhibit increased surface levels of MICA (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4) which can more easily be targeted by NK cells (Abstract, p1; Author Summary, p2).
Furthermore, as taught by Leviton, development of vaccines against CMV is a public health priority, that CMVs encode immune evasion genes that complicate live virus vaccine design, but that deletion of genes can result in an attenuated CMV vaccine (Title, Abstract, p1).
Therefore, a person of ordinary skill in the art would have been motivated to delete UL18 because it would decrease HCMV replicability in cells, would reduce the ability of the vector to evade the immune cell, and would allow production of an attenuated vaccine.
Furthermore, because Fielding teaches that there are known CMV vectors that lack UL18 (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4), it could have been done with predictable results and a reasonable expectation of success.
The patent does explicitly require that the vector does not comprise UL128.
However, a person of ordinary skill in the art would have been motivated to engineer a vector that does not comprise UL128 because Leviton teaches that deletion of the MIP gene (which comprises UL128 along with UL130) establishes virus-based vaccine that attenuates the pathogenicity of HMV while retaining immunogenicity and demonstrates efficacy against congenital infection and disease (Title, Abstract, p1). Furthermore, because Leviton demonstrates that UL128 can be effectively deleted from the CMV genome by explicitly well-known methods (Results, p6), it could have been done with predictable results and a reasonable expectation of success.
Claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31 provisionally 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 Fielding et al. (PLOS ONE, 2014) and Leviton et al. (Clinical and Developmental Biology, 2013).
Although the conflicting claim 18 of U.S. Patent No. 11,834,669 is not identical to the currently prosecuted claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31, they are not patently distinct from each other because said claims of both inventions are drawn to a CMV vector that does express UL130.
The patent does explicitly require that the vector does not comprise UL18.
However, Fielding teaches that UL18 helps HCMV evade NK cells (Introduction, p2), but that CMV vectors lacking UL18 replicate less efficiently and exhibit increased surface levels of MICA (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4) which can more easily be targeted by NK cells (Abstract, p1; Author Summary, p2).
Furthermore, as taught by Leviton, development of vaccines against CMV is a public health priority, that CMVs encode immune evasion genes that complicate live virus vaccine design, but that deletion of genes can result in an attenuated CMV vaccine (Title, Abstract, p1).
Therefore, a person of ordinary skill in the art would have been motivated to delete UL18 because it would decrease HCMV replicability in cells, would reduce the ability of the vector to evade the immune cell, and would allow production of an attenuated vaccine.
Furthermore, because Fielding teaches that there are known CMV vectors that lack UL18 (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4), it could have been done with predictable results and a reasonable expectation of success.
The patent does explicitly require that the vector does not comprise UL128.
However, a person of ordinary skill in the art would have been motivated to engineer a vector that does not comprise UL128 because Leviton teaches that deletion of the MIP gene (which comprises UL128 along with UL130) establishes virus-based vaccine that attenuates the pathogenicity of HMV while retaining immunogenicity and demonstrates efficacy against congenital infection and disease (Title, Abstract, p1). Furthermore, because Leviton demonstrates that UL128 can be effectively deleted from the CMV genome by explicitly well-known methods (Results, p6), it could have been done with predictable results and a reasonable expectation of success.
Claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31 provisionally 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 Fielding et al. (PLOS ONE, 2014) and Leviton et al. (Clinical and Developmental Immunology, 2013).
Although the conflicting claims 1-26 of U.S. Patent No. 10,894,078 is not identical to the currently prosecuted claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31, they are not patently distinct from each other because said claims of both inventions are drawn to a CMV vector that does express UL128 or UL130.
The patent does explicitly require that the vector does not comprise UL18.
However, Fielding teaches that UL18 helps HCMV evade NK cells (Introduction, p2), but that CMV vectors lacking UL18 replicate less efficiently and exhibit increased surface levels of MICA (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4) which can more easily be targeted by NK cells (Abstract, p1; Author Summary, p2).
Furthermore, as taught by Leviton, development of vaccines against CMV is a public health priority, that CMVs encode immune evasion genes that complicate live virus vaccine design, but that deletion of genes can result in an attenuated CMV vaccine (Title, Abstract, p1).
Therefore, a person of ordinary skill in the art would have been motivated to delete UL18 because it would decrease HCMV replicability in cells, would reduce the ability of the vector to evade the immune cell, and would allow production of an attenuated vaccine.
Furthermore, because Fielding teaches that there are known CMV vectors that lack UL18 (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4), it could have been done with predictable results and a reasonable expectation of success.
Claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31 provisionally 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 Fielding et al. (PLOS ONE, 2014) and Leviton et al. (Clinical and Developmental Immunology, 2013).
Although the conflicting claims 1-24 of U.S. Patent No. 11,554,168 is not identical to the currently prosecuted claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31, they are not patently distinct from each other because said claims of both inventions are drawn to a CMV vector that does express UL128 or UL130.
The patent does explicitly require that the vector does not comprise UL18.
However, Fielding teaches that UL18 helps HCMV evade NK cells (Introduction, p2), but that CMV vectors lacking UL18 replicate less efficiently and exhibit increased surface levels of MICA (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4) which can more easily be targeted by NK cells (Abstract, p1; Author Summary, p2).
Furthermore, as taught by Leviton, development of vaccines against CMV is a public health priority, that CMVs encode immune evasion genes that complicate live virus vaccine design, but that deletion of genes can result in an attenuated CMV vaccine (Title, Abstract, p1).
Therefore, a person of ordinary skill in the art would have been motivated to delete UL18 because it would decrease HCMV replicability in cells, would reduce the ability of the vector to evade the immune cell, and would allow production of an attenuated vaccine.
Furthermore, because Fielding teaches that there are known CMV vectors that lack UL18 (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4), it could have been done with predictable results and a reasonable expectation of success.
Claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31 provisionally 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 Fielding et al. (PLOS ONE, 2014) and Leviton et al. (Clinical and Developmental Immunology, 2013).
Although the conflicting claims 1-24 of U.S. Patent No. 9,783,823 are not identical to the currently prosecuted claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31, they are not patently distinct from each other because said claims of both inventions are drawn to a CMV vector that does express UL128 or UL130.
The patent does explicitly require that the vector does not comprise UL18.
However, Fielding teaches that UL18 helps HCMV evade NK cells (Introduction, p2), but that CMV vectors lacking UL18 replicate less efficiently and exhibit increased surface levels of MICA (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4) which can more easily be targeted by NK cells (Abstract, p1; Author Summary, p2).
Furthermore, as taught by Leviton, development of vaccines against CMV is a public health priority, that CMVs encode immune evasion genes that complicate live virus vaccine design, but that deletion of genes can result in an attenuated CMV vaccine (Title, Abstract, p1).
Therefore, a person of ordinary skill in the art would have been motivated to delete UL18 because it would decrease HCMV replicability in cells, would reduce the ability of the vector to evade the immune cell, and would allow production of an attenuated vaccine.
Furthermore, because Fielding teaches that there are known CMV vectors that lack UL18 (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4), it could have been done with predictable results and a reasonable expectation of success.
Claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31 provisionally 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 Fielding et al. (PLOS ONE, 2014) and Leviton et al. (Clinical and Developmental Immunology, 2013).
Although the conflicting claims 1-23 of U.S. Patent No. 10,316,334 are not identical to the currently prosecuted claims 1, 5-8, 12-13, 16-17, 20-23, 25, and 31, they are not patently distinct from each other because said claims of both inventions are drawn to a CMV vector that does express UL128 or UL130.
The patent does explicitly require that the vector does not comprise UL18.
However, Fielding teaches that UL18 helps HCMV evade NK cells (Introduction, p2), but that CMV vectors lacking UL18 replicate less efficiently and exhibit increased surface levels of MICA (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4) which can more easily be targeted by NK cells (Abstract, p1; Author Summary, p2).
Furthermore, as taught by Leviton, development of vaccines against CMV is a public health priority, that CMVs encode immune evasion genes that complicate live virus vaccine design, but that deletion of genes can result in an attenuated CMV vaccine (Title, Abstract, p1).
Therefore, a person of ordinary skill in the art would have been motivated to delete UL18 because it would decrease HCMV replicability in cells, would reduce the ability of the vector to evade the immune cell, and would allow production of an attenuated vaccine.
Furthermore, because Fielding teaches that there are known CMV vectors that lack UL18 (US18–US22 is a major HCMV locus controlling cell surface expression of MICA, p4), 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