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 .
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 04/29/2026 has been entered.
Claim Status
Claims 1-10 and 12-30 are pending.
Claims 14-30 are withdrawn from examination as being part of non-elected inventions.
Claims 1-10 and 12-13 are being examined.
All previous objections and rejections not set forth below have been withdrawn in view of applicant’s amendments to the claims.
Claim Objections
Claim 30 is objected to because of the following informalities:
It is suggested to add “a” between “comprising” and “mammalian promoter” in line 6 in claim 30.
Appropriate correction is required.
Claim Rejections - 35 USC § 102
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 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.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 1-2, 4-8, 10 and 12-13 remain rejected under 35 U.S.C. 102(a)(1)) as anticipated by Rybicki et al. (GB2574609A) in evidence of Nath et al. (Structural Perspectives of Beak and Feather Disease Virus and Porcine Circovirus Proteins, 2021, Viral Immunology, 34:49-59), Tepfer et al. (Transient expression in mammalian cells of transgenes transcribed from the Cauliflower mosaic virus 35S promoter, Environ. Biosafety Res. 3:91–97) and Durocher et al. (High-level and high-throughput recombinant protein production by transient transfection of suspension-growing human 293-EBNA1 cells, 2002, Nucleic acids research, 30:e9).
Rybicki et al. describes a mammalian porcine circovirus (PCV) pseudovirion (reads on to VLP, as discussed below) comprising a PCV capsid protein encoded by a replicating geminiviral (BeYDV) vector (which reads on to “replicon”) (abstract) and produced in a plant cell (page 2. Para 2, line 2-3), as recited in claim 2. It is known in the art that the circovirus capsid protein is icosahedral (Nath et al.; page 50, left column, 1st para). The replicating vector (replicon) comprises a mammalian promoter operably linked to the heterologous capsid polypeptide (Abstract) and, thus, replicates in a mammalian cells, as recited in claim 12. Rybicki et al. teaches that pseudovirions (PsVs) are produced in animals while the same or similar substances produced in plants are termed as “virus like particles” (VLPs) (page 1, last para; page 2, first para).
Rybicki et al. describes 5' and 3' ends of the amplicon (also known as replicon) consisting of a geminiviral long intergenic region (LIR) sequence of geminivirus BeYDV (Fig. 2; page 5, para 2; page 11 last line and page 12 first 2 lines).
Rybicki et al. teaches that the gene encoding the Rep/RepA protein can be present on another vector (page 10, para 1, line 1-2), which reads on to “a construct”, within the VLP which results in the production of the replicon/amplicon to high copy number in the target (mammalian) cell (p.10, para 1, last 2 lines). Rybicki et al. describes Rep and/or RepA being expressed under the control of the CaMV 35S promoter in an expression cassette (page 12, para 1, like 2-3). CaMV35 promoter does qualify as a “mammalian promoter” as it is functional in mammalian cells (Tepfer et al., Title and abstract), as recited in claims 1 and 12 and reads on to the definition of "mammalian promoter" as described by the Applicant (Spec, page 6, line 1-2). If it is determined that CaMV 35S is not a mammalian promoter, then it would have been obvious to use (other) mammalian promoters, as discussed below.
Regarding claim 4, Rybicki et al. describes a cytomegalovirus expression cassette (page 18, para 3, line 14-16). It is acknowledged in the art that a cytomegalovirus expression cassette includes a cytomegalovirus promoter (Durocher et al.; abstract; page 1, right column, para 2, line 16-25).
Regarding claim 5, Rybicki et al. teaches a heterologous polynucleotide encoding the capsid protein (abstract; page 2, para 2, line 8-9).
Regarding claim 6, Rybicki et al. teaches an antigenic polypeptide, a hormone, an antibody, or an enzyme (page 3, pare 2, line 1-4).
Regarding claim 7, Rybicki et al. describes expressing PCV capsid protein in the VLP, as discussed above. VLPs minimally require a viral capsid protein for spontaneous formation of a VLP structure (spec, page 3, last 2 lines). The structure of VLPs mimics the native virus from which the capsid proteins are derived, and the capsid proteins are exposed on the surface of a virus. Naturally, the VLPs, as described by Rybicki et al., present the capsid protein encoded by the heterologous polynucleotide on its surface.
Regarding claim 8, the heterologous polynucleotide encoding the capsid protein, encodes an RNA (mRNA) which is needed to make the protein.
Regarding claim 10, Rybicki et al. describes a replicon (an amplicon produced by the amplification/replication of the PCV genome in the host cell) comprising a geminiviral short intergenic region (SIR) sequence (page 5, para 2, line 6; Fig. 2; page 6, para 3, line 1; Fig. 7; page 12, para 1, line 1-2 and 5) that flanks the heterologous polynucleotide on its 3'end (Fig. 2A).
Regarding claim 12, Rybicki et al. describes a replicon which is capable of replicating in mammalian cells (page 9, para 3, line 1-3).
Regarding claim 13, Rybicki et al. teaches a pharmaceutical composition comprising the VLP of claim 1 and a pharmaceutically acceptable carrier (Abstract and claim 14).
Response to Applicants’ arguments regarding 35 U.S.C. § 102(a)(1) rejections: The Applicant argues, “the Rep/RepA protein in Rybicki is expressed from a plant promoter, which Rybicki states cannot be recognized in a mammalian cell. See, e.g. Rybicki at page 9, second full paragraph” (response, page 6, para 3, line 8-9).
The Examiner disagrees. Tepfer et al. explicitly teaches that CaMV 35S promoter is functional in mammalian cells (title and abstract) and reads on to the definition of a “mammalian promoter” by the Applicant (spec, p. 6, line 1-2), as discussed above. In that sense, 35S CaMV is not a typical “plant-specific” promoter. Moreover, Rybicki et al. does not define what is “plant specific promoter” and/or mention the 35S CaMV promoter while describing plant-specific promoter sequence at page 9, second full paragraph. Rybicki et al. also does not define “mammalian promoter”.
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.
Claims 3 is rejected under 35 U.S.C. 103 as being unpatentable over Rybicki et al. as applied to claims 1-2, 4-8, 10 and 12-13 above, and further in view of Lai et al. (Robust production of virus-like particles and monoclonal antibodies with geminiviral replicon vectors in lettuce, 2012, Plant Biotechnol J., 10:95–104).
Claim 3 depends from claim 1 and is drawn to a icosahedral mammalian virus capsid protein is a Norwalk virus capsid protein (NVCP).
Rybicki et al. describes plant derived virus-like particles (VLPs) comprising an icosahedral mammalian viral capsid protein and containing a replicon comprising a mammalian promoter operably linked to a heterologous polynucleotide encoding Rep and/or RepA, wherein the 5' and 3' ends of the replicon consist of a geminiviral long intergenic region (LIR) sequence; and a construct (a vector, a replicon) comprising mammalian promoter operably linked to a polynucleotide encoding Rep and/or RepA, as discussed above.
However, Rybicki et al., does not describe any Norwalk virus capsid protein (NVCP).
Lai et al. describes a method to obtain high-level expression of virus-like particles (VLP) derived from the Norwalk virus capsid protein (NVCP) in a plant using the same geminiviral (bean yellow dwarf virus, BYDV) based replicon system (abstract). The NVCP based VLPs are used as a therapeutic agent against Ebola and West Nile viruses (abstract).
Before the effective filing date of the invention, it would have been obvious to an ordinarily skilled artisan to modify the method described by Rybicki et al. to use the Norwalk virus capsid protein (NVCP) (replacing the porcine circovirus capsid protein) for high level expression, as described by Lai et al., and consequently more efficient production of the NVCP based VLP.
Before the effective filing date, one ordinarily skilled artisan would have been motivated to use the Norwalk virus capsid protein (NVCP) for high level expression, and consequently more efficient production, of the NVCP based VLP to be used as a therapeutic agent against Ebola and West Nile viruses.
Claim 9 is rejected under 35 U.S.C. 103 as being unpatentable over Rybicki et al. as applied to claims 1-2, 4-8, 10 and 12-13 above, and further in view of Arhancet et al. (US 20180030445A1)
Claim 9 depends from claim 8 and recites, “… wherein the RNA is a small interfering RNA (siRNA), short hairpin RNA (shRNA), anti-sense RNA, microRNA (miRNA), or guide RNA (gRNA)”
Rybicki et al. describes plant derived virus-like particles (VLPs) comprising an icosahedral mammalian viral capsid protein and containing a replicon comprising a mammalian promoter operably linked to a heterologous polynucleotide encoding Rep and/or RepA, wherein the 5' and 3' ends of the replicon consist of a geminiviral long intergenic region (LIR) sequence; and a construct (a vector, a replicon) comprising mammalian promoter operably linked to a polynucleotide encoding Rep and/or RepA, as discussed above.
However, Rybicki et al. does not describe any heterologous polynucleotide encoding a small interfering RNA (siRNA), short hairpin RNA (shRNA), anti-sense RNA, microRNA (miRNA), or guide RNA (gRNA)”.
Arhancet et al. describes producing VLPs expressing nucleic acid constructs comprising short RNAs selected from siRNA, shRNA, sshRNA, lshRNA and miRNA (page 1, para 0010; claims 5-6). Such VLPs are used to produce double stranded RNA molecules (claim 5) in the target host cells for various purposes including- silencing one or more endogenous gene(s) using RNA interference (RNAi) (page 8, para 0068); introducing short RNA sequences aimed at inducing RNAi in specific target cells (page 9, para 0071); targeting endogenous RNA strands essential for the survival of the host taking up such RNAs within VLPs (page 23, para 0202).
Before the effective filing date of the invention, it would have been obvious to an ordinarily skilled artisan to modify the method described by Rybicki et al. to express an RNA molecule encoded by the heterologous polynucleotide and encapsulated in the VLP with the realistic objective to silencing one or more endogenous gene(s) in the target host cells using RNA interference (RNAi), as described by Arhancet et al.
Before the effective filing date, one ordinarily skilled artisan would have been motivated to express an RNA molecule encoded by the heterologous polynucleotide and being encapsulated in the VLP with the realistic objective to silencing one or more endogenous gene(s) in the target host cells using RNA interference (RNAi).
The rejections under 35 U.S.C. 103 below are alternatively presented, if it is determined that CaMV 35S is not a mammalian promoter because it is not derived from a mammalian genomic sequence (alternative definition).
Claims 1-2, 4-8, 10 and 12 are rejected under 35 U.S.C. 103 as being unpatentable over Rybicki et al. in view of Kennedy, P. (HPV Pseudovirion Production in Plants, 2013, Thesis presented for the degree of Master of Science in the department of Molecular Biology, University of Cape Town, South Africa).
Claim 1 are drawn to a virus-like particle (VLP) comprising an icosahedral mammalian virus capsid protein and containing– i) a replicon comprising a mammalian promoter operably linked to a heterologous polynucleotide encoding Rep and/or RepA, wherein the 5' and 3' ends of the replicon consist of a geminiviral long intergenic region (LIR) sequence; and ii) a construct comprising mammalian promoter operably linked to a polynucleotide encoding Rep and/or RepA.
Rybicki et al. describes a mammalian porcine circovirus (PCV) pseudovirion (reads on to VLP) comprising a PCV capsid protein encoded by a replicating geminiviral (BeYDV) vector (which reads on to “replicon”) (abstract). It is known in the art that all circovirus capsid protein is icosahedral (Nath et al.; page 50, left column, 1st para). The replicating vector comprises a mammalian promoter operably linked to the heterologous capsid polypeptide (Abstract) and, thus, replicated in a mammalian cell (as recited in claim 12). Rybicki et al. teaches that pseudovirions (PsVs) are produced in animals while the same or similar substances produced in plants are termed as “virus like particles” (VLPs) (page 1, last para; page 2, first para). Rybicki et al. describes 5' and 3' ends of the amplicon (also known as replicon) consisting of a geminiviral long intergenic region (LIR) sequence of geminivirus BeYDV (Fig. 2; page 5, para 2; page 11 last line and page 12 first 2 lines).
Rybicki et al. teaches that the gene encoding the Rep/RepA protein can be present on another vector, which reads on to “a construct”, (page 10, para 1, line 1-2) within the VLP. It also teaches Rep and/or RepA being expressed under the control of the CaMV 35S promoter in an expression cassette (page 12, para 1, like 2-3), which reads on to the definition of "mammalian promoter" as defined by the Applicant as “a promoter that drives gene expression in mammalian cells” (Spec, page 6, line 1-2).
Rybicki et al. uses a replicating vectors derived from the geminivirus BeYDV (abstract, line 2-3) while Kennedy, P. describes that the Rep and RepA are the only (Gemini)viral components required for replication (page 26, last para, line 6) which is capable to initiate replication in a host cell (page 31, para 1, line 4-5). Kennedy, P. also describes that insertion of a mammalian promoter into the vector present in high copy number leading to increased expression of the gene(s) under the control of the mammalian promoter (page 33, para 2, line 3-7). Any gene including Rep/RepA, cloned in the vector under the control of a mammalian promoter would have increased expression.
Before the effective filing date of the invention, it would have been obvious to an ordinarily skilled artisan to modify the method described by Rybicki et al. to make a vector construct comprising a mammalian promoter operably linked to a polynucleotide encoding Rep and/or RepA to achieve higher copy number of the replicon leading to higher expression of the heterologous polynucleotide encoded by the vector in mammalian host cells, as described by Kennedy, P.
Before the effective filing date, one ordinarily skilled artisan would have been motivated to make a vector construct comprising a mammalian promoter operably linked to a polynucleotide encoding Rep and/or RepA to achieve increased copy number of the replicon leading to higher expression of the gene(s) encoded by the vector/replicon in mammalian host cells.
Regarding claim 12, Rybicki et al. describes a replicon which is capable of replicating in mammalian cells (page 9, para 3, line 1-3).
Claims 3 is rejected under 35 U.S.C. 103 as being unpatentable over Rybicki et al. in view of Kennedy, P. as applied to claims 1-2, 4-8, 10 and 12-13 above, and further in view of Lai et al. (Robust production of virus-like particles and monoclonal antibodies with geminiviral replicon vectors in lettuce, 2012, Plant Biotechnol J., 10:95–104).
Claim 3 depends from claim 1 and is drawn to a icosahedral mammalian virus capsid protein is a Norwalk virus capsid protein (NVCP).
Rybicki et al. describes plant derived virus-like particles (VLPs) comprising an icosahedral mammalian viral capsid protein and containing a replicon comprising a mammalian promoter operably linked to a heterologous polynucleotide encoding Rep and/or RepA, wherein the 5' and 3' ends of the replicon consist of a geminiviral long intergenic region (LIR) sequence; and a construct (a vector, a replicon) comprising mammalian promoter operably linked to a polynucleotide encoding Rep and/or RepA, as discussed above.
However, Rybicki et al., does not describe any Norwalk virus capsid protein (NVCP).
Lai et al. describes a method to obtain high-level expression of virus-like particles (VLP) derived from the Norwalk virus capsid protein (NVCP) in a plant using the same geminiviral (bean yellow dwarf virus, BYDV) based replicon system (abstract). The NVCP based VLPs are used as a therapeutic agent against Ebola and West Nile viruses (abstract).
Before the effective filing date of the invention, it would have been obvious to an ordinarily skilled artisan to modify the method described by Rybicki et al. to use the Norwalk virus capsid protein (NVCP) (replacing the porcine circovirus capsid protein) for high level expression, as described by Lai et al., and consequently more efficient production of the NVCP based VLP.
Before the effective filing date, one ordinarily skilled artisan would have been motivated to use the Norwalk virus capsid protein (NVCP) for high level expression, and consequently more efficient production, of the NVCP based VLP to be used as a therapeutic agent against Ebola and West Nile viruses.
Claim 9 is rejected under 35 U.S.C. 103 as being unpatentable over Rybicki et al. in view of Kennedy, P. as applied to claims 1-2, 4-8, 10 and 12-13 above, and further in view of Arhancet et al. (US 20180030445A1)
Claim 9 depends from claim 8 and recites, “… wherein the RNA is a small interfering RNA (siRNA), short hairpin RNA (shRNA), anti-sense RNA, microRNA (miRNA), or guide RNA (gRNA)”
Rybicki et al. describes plant derived virus-like particles (VLPs) comprising an icosahedral mammalian viral capsid protein and containing a replicon comprising a mammalian promoter operably linked to a heterologous polynucleotide encoding Rep and/or RepA, wherein the 5' and 3' ends of the replicon consist of a geminiviral long intergenic region (LIR) sequence; and a construct (a vector, a replicon) comprising mammalian promoter operably linked to a polynucleotide encoding Rep and/or RepA, as discussed above.
However, Rybicki et al. does not describe any heterologous polynucleotide encoding an small interfering RNA (siRNA), short hairpin RNA (shRNA), anti-sense RNA, microRNA (miRNA), or guide RNA (gRNA)”.
Arhancet et al. describes producing VLPs expressing nucleic acid constructs comprising short RNAs selected from siRNA, shRNA, sshRNA, lshRNA and miRNA (page 1, para 0010; claims 5-6). Such VLPs are used to produce double stranded RNA molecules (claim 5) in the target host cells for various purposes including- silencing one or more endogenous gene(s) using RNA interference (RNAi) (page 8, para 0068); introducing short RNA sequences aimed at inducing RNAi in specific target cells (page 9, para 0071); targeting endogenous RNA strands essential for the survival of the host taking up such RNAs within VLPs (page 23, para 0202).
Before the effective filing date of the invention, it would have been obvious to an ordinarily skilled artisan to modify the method described by Rybicki et al. to express an RNA molecule encoded by the heterologous polynucleotide and encapsulated in the VLP with the realistic objective to silencing one or more endogenous gene(s) in the target host cells using RNA interference (RNAi), as described by Arhancet et al.
Before the effective filing date, one ordinarily skilled artisan would have been motivated to express an RNA molecule encoded by the heterologous polynucleotide and being encapsulated in the VLP with the realistic objective to silencing one or more endogenous gene(s) in the target host cells using RNA interference (RNAi).
Response to Applicants’ arguments 35 U.S.C. § 103 rejections: The Applicant argues, “Regarding Kennedy, the Examiner cites page 33, paragraph 2, lines 3-7 as disclosure of the gene encoding Rep/RepA under control of a mammalian promoter. …. This cited passage only states the use of a mammalian promoter with a reporter gene and polyadenylation signal elements. Rep/RepA is not mentioned” (response, page 7, para 5). The Applicant continues to argue that “Kennedy discusses that the purpose of its described methods is for "high-titre HPV PsV production in plants…. In contrast, the present application utilizes a mammalian promoter for expressing Rep/RepA to allow the replicon encoding the heterologous polynucleotide to be replicated in a mammalian host cell” (response, p.7, last para, line 5-8).
The Examiner disagrees. Although Kennedy, P. does not explicitly teach cloning Rep/RepA under the control of a mammalian promoter on p. 33, paragraph 2, the teaching clearly implies that an ordinarily skilled artisan can clone any gene under the control of a mammalian promoter (page 33, para 2, line 3-7), and that includes Rep/RepA gene as well, with a clear motivation to express higher copy number and thus, enhance expression of the protein encoded by the gene including Rep/RepA, as discussed above.
Kennedy describes, “Geminiviruses in the genus Mastrevirus commonly encode only four proteins, namely coat protein (CP), movement protein (MP), and the replication-associated protein Rep and RepA….. Rep and RepA are the only viral components required for replication, which occurs by a rolling circle mechanism and amplifies the circular genome to high copy number” (p. 26, last para para, line 4-7).
It is well-known in the art that a promoter is responsible to express (i.e. transcribe) any polynucleotide sequence, encoding one or more gene(s), being controlled by the promoter. The polynucleotide sequence under the control of the promoter can encode basically any RNA/protein. It is the promoter sequence which decides where the promoter would be functional (i.e., where it will be expressed, in which organism- prokaryotes, eukaryotes like plant or animal/mammal etc., besides other specific regulations in terms of transcription). The Rep and/or RepA protein would express in any host cell depending on the promoter sequence controlling its transcription while the Rep/RepA protein would replicate a geminiviral replicon by a rolling circle mechanism and amplifies the circular genome to high copy number, as taught by Kennedy P. Thus, a promoter, which is functional in a mammalian cell, would express/transcribe any polynucleotide sequence encoding any protein including Rep and/or RepA in a mammalian cell.
Kennedy or any other cited reference does not need to do the exact same experiment and/or for the same objective(s) as the instant invention. The information provided by the cited reference(s) would have made it obvious and motivate an ordinarily skilled artisan to express Rep and/or RepA in a VLP to replicate the target (geminiviral) replicon that would increase the copy number of the replicon resulting in increased production of the VLP.
Moreover, the Applicant does not provide any evidence to show that Rep and/or RepA would not be functional in a mammalian cell. Applicant’s opinion cannot take the place of evidence (MPEP 716.01(c)(II), 2145(I)).
Conclusion
No claim is allowed.
Communication
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Jay Chatterjee
Patent Examiner
Art Unit 1662
/Jay Chatterjee/Examiner, Art Unit 1662
/BRATISLAV STANKOVIC/Supervisory Patent Examiner, Art Units 1661 & 1662
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