DETAILED ACTION
Applicant’s response to the restriction/election requirement received on 6/10/26 has been entered. Claims 1-15 are pending in the instant application. Applicant’s election with traverse of the species alphavirus as the species of positive stranded RNA virus and HPV16 as the species of viral innate inhibitor protein (IIP) is acknowledged. Applicant’s traversal argues that each of the species are linked by common inventive concept and therefore the search for art for the different species that a separate significant search effort is not necessary and therefore no serious burden. In response, the different species of positive stranded RNA viruses are materially different species of virus with distinct structural, physical, and functional properties such that each species of virus would require a separate search of the prior art and may further raise separate issues under other patent statues. Further, the species of viral innate inhibitor proteins are all individual and unique proteins with materially different sequences and structural and functional properties such that, again, each species of protein would require a separate search of the prior art and may further raise separate issues under other patent statues. In addition, the previous office action clearly set forth that the “common inventive concept” which is an RNA construct comprising a therapeutic protein and an IIP is not a special technical feature in view of Kamrud et al. (U.S. Patent Application Publication 2018/0171340 (21 June, 2018). Applicant’s traversal does not address Kamrud nor the uniqueness of the recited species. As such, applicant’s arguments are not found persuasive and the election of species requirements are both deemed proper and made FINAL.
Claims 6-13 are hereby withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to a nonelected species, there being no allowable generic or linking claim. Applicant timely traversed the restriction (election) requirement in the reply filed on 6/10/26. Claims 1-5 and 14-15 are currently under examination based on the elected species of alphavirus and HPV16. An action on the merits follows.
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Information Disclosure Statement
The information disclosure statements (IDS) submitted on 6/14/23, 7/10/25, and 4/17/26 are in compliance with the provisions of 37 CFR 1.97 and 1.98. Accordingly, the information disclosure statements have been considered by the examiner and initialed and signed copies of the 1449s are attached to this action.
Claim Rejections - 35 USC § 112
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.
Claims 4 and 14 are 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 4 recites in in regards to the positive stranded RNA virus that is selected from a genus consisting of in part “preferably an alphavirus, optionally VEEV”. The term “preferably” renders the claim indefinite because it is unclear how the limitation that the RNA virus is “preferably an alphavirus” affects the closed genus of positive stranded RNA virus already listed, which includes alphavirus. It is unclear whether this phrase is intended to limit the RNA virus to just this species. Furthermore, the use of the term “optionally” following the term “preferably” is indefinite and confusing as it is unclear whether the specific species of VEEV is a part of the “genus consisting of” or is simply an example of such an RNA. See MPEP § 2173.05(d). Thus, the metes and bounds of the closed genus recited in this claim cannot be determined. In the interests of compact prosecution, claim 4 has been interpreted to include any alphavirus.
Claim 14 recites that the therapeutic biomolecule comprises a therapeutic protein, “preferably the protein or peptide is an antigen, and more preferably a viral antigen”. It is first noted that “the protein or peptide” lacks antecedent basis as the claim previously only refers to a therapeutic protein. Second, the use of the term “preferably” and “most preferably” renders the claim indefinite as it is unclear whether the recitation that the protein is an antigen, or a viral antigen is an actual limitation of the claim or simply an example. See MPEP § 2173.05(d). Thus, the metes and bounds of claim 14 cannot be determined. In the interests of compact prosecution, claim 14 has been interpreted and reading on the inclusion of RNA coding for any therapeutic biomolecule.
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claim 5 is rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
Claim 5 recites that the innate inhibitor protein is HPV16 E6 or an “ortholog thereof”. However, while the specification discloses HPV16 E6, the specification neither provides a definition of “ortholog”, definition of an “ortholog” in regards to HPV16 or HPV16 E6, nor any description or examples of any protein which may qualify as an “ortholog” of HPV16 E6.
At the time of filing, the term “ortholog” was generally defined as follows:
ortholog or orthologue (ôr′thə-lôg′, -lŏg′)
n.
A homologous gene that is related to those in different organisms by descent from the DNA of a common ancestor and that may or may not have the same function.
See-“Ortholog”-The American Heritage® Medical Dictionary Copyright © 2007, 2004 by Houghton Mifflin Company. Published by Houghton Mifflin Company. Accessed via The Free Dictionary https://medical-dictionary.thefreedictionary.com/ortholog. However, as a unique virus, HPV16, and its encoded proteins including E6 are not taught in the prior art as having any related genes in other types of organisms, such as bacteria, fungi, or animals. Thus, the knowledge and level of skill in the art at the time of filing would not have permitted the ordinary artisan to immediately envisage the genus of orthologs of HPV16 E6 based on the sole recitation of the term “ortholog” in the specification. Further, based on the commonly understood definition of “ortholog” as presented above, the ortholog may not even have the same function as HPV16 E6. As such, the specification fails to describe any protein which can be considered an ortholog of HPV16 E6 by failing to describe any ortholog which has the same function as HPV16 E6 or any protein which may have a different function than HPV16 E6 but is still recognized as an “ortholog” of HPV16 E6. As such, neither the as filed specification nor the prior art at the time of filing provides the requisite written description for the genus of “orthologs” of HPV16 E6 recited in instant claim 5.
The following guidance provided in MPEP 2163 is informative. To satisfy the written description requirement, a patent specification must describe the claimed invention in sufficient detail that one skilled in the art can reasonably conclude that the inventor had possession of the claimed invention. See, e.g., Moba, B.V. v. Diamond Automation, Inc., 325 F.3d 1306, 1319, 66 USPQ2d 1429, 1438 (Fed. Cir. 2003); Vas-Cath, Inc. v. Mahurkar, 935 F.2d at 1563, 19 USPQ2d at 1116. The written description requirement for a claimed genus may be satisfied through sufficient description of a representative number of species by actual reduction to practice (see i)(A) above), reduction to drawings (see i)(B) above), or by disclosure of relevant, identifying characteristics, i.e., structure or other physical and/or chemical properties, by functional characteristics coupled with a known or disclosed correlation between function and structure, or by a combination of such identifying characteristics, sufficient to show the applicant was in possession of the claimed genus (see i)(C) above). See Eli Lilly, 119 F.3d at 1568, 43 USPQ2d at 1406. An invention described solely in terms of a method of making and/or its function may lack written descriptive support where there is no described or art-recognized correlation between the disclosed function and the structure(s) responsible for the function. In other words, describing a composition by its function alone typically will not suffice to sufficiently describe the composition. See for example Eli Lilly, 119 F.3 at 1568, 43 USPQ2d at 1406 (Holding that description of a gene’s function will not enable claims to the gene "because it is only an indication of what the gene does, rather than what it is."); see also Fiers, 984 F.2d at 1169-71, 25 USPQ2d at 1605-06 (discussing Amgen Inc. v. Chugai Pharm. Co., 927 F.2d 1200, 18 USPQ2d 1016 (Fed. Cir. 1991)). An adequate written description of a chemical invention also requires a precise definition, such as by structure, formula, chemical name, or physical properties, and not merely a wish or plan for obtaining the chemical invention claimed. See, e.g., Univ. of Rochester v. G.D. Searle & Co., 358 F.3d 916, 927, 69 USPQ2d 1886, 1894-95 (Fed. Cir. 2004) (The patent at issue claimed a method of selectively inhibiting PGHS-2 activity by administering a non-steroidal compound that selectively inhibits activity of the PGHS-2 gene product, however the patent did not disclose any compounds that can be used in the claimed methods. While there was a description of assays for screening compounds to identify those that inhibit the expression or activity of the PGHS-2 gene product, there was no disclosure of which peptides, polynucleotides, and small organic molecules selectively inhibit PGHS-2. The court held that "[w]ithout such disclosure, the claimed methods cannot be said to have been described."). Furthermore, written description issues may also arise if the knowledge and level of skill in the art would not have permitted the ordinary artisan to immediately envisage the claimed product arising from the disclosed process. See, e.g., Fujikawa v. Wattanasin, 93 F.3d 1559, 1571, 39 USPQ2d 1895, 1905 (Fed. Cir. 1996). While it has been held that what is conventional or well known to one of ordinary skill in the art need not be disclosed in detail, for inventions in emerging and unpredictable technologies, or for inventions characterized by factors not reasonably predictable which are known to one of ordinary skill in the art, more evidence is required to show possession.
Thus, as the prior art at the time of filing does not teach a genus of “orthologs” of HPV16 E6, and as the specification does not provide any definition for the term “ortholog”, or any disclosure of any “orthologs” of HPV16 E6, the specification fails to provide a description of a representative number of species of orthologs of HPV16 E6 by actual reduction to practice (see i)(A) above), reduction to drawings (see i)(B) above), or by disclosure of relevant, identifying characteristics, i.e., structure or other physical and/or chemical properties, by functional characteristics coupled with a known or disclosed correlation between function and structure, or by a combination of such identifying characteristics, sufficient to show the applicant was in possession of any of the claimed genus of orthologs of HPV16 E6 as claimed.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
Claims 1-5 and 14-15 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Daemen et al. (2000) Gene Ther., Vol. 7, 1859-1866, as evidenced by Schmaljohn et al. (1996) Medical Microbiology 4th edition, Chapter 54, pages 1-16, Ballesteros-Briones et al. (2020) Curr. Opin. Virol, Vol. 44, 145-153, available online 9/6/2020, and Chiang et al. (2018) J. Virol., Vol. 92(6), doi.org/10.1128/JVI.01737-17, pages 1-15.
Daemen 2000 teaches a vaccine expression system comprising an RNA construct derived from the alphavirus Semliki Forest virus (SFV) which is self-replicating and which encodes the SFV viral replicase but not the SFV viral structural genes and which further encodes both the HPV16 E6 and HPV16 E7 proteins (Daemen 2000, pages 1860 and 1864). Daemen 2000 teaches the RNA as either synthetic RNA or as RNA present as the genome of SFV particles (Daemen 2000, page 1864). Daemen 2000 further teaches a plasmid DNA nucleic acid sequence encoding the RNA sequence of the RNA construct (Daemen 2000, page 1864). Further, Daemen 2000 teaches immunization of mice with the SFV-E6E7 particles resulting in the induction of potent CTL response against HPV transformed tumor cells (Daemen 2000, page 1863).
While Daemen 2000 does not teach that the SFV replicon RNA is mRNA or saRNA, SFV RNA inherently qualifies as both these types of RNA. Schmaljohn et al. provides evidence that the positive strand RNA genome of alphaviruses including SFV is an mRNA by teaching that the genomic RNA of alphaviruses is capped and polyadenylated and serves as mRNA for nonstructural proteins (Schmaljohn et al., pages 1-2). Ballesteros-Briones et al. provides evidence that alphavirus RNA such as SFV RNA which includes sequence encoding the replicase and does not include sequence encoding the structural proteins is considered self-amplifying RNA (saRNA) (Ballesteros-Briones et al., page 145). Thus, Schmaljohn et al. and Ballesteros-Briones et al. provides evidence that the SFV replicon RNA of the SFV-E6E7 taught by Daemen 2000, which comprises sequence encoding the replicase and does not include sequence encoding the structural proteins, is inherently both mRNA and saRNA.
Further, while Daemen 2000 teaches the inclusion of the sequence encoding HPV16 E6 in the SFV replicon RNA, Daemen 2000 does not specifically teach that HPV16 E6 is an innate inhibitor protein. Chiang et al., however, provides evidence that HPV16 E6 inherently comprises the property of an inhibitor of the innate immune system by teaching that HPV16 E6 protein targets USP15 and TRIM25 in cells which suppresses innate immune signaling (Chiang et al., page 1). Thus, Chiang et al. provides evidence that the HVP16 E6 present in the SFV replicon RNA taught by Daemen 2000 inherently has the function of an innate inhibitor.
Thus, by teaching RNA and DNA which meets all the structural and functional limitations of the claims as written, Daemen 2000 as evidenced by Schmaljohn et al., Ballesteros-Briones et al., and Chiang et al. anticipates the instant invention as claimed.
Claims 1-5 and 14-15 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Daemen et al. (2004) Antiviral Ther., Vol. 9, 733-742, as evidenced by Schmaljohn et al. (1996) Medical Microbiology 4th edition, Chapter 54, pages 1-16, Ballesteros-Briones et al. (2020) Curr. Opin. Virol, Vol. 44, 145-153, available online 9/6/2020, and Chiang et al. (2018) J. Virol., Vol. 92(6), doi.org/10.1128/JVI.01737-17, pages 1-15.
Daemen et al. teaches a vaccine expression system comprising RNA derived from the alphavirus Semliki Forest virus (SFV) which is self-replicating and which encodes the SFV viral replicase but not the SFV viral structural genes and which further encodes a fusion protein comprising HPV16 E6 and HPV16 E7 proteins (SFV-enhE6,7) (Daemen et al., pages 734-735). Daemen et al. teaches the RNA as either synthetic RNA or as RNA present as the genome of SFV particles (Daemen et al., page 735). Daemen et al. further teaches a plasmid DNA nucleic acid sequence encoding the RNA sequence of the SFV RNA (Daemen et al., page 735). Further, Daemen et al. teaches immunization of mice with the SFV-enhE6,7 particles resulting in the induction of potent CTL response against HPV transformed tumor cells (Daemen et al., page 736-739).
While Daemen et al. does not teach that the SFV RNA is mRNA or saRNA, SFV RNA inherently qualifies as both these types of RNA. Schmaljohn et al. provides evidence that the positive strand RNA genome of alphaviruses including SFV is an mRNA by teaching that the genomic RNA of alphaviruses is capped and polyadenylated and serves as mRNA for nonstructural proteins (Schmaljohn et al., pages 1-2). Ballesteros-Briones et al. provides evidence that alphavirus RNA such as SFV RNA which includes sequence encoding the replicase and does not include sequence encoding the structural proteins is considered self-amplifying RNA (saRNA) (Ballesteros-Briones et al., page 145). Thus, Schmaljohn et al. and Ballesteros-Briones et al. provides evidence that the SFV replicon RNA of the SFV-enhE6,7 taught by Daemen et al., which comprises sequence encoding the replicase and does not include sequence encoding the structural proteins, is inherently both mRNA and saRNA.
Further, while Daemen et al. teaches the inclusion of the sequence encoding HPV16 E6 in the SFV replicon RNA, Daemen et al. does not specifically teach that HPV16 E6 is an innate inhibitor protein. Chiang et al., however, provides evidence that HPV16 E6 inherently comprises the property of an inhibitor of the innate immune system by teaching that HPV16 E6 protein targets USP15 and TRIM25 in cells which suppresses innate immune signaling (Chiang et al., page 1). Thus, Chiang et al. provides evidence that the HVP16 E6 present in the SFV r RNA taught by Daemen et al. inherently has the function of an innate inhibitor.
Thus, by teaching RNA and DNA which meets all the structural and functional limitations of the claims as written, Daemen et al. as evidenced by Schmaljohn et al., Ballesteros-Briones et al., and Chiang et al. anticipates the instant invention as claimed.
Claims 1-5 and 14-15 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Cassetti et al. (2004) Vaccine, Vol. 22, 520-527, as evidenced by Schmaljohn et al. (1996) Medical Microbiology 4th edition, Chapter 54, pages 1-16, Pushko et al. (1997) Virology, Vol. 239, 389-401, and Chiang et al. (2018) J. Virol., Vol. 92(6), doi.org/10.1128/JVI.01737-17, pages 1-15.
Cassetti et al. teaches a Venezuelan equine encephalitis virus (VEE) replicon RNA, a species of alphavirus, comprising sequences encoding HPV16 E6 and HPV16 E7 (Cassetti et al., page 521). Cassetti et al. further teaches a plasmid DNA encoding the VEE E7 E6 RNA (Cassetti et al., page 521). Cassetti et al. teaches the preparation of RNA from the plasmid and generation of non-replicating viral particles comprising the RNA using the split helper method, citing Pushko et al. (Cassetti et al., page 521). Cassetti et al. teaches that immunization with the VEE E7 E6 particles comprising the RNA induces potent anti-tumor CTL responses with therapeutic efficacy in a mouse tumor model (Cassetti et al., pages 523-524). Cassetti et al. also teaches that alphavirus replicons can be administered either as naked RNA or as viral particles comprising the RNA (Cassetti et al., page 526).
While Cassetti et al. does not teach that the VEE RNA is mRNA or saRNA, VEE RNA inherently qualifies as both these types of RNA. Schmaljohn et al. provides evidence that the positive strand RNA genome of alphaviruses including VEE is an mRNA by teaching that the genomic RNA of alphaviruses is capped and polyadenylated and serves as mRNA for nonstructural proteins (Schmaljohn et al., pages 1-2). In regards to whether the VEE RNA of Cassetti is saRNA it is first noted that Cassetti et al. states that the VEE E7 E6 RNA particles was prepared using the split helper method of Pushko et al. Pushko et al. provides evidence that VEE replicon used in the split helper method comprises the replicase encoding sequence but does not encode the structural proteins (Pushko et al., Figure 1). Ballesteros-Briones et al. provides evidence that alphavirus RNA such as VEE RNA which includes sequence encoding the replicase and does not include sequence encoding the structural proteins is considered self-amplifying RNA (saRNA) (Ballesteros-Briones et al., page 145). Thus, Schmaljohn et al., Pushko et al., and Ballesteros-Briones et al. provide evidence that the FEE replicon RNA of the VEE E6 E7 RNA taught by Cassetti et al., which comprises sequence encoding the replicase and does not include sequence encoding the structural proteins, is inherently both mRNA and saRNA.
Further, while Cassetti et al. teaches the inclusion of the sequence encoding HPV16 E6 in the VEE replicon RNA, Cassetti et al. does not specifically teach that HPV16 E6 is an innate inhibitor protein. Chiang et al., however, provides evidence that HPV16 E6 inherently comprises the property of an inhibitor of the innate immune system by teaching that HPV16 E6 protein targets USP15 and TRIM25 in cells which suppresses innate immune signaling (Chiang et al., page 1). Thus, Chiang et al. provides evidence that the HVP16 E6 present in the VEE replicon RNA taught by Cassetti et al. inherently has the function of an innate inhibitor.
Thus, by teaching RNA and DNA which meets all the structural and functional limitations of the claims as written, Cassetti et al. as evidenced by Schmaljohn et al., Pushko et al., Ballesteros-Briones et al., and Chiang et al. anticipates the instant invention 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 and 14-15 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-24 of U.S. Patent No. 12,569,548, hereafter referred to s the ‘548 patent in view of Cassetti et al. (2004) Vaccine, Vol. 22, 520-527, and Chiang et al. (2018) J. Virol., Vol. 92(6), doi.org/10.1128/JVI.01737-17, pages 1-15.
The ‘548 patent claims recite RNA and nucleic acid products which are both broader and narrower than the instant claimed products. Claim 1 of the ‘548 patent recites, “[a]n RNA construct encoding (i) at least one therapeutic biomolecule; and (ii) at least one innate inhibitor protein (IIP), wherein the RNA construct comprises or is derived from a virus selected from the group of species consisting of: Venezuelan Equine Encephalitis Virus (VEEV); enterovirus 71; Encephalomyocarditis virus; Kunjin virus; and Middle East respiratory syndrome virus”. ‘548 patent claim 2 recites that the RNA is saRNA, and claim 20 recites a nucleic acid encoding the RNA construct of claim 1. Thus, the ‘548 patent claims are narrower than the instant claims in that they are limited to five specific viral strains, but are broader in that they are not read on any innate inhibitor protein and do not specifically recite that the innate inhibitor protein is HPV16 E6.
However, at the time of filing, HPV16 E6 was known to have innate immunity inhibitory function, and VEEV encoding a therapeutic biomolecule and HPV16 E6 were also known in the prior art. Cassetti et al. teaches a Venezuelan equine encephalitis virus (VEE) replicon RNA comprising sequences encoding HPV16 E6 and HPV16 E7 (Cassetti et al., page 521). Cassetti et al. further teaches a plasmid DNA encoding the VEE E7 E6 RNA (Cassetti et al., page 521). Chiang et al. further teaches that HPV16 E6 inherently comprises the property of an inhibitor of the innate immune system by teaching that HPV16 E6 protein targets USP15 and TRIM25 in cells which suppresses innate immune signaling (Chiang et al., page 1). Thus, Chiang et al. provides evidence that the HVP16 E6 present in the VEE replicon RNA taught by Cassetti et al. inherently has the function of an innate inhibitor protein.
Therefore, based on the teachings of Chiang et al. that HPV16 E6 is an innate inhibitor, and the teachings of Cassetti et al. to include HPV16 E6 in a VEEV RNA which further encodes the therapeutic biomolecule HPV E7, it would have been obvious to the skilled artisan at the time of filing to make the RNA construct of the ‘548 patent claims using HPV16 E6 as the innate inhibitor protein.
No claims are allowed.
Any inquiry concerning this communication from the examiner should be directed to Anne Marie S. Wehbé, Ph.D., whose telephone number is (571) 272-0737. If the examiner is not available, the examiner’s supervisor, Maria Leavitt, can be reached at (571) 272-1085. For all official communications, the technology center fax number is (571) 273-8300. Please note that all official communications and responses sent by fax must be directed to the technology center fax number. For informal, non-official communications only, the examiner’s direct fax number is (571) 273-0737. For any inquiry of a general nature, please call (571) 272-0547.
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Dr. A.M.S. Wehbé
/ANNE MARIE S WEHBE/Primary Examiner, Art Unit 1634
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