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 .
Priority
The instant application is a national stage entry of PCT application PCT/KR2022/004159, filed 09/19/2023 under 35 USC 371. Acknowledgment is made of applicant's claim for foreign priority based on an application KR10-2021-0040269 filed in Republic of Korea on 03/29/2021, and an application KR10-2022-0034885 filed in Republic of Korea on 03/21/2022.
Claim Objections
Claim 8 is objected to because of the following informalities: claim 8 recites “the vector is shown in Figure 6 or Figure 8”. MPEP 2173.05(s) states: [W]here possible, claims are to be complete in themselves. Incorporation by reference to a specific figure or table "is permitted only in exceptional circumstances where there is no practical way to define the invention in words and where it is more concise to incorporate by reference than duplicating a drawing or table into the claim. Incorporation by reference is a necessity doctrine, not for applicant’s convenience." Ex parte Fressola, 27 USPQ2d 1608, 1609 (Bd. Pat. App. & Inter. 1993). In instant case, Applicant is recommended to describe the vector by words (i.e., from 5’ to 3’ ) to provide the components in the vector of the claim instead of just referring the figures in the Drawing.
Appropriate correction is required.
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.
Claim 1-12 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 1 recites “the knob domain of the end of the fiber protein of human adenovirus type 5 has been replaced with the knob gene of chimpanzee adenovirus serotype 6” renders instant claim indefinite. The phrase “the knob domain of the end of the fiber protein” refers to a region of a protein, it is not clear how a protein (domain/region) be replaced by a gene. Therefore the scope of instant claim is not clear.
Claims 2-12 depend from, at least, claim 1, and thus inherit the deficiency and are rejected on the same basis.
Claim 5 recites the vector “further” comprises a fiber protein renders instant claim indefinite. It is known that fiber protein consists of a tail, a shaft and a knob domain. In independent claim 1 which instant claim 5 depends from, the gene which encoding knob domain has been replaced with the knob gene of chimpanzee adenovirus serotype 6, therefore forms a fiber protein combined with the tail and shaft domains of human adenovirus type 5 and the knob domain of chimpanzee adenovirus serotype 6. It is not clear what “further comprises a fiber protein” here refers to, the scope of instant claim is not clear.
Claim Interpretation
As stated above, claim 1 is indefinite. In the interest of compacted prosecution, claim 1 is interpreted as a chimeric adenovirus vector in which the gene/polynucleotides encoding knob domain of the end of the fiber protein of human adenovirus type 5 has been replaced with the knob gene of chimpanzee adenovirus serotype 6.
Claim 5 is interpreted as the chimeric adenovirus vector comprises a fiber protein combined with the tail and shaft domains of human adenovirus type 5 and the knob domain of chimpanzee adenovirus serotype 6.
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.
Claims 1, 5 and 10-12 are rejected under 35 U.S.C. 103 as being unpatentable over Barouch et al. (WO 2013/036791 A2) in view of Ersching et al. (Virology. 2010 Nov 10;407(1):1-6).
Barouch et al. teach recombinant adenovirus serotype 5 (Ad5) vectors which harbor chimeric capsid proteins including substitutions of the corresponding regions from adenovirus serotypes having a lower seroprevalence relative to Ad5 (Abstract).
Regarding claim 1, Barouch et al. teach producing chimeric Ad5 vectors having substitutions of specific regions of the adenoviral hexon protein (e.g., the hexon HVRs) and fiber protein (e.g., the fiber knob domain) that evade pre-existing vector immunity more effectively than Ad5 vectors having substitutions in only the HVRs (p12, parag 1). Barouch et al. teach any fiber knob domain from an adenovirus serotype having a lower seroprevalence compared to Ad5, can be used to replace the fiber knob domain of Ad5. The preferred serotypes that are used to provide their fiber protein, or relevant parts thereof, are Ad11, Ad15, Ad34, Ad35, Ad48, and Pan9/AdC68; Ad15 and Pan9/ AdC68 are the most preferred serotypes (p14, parag 1). Barouch et al. do not specifically point out using the knob gene of chimpanzee adenovirus serotype 6 to replace the gene encoding the knob domain of the end of the fiber protein of human adenovirus type 5. However, this was disclosed by Ersching et al. at the time of instant invention.
Ersching et al. teach sera from 200 Brazilian human subjects and New-World monkeys were tested for neutralizing antibodies (Nab) titers to human adenovirus serotypes AdHu5 and AdHu26 and chimpanzee-origin Ad viruses of serotype 6 (AdC6) and serotype 68 (AdC68) (Abstract).
Regarding claim 1, Ersching et al. teach seroprevalence rates of NAb in humans were 69.5% for AdHu5, 44% for AdHu26, 21% for AdC6 and 23.5% for AdC68 (Abstract).
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to modify Barouch et al.’s chimeric Ad5 vectors having substitutions of fiber protein knob domain, and use the fiber knob domain of chimpanzee-origin Ad viruses of serotype 6 (AdC6) as taught by Ersching et al.. The only difference between instant claim and Barouch et al.’s chimeric Ad5 vectors having substitutions of fiber knob domain is instant claim has the knob domain of the end of the fiber protein of human adenovirus type 5 been replaced with the knob domain of chimpanzee adenovirus serotype 6. Given that Barouch et al. teach any fiber knob domain from an adenovirus serotype having a lower seroprevalence compared to Ad5 can be used to replace the fiber knob domain of Ad5, and Ersching et al. teach AdC6 has a lower seroprevalence than Ad5, one of ordinary skill in the art would have substituted the fiber knob domain of human Ad5 with AdC6, depends on their research interest or preference. This simple substitution of one known element (the fiber knob domain of chimpanzee adenovirus serotype 6) for another known element (the fiber knob domain of human adenovirus type 5) to form a chimeric adenovirus vector is likely to be obvious when predictable results are achieved. See KSR International Co. v. Teleflex Inc., 550 U.S. 398, 415-421, USPQ2d 1385, 1395 — 97 (2007) (see MPEP § 2143, B.).
Regarding claim 5, Barouch et al. teach by "fiber protein" is meant an adenoviral capsid protein, which is bound to, and projects from, a penton protein base. The fiber protein assembles into homotrimers, each fiber protein consisting of a tail, a shaft, and a knob domain (p7, parag 7). Following the discussion above, Barouch et al. teach any fiber knob domain from an adenovirus serotype having a lower seroprevalence compared to Ad5 can be used to replace the fiber knob domain of Ad5 (p14, parag 1), and Ersching et al. teach AdC6 has a lower seroprevalence than Ad5 (Abstract), indicates the knob domain of the end of the fiber protein of human Ad5 can replaced with the knob domain of AdC6, while keep the other components of the fiber protein in human Ad5. Therefore the chimeric vector comprises a fiber protein combined with the tail and shaft domains of human adenovirus type 5 and the knob domain of chimpanzee adenovirus serotype 6.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to modify Barouch et al.’s chimeric Ad5 vectors having substitutions of fiber knob domain, and use the fiber knob domain of chimpanzee-origin Ad viruses of serotype 6 (AdC6) as taught by Ersching et al. to make a chimeric adenovirus vector comprising a fiber protein combined with the tail and shaft domains of human Ad5 and the knob domain of AdC6. The only difference between instant claim and Barouch et al.’s chimeric Ad5 vectors having substitutions of fiber knob domain is instant claim has the knob domain of the end of the fiber protein of human adenovirus type 5 been replaced with the knob domain of chimpanzee adenovirus serotype 6. Given that Barouch et al. teach any fiber knob domain from an adenovirus serotype having a lower seroprevalence compared to Ad5 can be used to replace the fiber knob domain of Ad5, and Ersching et al. teach AdC6 has a lower seroprevalence than Ad5, one of ordinary skill in the art would have substituted the fiber knob domain of human Ad5 with AdC6, depends on their research interest or preference, therefore obtain a make a chimeric adenovirus vector comprising a fiber protein combined with the tail and shaft domains of human Ad5 and the knob domain of AdC6. This simple substitution of one known element (a chimeric adenovirus vector comprising a fiber protein combined with the tail and shaft domains of human Ad5 and the knob domain of AdC6) for another known element (an adenovirus vector comprising a fiber protein of human Ad5) to form a chimeric adenovirus vector is likely to be obvious when predictable results are achieved. See KSR International Co. v. Teleflex Inc., 550 U.S. 398, 415-421, USPQ2d 1385, 1395 — 97 (2007) (see MPEP § 2143, B.).
Regarding claims 10 and 11, Barouch et al. do not teach a host cell transformed with the chimeric adenovirus vector, wherein the cell is HEK293, PERC6 or 911 cell. However, Ersching et al. teach recombinant vectors (AdHu5, AdHu26, AdC6 and AdC68) were serially passaged on complementing HEK293 cells to generate high-titer viral stocks (p4, right column). This teaching reads on a host HEK293 cell can be transformed with both human adenovirus type 5 and chimpanzee adenovirus serotype 6.
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to modify Barouch et al.’s chimeric Ad5 vectors having substitutions of fiber knob domain, use the fiber knob domain of chimpanzee-origin Ad viruses of serotype 6 (AdC6) and transform the chimeric adenoviral vectors to host cells such as HEK293 cells as taught by Ersching et al.. The skilled artisan would have been motivated to transform the chimeric adenovirus vector to host cells such as HEK293 cells in order to obtain viral stocks. There would be a reasonable expectation of success of transforming the recombinant adenoviral vectors to host cells such as HEK293 cells since Ersching et al. teach both human Ad5 and chimpanzee adenovirus AdC6 can be obtained in HEK293 cells (see p4, right column).
Regarding claim 12, following the discussion above, Barouch et al. teach the compositions of the invention include a recombinant replication-defective Ad5 vector with chimeric hexon and fiber proteins, containing a heterologous nucleic acid molecule encoding an antigenic gene product or fragment thereof (p19, parag 4). By "gene product" is meant to include mRNAs transcribed from a gene as well as polypeptides translated from those mRNAs (p7, parag 8). This teaching indicates the polypeptide (gene product) can be encoded by the chimeric adenovirus vector, as recited in instant claim.
Claims 1, 2, 5 and 10-12 are rejected under 35 U.S.C. 103 as being unpatentable over Barouch et al. (WO 2013/036791 A2) in view of Ersching et al. (Virology. 2010 Nov 10;407(1):1-6), as applied to claim 1, 5 and 10-12 above, further in view of Kahl et al. (Vaccine. 2010 Aug 9;28(35):5691-702).
The teaching of Barouch et al. and Ersching et al. is set for the above.
Regarding claim 2, following the discussion above, Barouch et al. teach the invention features recombinant, replication-deficient Ad5 vectors having both chimeric hexon and fiber proteins, in which
regions of the Ad5 hexon and fiber proteins have been replaced with corresponding regions from adenoviruses having lower seroprevalence compared to that of Ad5 (p1, parag 4). Barouch et al. do not specifically point out using hypervariable regions 1-7 of human adenovirus serotype 28 for the substitution of hexon protein of human adenovirus type 5, However, this was disclosed by KahL et al. at the time of instant invention.
KahL et al. teach a vector derived from a representative serotype, Ad28, induced significantly higher transgene-specific T cell responses than an Ad35 vector (Abstract).
Regarding claim 2, KahL et al. teach the seroprevalence of Ad28 was confirmed to be <10% in the United States (Abstract) and lower than human AD5 (see p5696, figure 4).
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to modify Barouch et al.’s chimeric Ad5 vectors having substitutions of hexon protein, and use the hypervariable regions 1-7 of human adenovirus serotype 28 as taught by KahL et al.. The only difference between instant claim and Barouch et al.’s chimeric Ad5 vectors having substitutions of hexon protein is instant claim has the hypervariable regions 1-7 of human adenovirus serotype 28. Given that Barouch et al. teach any hexon hypervariable region (HVR) sequences from an adenovirus serotype having a lower seroprevalence compared to Ad5 can be used to replace the hexon HVR sequences of Ad5, and KahL et al. teach Ad28 has a lower seroprevalence than Ad5 (see p5696, figure 4), one of ordinary skill in the art would have substitute hexon protein of human Ad5 with hypervariable regions 1-7 of human adenovirus serotype 28, depends on their research interest or preference. This simple substitution of one known element (the hypervariable regions 1-7 of human adenovirus serotype 28) for another known element (the hexon protein of human adenovirus type 5) to form a chimeric adenovirus vector is likely to be obvious when predictable results are achieved. See KSR International Co. v. Teleflex Inc., 550 U.S. 398, 415-421, USPQ2d 1385, 1395 — 97 (2007) (see MPEP § 2143, B.).
Claims 1, 3-5 and 10-12 are rejected under 35 U.S.C. 103 as being unpatentable over Barouch et al. (WO 2013/036791 A2) in view of Ersching et al. (Virology. 2010 Nov 10;407(1):1-6), as applied to claims 1, 5 and 10-12 above, further in view of Wilson et al. (US 2015/0352203 A1).
The teaching of Barouch et al. and Ersching et al. is set for the above.
Regarding claims 3 and 4, Barouch et al. and Ersching et al. do not teach the protein expressed by the knob gene of chimpanzee adenovirus serotype 6 comprises the amino acid sequence of SEQ ID NO: 1, as well as the knob gene sequence of chimpanzee adenovirus serotype 6 comprises the nucleic acid sequence of SEQ ID NO: 2. However, this was disclosed by Wilson et al. at the time of instant invention.
Wilson et al. teach a recombinant vector comprises simian adenovirus sequences and a heterologous gene under the control of regulatory sequences (Abstract).
Regarding claim 3, Wilson et al. teach the sequence of the amino acid sequences of the fiber knob domains of chimpanzee Pan-6 (SEQ ID NO:19). Herein the SEQ ID NO:1 in instant claim is 100% identical the SEQ ID NO:19 of Wilson et al. (sequence alignment is provided below).
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to modify Barouch et al.’s chimeric Ad5 vectors having substitutions of fiber knob domain, and use the chimpanzee-origin Ad viruses of serotype 6 (AdC6) as taught by Ersching et al, which has amino acid sequences same as the amino acid sequences of the fiber knob domains of chimpanzee adenovirus serotype 6 (also named Pan-6) as taught by Wilson et al.. The only difference between instant claim and Barouch et al.’s chimeric Ad5 vectors having substitutions of fiber knob domain is instant claim has the knob domain of the end of the fiber protein of human adenovirus type 5 been replaced with the knob domain of chimpanzee adenovirus serotype 6 and having the amino acid sequences of the knob domain of chimpanzee adenovirus serotype 6. Given that Barouch et al. teach any fiber knob domain from an adenovirus serotype having a lower seroprevalence compared to Ad5 can be used to replace the fiber knob domain of Ad5, Ersching et al. teach AdC6 has a lower seroprevalence than Ad5, and Wilson et al. provide the amino acid sequences of the fiber knob domains of chimpanzee adenovirus serotype 6, one of ordinary skill in the art would have substituted the fiber knob domain of human Ad5 with AdC6, and use the amino acid sequences of AdC6 as provided by Wilson et al. depends on their research interest or preference. This simple substitution of one known element (the fiber knob domain of chimpanzee adenovirus serotype 6) for another known element (the fiber knob domain of human adenovirus type 5) to form a chimeric adenovirus vector is likely to be obvious when predictable results are achieved. See KSR International Co. v. Teleflex Inc., 550 U.S. 398, 415-421, USPQ2d 1385, 1395 — 97 (2007) (see MPEP § 2143, B.).
Regarding claim 4, Wilson et al. teach the sequence of chimpanzee adenovirus serotype Pan6 (Ad Pan-6) SEQ ID NO: 5 (see p3, right column, and p51), Herein the SEQ ID NO:1 in instant claim is 100% identical the SEQ ID NO:5 of Wilson et al. (sequence alignment is provided below).
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to modify Barouch et al.’s chimeric Ad5 vectors having substitutions of fiber knob domain, and use the chimpanzee-origin Ad viruses of serotype 6 (AdC6) as taught by Ersching et al, which has nucleic acid sequences same as the nucleic acid sequences of chimpanzee adenovirus serotype 6 (also named Pan6, Ad Pan-6) as taught by Wilson et al.. The only difference between instant claim and Barouch et al.’s chimeric Ad5 vectors having substitutions of fiber knob domain is instant claim has the knob domain of the end of the fiber protein of human adenovirus type 5 been replaced with the knob domain of chimpanzee adenovirus serotype 6 and having the nucleic acid sequences of the knob domain of the chimpanzee adenovirus serotype 6. Given that Barouch et al. teach any fiber knob domain from an adenovirus serotype having a lower seroprevalence compared to Ad5 can be used to replace the fiber knob domain of Ad5, Ersching et al. teach AdC6 has a lower seroprevalence than Ad5, and Wilson et al. provide the nucleic acid sequences of the chimpanzee adenovirus serotype 6 which comprising the nucleic acid sequence of the fiber knob domain, one of ordinary skill in the art would have substituted the fiber knob domain of human Ad5 with AdC6, and use the nucleic acid sequences of AdC6 as provided by Wilson et al. depends on their research interest or preference. This simple substitution of one known element (the fiber knob domain of chimpanzee adenovirus serotype 6) for another known element (the fiber knob domain of human adenovirus type 5) to form a chimeric adenovirus vector is likely to be obvious when predictable results are achieved. See KSR International Co. v. Teleflex Inc., 550 U.S. 398, 415-421, USPQ2d 1385, 1395 — 97 (2007) (see MPEP § 2143, B.).
Claims 1, 5, 8 and 10-12 are rejected under 35 U.S.C. 103 as being unpatentable over Barouch et al. (WO 2013/036791 A2) in view of Ersching et al. (Virology. 2010 Nov 10;407(1):1-6), as applied to claims 1, 5 and 10-12 above, further in view of Saha et al. (Viruses 2014, 6, 3563-3583) and Makrides (New Comprehensive Biochemistry. 2003;38:9–26).
The teaching of Barouch et al. and Ersching et al. is set for the above.
Regarding claim 8, Barouch et al. do not teach the detailed chimeric adenovirus vector comprising a fiber protein combined with the tail and shaft domains of human adenovirus type 5 and the knob domain of chimpanzee adenovirus serotype 6. However, this was disclosed by Saha et al. and Makrides.
Saha et al. discusses the impact of the genome size on Ad virion stability and emphasizes the need to consider this aspect of virus biology in Ad-based vector design (Abstract).
Makrides teaches virus-based vectors for gene therapy, protein production, vaccine development and other applications (Abstract).
Regarding claim 8, Saha et al. teach the schematic representation of the adenovirus genome and various adenoviral vectors (p3566, figure 1). The vector includes components such as ITR, Ψ, GOI, HAdV-5 genome ( E1/E3 deleted). Makrides teaches Virus-based vectors for gene delivery and expression in mammalian cells (see p10, table 1). Makrides also teaches components in a vector such as regulatory elements including CMV (pp17, parag 3) and poly A (p19, parag 3).
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to modify Barouch et al.’s chimeric Ad5 vectors having substitutions of fiber knob domain, use the chimpanzee-origin Ad viruses of serotype 6 (AdC6) as taught by Ersching et al., and further have a chimeric adenovirus vector comprising the adenoviral genome with a fiber protein combined with the tail and shaft domains of human Ad5 and the knob domain of chimpanzee AdC6 as well as other components such as gene of interest (GOI) and regulatory elements as taught by Saha et al. and Makrides. The difference between instant claim and Barouch et al.’s chimeric Ad5 vectors having substitutions of fiber knob domain is instant claim has the knob domain of the end of the fiber protein of human adenovirus type 5 been replaced with the knob domain of chimpanzee adenovirus serotype 6, and further forming an chimeric adenovirus vector comprising the chimeric adenovirus genome and other regulatory elements. Given that Barouch et al. teach any fiber knob domain from an adenovirus serotype having a lower seroprevalence compared to Ad5 can be used to replace the fiber knob domain of Ad5, Ersching et al. teach AdC6 has a lower seroprevalence than Ad5, and Saha et al. as well as Makrides teach an adenovirus vector for gene expressing, one of ordinary skill in the art would have substituted the fiber knob domain of human Ad5 with AdC6, and have a an adenovirus vector comprising the chimeric adenoviral genome in the vector for gene expressing depends on their research interest or preference. This simple substitution of one known element (a chimeric adenovirus vector comprising adenovirus genome having a fiber protein combined with the tail and shaft domains of human Ad 5 and the knob domain of chimpanzee AdC6) for another known element (a recombinant adenovirus vector comprising human Ad5 adenovirus genome) to form a chimeric adenovirus vector is likely to be obvious when predictable results are achieved. See KSR International Co. v. Teleflex Inc., 550 U.S. 398, 415-421, USPQ2d 1385, 1395 — 97 (2007) (see MPEP § 2143, B.).
Claim 1, 5 and 9-12 are rejected under 35 U.S.C. 103 as being unpatentable over Barouch et al. (WO 2013/036791 A2) in view of Ersching et al. (Virology. 2010 Nov 10;407(1):1-6), as applied to claims 1, 5 and 10-12 above, further in view of Khallouf et al. (Vaccines (Basel). 2014 Jun 13;2(2):422-62).
The teaching of Barouch et al. and Ersching et al. is set for the above.
Regarding claim 9, Barouch et al. and Ersching et al do not teach the chimeric adenovirus vector comprises as an insert a) a gene encoding the spike protein of the coronavirus, or b) a gene encoding the E6 and E7 proteins of human papillomavirus type 16 or 18. However, this was disclosed by Khallouf et al. at the time of instant invention.
Khallouf et al. teach a comprehensive overview of completed and ongoing clinical trials in therapeutic HPV vaccination, and also highlights selected promising preclinical studies (Abstract).
Regarding claim 9, Khallouf et al. teach preclinical studies in a murine model have shown that immunization with a rAd5 vector expressing HPV16 E6/E7 (Ad5 E6/E7) can induce HPV antigen-specific immune responses and can prevent development of HPV16-positive tumors (p439-440).
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to modify Barouch et al.’s chimeric Ad5 vectors having substitutions of fiber knob domain, and use the chimpanzee-origin Ad viruses of serotype 6 (AdC6) as taught by Ersching et al., and further have an insert comprising a gene encoding the E6 and E7 proteins of human papillomavirus type 16 or 18 as taught by Khallouf et al.. The skilled artisan would have been motivated to have an insert comprising a gene encoding the E6 and E7 proteins of human papillomavirus type 16 or 18 since Khallouf et al. teach immunization with a rAd5 vector expressing HPV16 E6/E7 (Ad5 E6/E7) can induce HPV antigen-specific immune responses and can prevent development of HPV16-positive tumors (p439-440), which is beneficial for the prevention or the treatment of HPV16-positive tumors. There would be a reasonable expectation of success of having an insert comprising a gene encoding the E6 and E7 proteins of human papillomavirus type 16 or 18, since Khallouf et al. teach the evidence from preclinical studies having rAd5 vector expressing HPV16 E6/E7 (Ad5 E6/E7) (see p439-440).
Allowable Subject Matter
Claims 6 and 7 would be allowable if rewritten to overcome the rejection(s) under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), 2nd paragraph, set forth in this Office action and to include all of the limitations of the base claim and any intervening claims.
Claims 6 and 7 are directed to the chimeric protein in which the hexon protein of human adenovirus type 5 is replaced with the hypervariable region 1-7 of human adenovirus serotype 28 comprises the amino acid sequence of SEQ ID NO: 3, as well as the gene encoding a chimeric protein in which the hexon protein of human adenovirus type 5 is replaced with hypervariable regions 1-7 of human adenovirus serotype 28 comprises the nucleic acid sequence of SEQ ID NO: 4. The SEQ ID NOs 3 and 4 are art free in sequence search in the databases.
Conclusion
No claim is allowed.
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/Q.G./Examiner, Art Unit 1633
/FEREYDOUN G SAJJADI/Supervisory Patent Examiner, Art Unit 1699
Sequence alignment
SEQ ID NO:1 v.s. SEQ ID NO:19 in US 2015/0352203 A1
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83
626
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Greyscale
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308
762
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Greyscale
SEQ ID NO:2 v.s. SEQ ID NO:5 in US 2015/0352203 A1
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76
475
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Greyscale
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755
797
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