DETAILED ACTION
Final Rejection
Notice of Pre-AIA or AIA Status
1. 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
2. Applicant’s election of Group II claims 9-16 and further election of African Swine Fever Virus as a specie, in the reply filed on 05/05/2025 is acknowledged. Because applicant did not distinctly and specifically point out the supposed errors in the restriction requirement, the election has been treated as an election without traverse (MPEP § 818.01(a)). The restriction is made Final.
Status of Claims
3. Claims 1-13, and 15-26 as amended on 01/02/2026 are pending.
4. Claims 1-8, 17-24 and 25-26 are withdrawn from examination as non-elected.
5. Claims 9-13, and 15-16 are under examination in this office action.
Information Disclosure Statement
6. Applicant has not filed information disclosure statement. The listing of references in the specification is not a proper information disclosure statement. 37 CFR 1.98(b) requires a list of all patents, publications, or other information submitted for consideration by the Office, and MPEP § 609.04(a) states, "the list may not be incorporated into the specification but must be submitted in a separate paper." Therefore, unless the references have been cited by the examiner on form PTO-892, they have not been considered. Applicant has listed 41 references on page numbers 52-54 of the specification.
Priority (modified)
7. This application is a CIP of International Patent Application No. PCT/US2020/50939, filed on 16 September 2020, which claims the benefit of U.S. Provisional Application No. 62/900,816 filed on 16 September 2019.
The amended instant claim 9 and dependent claims under examination do not have support for claimed elements “endocytosis” and “phagocytosis” in context to the ASFV proteins both in the provisional application 62/900,816 and PCT/US2020/50939.
However, the instant application 17/535,545 filing date 11/24/2021 has support for the amended claim 9 claimed elements “endocytosis” and “phagocytosis” in context to the method administering the instant claimed ASFV proteins/antigens.
Withdrawn Rejection under 35 U.S.C 102
8. Withdrawn rejection of claims 9-13, and 15-16 under 35 U.S.C. 102 (a)(1) or (a)(2) or both in view of amendment of claim 9 that affected dependent claims 10 and 16.
Withdrawn Rejection under 35 U.S.C 112
9. Withdrawn rejection of claims 9-10 and 16 under 35 U.S.C. 112 (a) and 112(b) in view of applicant’s arguments/response.
Withdrawn Objection to Drawing
10. Withdrawn objection to the drawings in view of replacement filed on 01/02/2026.
11. Withdrawn provisional double patenting rejection of claims 9-10 and 14-16 under 35 USC §101 in view of applicant’s amendment of instant claim 9.
Claim Objections
12. Claim 9 is objected to because of the following informalities:
The instant claim 9 in line 9 recited “macropinoocytosis” that is a spelling error.
Appropriate correction is required.
Claim Interpretation (modified)
13. The claims in this application are given their broadest reasonable interpretation using the plain meaning of the claim language in light of the specification as it would be understood by one of ordinary skill in the art.
In summary, the instant elected claims 9-13 and 15-16 are directed to a method of immunization or treating ASFV viral infection in porcine (swine/pigs), by administering ASFV proteins including whole and/or partial domains of proteins that induce antibody and immune response to inhibit viral ligand interactions with critical cellular receptors that are involved either directly (endocytosis and/or macropinocytosis) or indirectly (phagocytosis of RBCs that have been aggregated by viral interactions) with binding of ASFV to host cell and cellular entry and thus inhibit the viral infection and spread in porcine or other susceptible animal species.
The ASFV that is “lysogenic” (as termed by the applicant) is interpreted as an ASFV that has viral envelop derived from cell membrane and the ASFV acquired the cell membrane envelope via “budding mechanism”. Many animal and human viruses are known in the art to acquire viral envelope by cellular membrane budding mechanism.
The ASFV that is lytic (as termed by the applicant) is interpreted as an ASFV that does not have a viral envelope. Because the virus did not undergo the budding mechanism for release from the cell and the virus released from the cell by of burst of the cell likely due to pathological and structural changes of the cells due to large number of virus particle replication and accumulation and swelling of a cell like a balloon, thereby the virus has only capsid and not the viral envelope derived from cell membrane. Many animal and human viruses are known in the art to acquire viral envelope by cellular membrane budding mechanism. The same infected animal however would produce both type of viruses having viral enveloped or no viral envelope. There is no ASFV known in the art that produce only enveloped or non-enveloped ASFV as progeny.
The instant claims 9-13, and 15-16 are interpreted as directed to: a method of treating a viral infection in an individual that is an enveloped virus that has both an outer membrane protein known as an outer/external envelope (See, abstract and Fig. 1-C of Salsas et al 2013 (Virus Research 173 (2013) 29– 41) whereas applicant recited a phrase lysogenic for an outer membrane protein of a virus; and a capsid (See, Salsas et al 2013, abstract as referred supra) whereas applicant recited a phrase lytic for capsid protein of a virus, including the steps of: administering a viral antigen that targets protein on an outer/external envelope of the virus; administering a viral antigen that induce antibody response or immune response to target the viral capsid or the viral envelope - the claim limitation is interpreted as administering a viral antigen that induces antibodies and immune response that targets outer envelope protein and viral capsid protein, respectively; and treating the viral infection. The ASFV viral antigen is derived from a protein chosen from the group consisting of pE402R (CD2v), EP153R, E183L (p54), pE102R, B646L (p72), CP204L (p30), B438L (p49), O61R (p12), and combinations thereof (claim 9 limitations); wherein the individual is a swine (claim 10 limitations dependent on claim 9); wherein said administering a viral antigen that targets outer/external envelope protein of the virus is further defined as targeting pE402R (claim 11 dependent on claim 9); wherein said administering a viral antigen that targets protein on a capsid of the virus is further defined as targeting a protein chosen from the group consisting of pE102R, p72, p49, and combinations thereof (claim 12 dependent on claim 9); wherein each of said administering steps include administering a composition chosen from the group consisting of whole protein, a peptide, peptide segments, and a mixture of peptides derived from target proteins (claim 12 dependent on claim 9); wherein each of said administering steps include administering a composition chosen from the group consisting of whole protein, a peptide, peptide segments, and a mixture of peptides derived from target protein (claim 13 dependent on claim 9); wherein said administering steps are performed with a single injection or separate injections (claim 15 dependent on claim 9); wherein said treating step further includes the step of inducing a B-cell response in the individual and creating an immune stimulating response (claim 16 dependent on claim 9).
Claim Rejections - 35 USC § 103
14. 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.
15: Claims 9-10 and 16 are rejected under 35 U.S.C. 103 as being unpatentable over Guelen et al 2019 (US20170056492A1 published 03/02/2017), and further in view of Salsas et al 2013 (Virus Research 173 (2013) 29– 41), Rath et al 2008 (US20080131449A1 published 06/05/2008), Neilan et al 2004 (Virology 319 (2004) 337– 342), Pérez-Núñez et al 2019 (Veterinary Immunology and Immunopathology 208 (2019) 34–43), Gaudreault et al 2019 (Vaccines 2019, 7, 56), Netherton et al 2019 (Frontiers in Immunology, vol 10, article 1318), Jia et al 2017 (J Vet Res. 2017 Dec 6;61(2):135-143), Sánchez et al 2012 (PLoS Pathog. 2012;8(6): e1002754), Sánchez et al 2017 (Vaccines (Basel). 2017 Nov 8;5(4):42), Yang et al 2021 (Drug Delivery, Vol. 28, No. 1, 957–962) and Galindo et al 2015 (Virus Research, 200 (2015) 45–55).
Claims 9-10: Guelen et al 2019 (US20170056492A1) is in the art and discloses, a method of treating a viral infection in an individual with a virus that is both lysogenic and lytic (therapeutic vaccination once the virus is diagnosed in an infected animal that is not yet suffering from the syndrome is equally efficient (See, para. [0099]); Therefore, the invention relates to a vaccine, wherein the virus pathogenic to swine is selected from the group of... African Swine Fever virus (See, para. [0169]), including the steps of: administering a viral antigen that targets envelope protein of a virus (protein on an outer membrane of a lysogenic phase) of the virus (antigenic material of the virus is interpreted in a broad sense). Antigen can be e.g. viral envelope material comprising viral outer membrane proteins (See, para. [0180)]; administering a viral antigen that targets protein on a capsid of a lytic phase of the virus (Such DNA vaccination is based upon the introduction of a DNA fragment carrying the gene encoding the Capsid protein under the control of a suitable promoter, into the host animal (para. [0146]); the DNA fragment comprising a gene encoding a Capsid protein should be expressing an immunogenically effective amount of the Capsid protein (See, para. [0151]); and treating the viral infection (the term "immunogenically effective amount" as used herein relates to the amount of empty capsid, live recombinant vector or DNA vaccine that is necessary to induce an immune response in pigs (instant claim 10 limitation) to the extent that it decreases the pathological effects caused by infection (See, para. [0153]).
Guelen et al 2019 (US20170056492A1) does not teach the added limitations of the amended instant claim 9, interrupting phagocytosis, and interrupting macropinocytosis and endocytosis, wherein the virus is African Swine Fever Virus (ASFV), wherein the viral antigen is derived from a protein chosen from the group consisting of pE402R (CD2v), EP153R, E183L (p54), pE102R, B646L (p72), CP204L (p30), B438L (p49), O61R (p12), and combinations thereof. The prior arts given below teaches the added limitations of the amended instant claim 9 as recited below.
Rath et al 2008 (US20080131449A1) teaches an invention directed to administration of polypeptides from African Swine Fever virus as vaccines for preventive and therapeutic use (See, US20080131449A1, abstract, claim 24, para [0005]-[0006], [0009], [0012]). The protein p12 of the African Swine Virus (para [0048]), the protein p72 of the African Swine Virus (para [0054]), the protein p54, a 183 amino acid long structural protein of the ASFV (para [0007], [0009], p30 (para [0052]),
Salsas et al 2013 teaches outer envelope proteins pE402R (CD2v), p24 and p12, and capsid proteins B646L (p72) (See, Salsas et al 2013, Fig 1-C).
Neilan et al 2004 teaches neutralizing antibodies to African swine fever virus protein p30, an inner envelope protein p54, and a capsid protein p72 are not sufficient for antibody-mediated protection in pigs (See, Neilan et al 2004, abstract, entire article)
Pérez-Núñez et al 2019 teaches evaluation of a viral DNA-protein immunization strategy against African Swine Fever in domestic pigs. Different groups of pigs were immunized using a modified prime-boost approach with combinations of previously selected viral proteins CD2v-E and p72 expressing DNA; and p72 protein and p72 expressing DNA resulting in induction of antibodies and specific cell-mediated immune response, measured by IFN-γ ELISpots. The ability of antibodies from pigs immunized with various combinations of ASFV-specific antigens to neutralize infection in vitro, and antigen-specific activation of the cellular immune response were analyzed (See, Pérez-Núñez et al 2019, abstract, pages 35-42 methods and results and entire article).
Gaudreault et al 2019 reviewed subunit vaccine approaches for African Swine Fever Virus and discloses that a number of immunogenic ASFV proteins have been identified and investigated for a role in protection against ASF, which are summarized and discussed later in this review. ASFV structural proteins p30, p54, p72, pp62, and CD2v encoded by genes CP204L, E183L, B646L, CP530R, and EP402R, respectively, have been the main targets of subunit and DNA vaccine strategies, including vaccination with either individual ASFV antigen targets or as multitarget cocktails (See, Gaudreault et al 2019, abstract, and page 2 para 3 on Subunit vaccines).
Netherton et al 2019 teaches an approach and method for identification and assessing immunogenicity of ASFV antigens by screening >150 ASFV viral proteins for peptides corresponding to 133 proteins using a gamma interferon ELIspot assay to screen for viral proteins recognized by lymphocytes from ASF-immune pigs (See, Netherton et al 2019, abstract and entire article). The approach can be adopted to screen the ASFV protein peptides for induction of B-cell immune response leading to antibody production in pigs and using ASFV in vitro neutralization and ELISA assays for screening of proteins and peptide antigens.
The instant claim 9 is amended to comprise functional limitations that include/comprise inhibit the micropinocytosis or endocytosis. The claimed ASFV structural proteins are antigens and known to reasonably induce the humoral (antibody) and cellular immune response as recited in the prior art above. The antibodies are expected to bind to the epitopes / antigenic determinants on the viral capsid or envelope structure (viral ligands). The viral ligands normally interact with cellular receptors on the host cells membrane and host cell organelles that results in micropinocytosis or endocytosis or phagocytosis mechanism-based entry into the host cell. Blocking of the viral sub-structure /viral ligands with the immunization induced antibody /immune response to the claimed ASFV proteins would block or bind to the viral ligands and interrupt both micropinocytosis or endocytosis or phagocytosis-based entry and thus replication of the ASFV in the host cells. The prior arts given below recites role of the instant claimed ASFV proteins in micropinocytosis or endocytosis or phagocytosis mechanism. Therefore, antibody response to these proteins would block viral ligands and interrupt micropinocytosis or endocytosis or phagocytosis mechanism.
Sánchez et al 2012 is in the art and teaches ASFV uses macropinocytosis to enter host cells (See, abstract, entire article).
Sánchez et al 2017 is in the art and teaches mechanisms of entry and endosomal pathway of ASFV, the ASFV enters host cells by receptor-mediated endocytosis (See, title and abstract). Alternative mechanisms such as phagocytosis have been suggested to be used by ASFV to enter primary macrophages (see, page 6 last para last 7-8 lines, entire article). After internalization, ASFV traffics through the endolysosomal system. The capsid and inner envelope are found in early endosomes or macropinosomes early after infection (See, abstract, entire article).
Yang et al 2021 is in the art and teaches identification of a new cell-penetrating peptide derived from the ASFV CD2v (EP402R) protein contains a repetitive RAAS sequence, and the RAAS enter the cells via the macropinocytosis or the clathrin-mediated endocytosis and RAAS function as a cell-penetrating peptide (See, abstract, entire article).
Galindo et al 2015 is in the art and teaches ASFV infects macrophages, the natural host cells by endocytosis, a recombinant ASFV expressing GFP fused ASFV protein p54 was used to demonstrate endocytosis (See, abstract, entire article).
Jia et al 2017 is in the art and teaches that there is evidence that the ASFV enters through a dynamin-dependent and clathrin-mediated micropinocytosis process in monocyte or macrophage cells (See, abstract, entire article).
Claim 16: Guelen et al 2019 (US20170056492A1) discloses the added limitation of instant claim 16, wherein said treating step further includes the step of inducing a B-cell response in the individual and creating an immune stimulating response by disclosing "immunogenically effective amount" as used herein relates to the amount of empty capsid, live recombinant vector or DNA vaccine that is necessary to induce an immune response in pigs to the extent that it decreases the pathological effects caused by infection, (See, para. [0153]; the capsid proteins of the virus according to the invention are highly suitable because they are suitable for use in vaccines, more specifically in subunit vaccines (See, para. [0078]); an immunogen or immunogenic component is a compound that induces an immune response in an animal. It can e.g. be a whole virus, or a protein or a sugar moiety of that virus (See, para [0167]. Thus, another embodiment of the present invention relates to antibodies (a B-cell response) or antisera that are reactive with the virus according to the invention (See, para. [0178]).
The instant claim 9 (and dependent claims) method(s) have a functional limitation interrupting phagocytosis, and interrupting micropinocytosis, and interrupting endocytosis. These functional limitations are achieved by administration of ASFV viral antigen(s) that is/are derived from a protein chosen from the group consisting of pE402R (CD2v), EP153R, E183L (p54), pE102R, B646L (p72), CP204L (p30), B438L (p49), O61R (p12), and combinations thereof. The claimed functional mechanisms interrupting phagocytosis, and interrupting micropinocytosis, and interrupting endocytosis is inherent to the claimed method that is rendered obvious by the combined prior art teachings, as applied and recited supra, comprising the claimed administration of ASVF viral antigens (ASFV proteins) derived from the ASFV outer envelope and the ASFV outer capsid. See, MPEP § 2112.02: In re Best, 562 F.2d 1252, 1255, 195 USPQ 430, 433 (CCPA 1977).
It would have been obvious to one of ordinary skills in the art before the effective filing date of the claimed invention to modify prior art teachings of Guelen et al 2019 to incorporate the teachings of Salsas et al 2013, Rath et al 2008, Neilan et al 2004, Pérez-Núñez et al 2019, Gaudreault et al 2019, and Netherton et al 2019 on the claimed ASFV structural proteins pE402R (CD2v), EP153R, E183L (p54), pE102R, B646L (p72), CP204L (p30), B438L (p49), O61R (p12), and combinations thereof and their role in entry of ASFV into the host cells by mechanism of micropinocytosis or endocytosis as taught by the teachings of Jia et al 2017, Sánchez et al 2012, Sánchez et al 2017, Yang et al 2021 and Galindo et al 2015 to arrive at the inventions of claims 9-10 and 16. The combined prior art teachings including Guelen et al 2019 teaches the claimed ASFV structural proteins induce immune response (antibody and cellular), and the antibodies and immune response is directed to the viral envelope and viral outer capsid and bind to the viral envelope (applicant termed lysogenic) and capsid (applicant termed lytic) and prevent ligand interaction with cellular receptor to prevent entry into the cells by the micropinocytosis or endocytosis or phagocytosis mechanisms taught by the applied prior art teachings. Thus, the challenges to develop an effective composition comprising ASFV outer envelope antigens and capsid antigens for the claimed method for treatment of ASFV infection in pigs is taught by the combined prior art teachings as applied and recited supra. One of ordinary skills in the art would have been motivated to incorporate the combined teachings of the applied prior arts as recited supra to develop an effective method of treatment using multiple antigens or peptides derived from outer envelope and capsid of ASFV to arrive at the invention of claims 9-10 and 16 for commercial success having knowledge in the art that there is no effective vaccine or treatment available for ASFV infection in pigs; and the natural host of ASFV is pig which is domestic food animal and contribute to food security and commercial success. One of the ordinary skills in the art would have a reasonable expectation of success to arrive at the invention of claims 9-10 and 16 given the prior teachings as applied to the claims as recited supra. This is analogous to some teaching, suggestion, or motivation in the prior art that would have led one of ordinary skill to modify the prior art reference or to combine prior art reference teachings to arrive at the invention as claimed in claims 9-10 and 16. See KSR Int'l Co. v. Teleflex Inc., 550 U.S. 398, 415-421, 82 USPQ2d 1385, 1395-97 (2007) (see MPEP § 2143, example of rationales, A-G).
16. Claim 11 is rejected under 35 U.S.C. 103 as being unpatentable over combined teachings of Guelen et al 2019 (US20170056492A1 published 03/02/2017), Salsas et al 2013 (Virus Research 173 (2013) 29– 41), Rath et al 2008 (US20080131449A1 published 06/05/2008), Neilan et al 2004 (Virology 319 (2004) 337– 342), Pérez-Núñez et al 2019 (Veterinary Immunology and Immunopathology 208 (2019) 34–43), Gaudreault et al 2019 (Vaccines 2019, 7, 56), Netherton et al 2019 (Frontiers in Immunology, vol 10, article 1318), Jia et al 2017 (J Vet Res. 2017 Dec 6;61(2):135-143), Sánchez et al 2012 (PLoS Pathog. 2012;8(6): e1002754), Sánchez et al 2017 (Vaccines (Basel). 2017 Nov 8;5(4):42), Yang et al 2021 (Drug Delivery, Vol. 28, No. 1, 957–962), and Galindo et al 2015 (Virus Research, 200 (2015) 45–55), and further in view of Burmakina et al 2016 (J Gen Virol, 97 (7): 1670-1675) and Rodríguez et al 1993 (J Virol. 1993 Sep;67(9):5312-20).
The combined teachings Guelen et al 2019, and other additional prior arts as applied to claims 9-10 and 16 teaches method of claims 9 as recited supra. However, does not teach added limitation of claim 11, wherein said administering a viral antigen that targets protein on an outer membrane of a lysogenic phase of the virus step is further defined as targeting pE402R.
Burmakina et al 2016 further teaches ASFV protein CD2v (EP402R or pE402R) is ASFV serotype-specific proteins are significant protective antigens for ASFV. Vaccination/challenge experiments in pigs indicate that ASF protective immunity is by haemadsorption inhibition (HAI) antibodies that are serotype specific (See, abstract).
Rodríguez et al 1993 teaches pEP402R gene encoded protein, also designated CD2v or CD2-like, is required for the attachment/binding of red blood cells to infected macrophages and is directly involved in hemadsorption phenomenon induced by the infection of susceptible cells with ASFV and contribute to ASFV pathogenesis and progression of pathogenicity through circulation to different organ system of red blood cells to which the ASFV is bound (See, Rodríguez et al 1993, abstract and entire article).
It would have been obvious to one of ordinary skills in the art before the effective filing date of the claimed invention to modify the combined prior art teachings as applied to claim 9 with additional teachings of prior arts by Burmakina et al 2016 and Rodríguez et al 1993 on pEP402R protein (CD2v protein) to arrive at the invention of claim 11. One of ordinary skills in the art would have been motivated to incorporate the teachings of Burmakina et al 2016 and Rodríguez et al 1993 on pEP402R protein (CD2v protein) to develop an effective method of treatment by incorporating pEP402R protein (CD2v protein) to induce antibodies that prevent the attachment of ASFV to red blood cells and prevent hemadsorption of ASFV from infected cells and extracellular ASFV in blood (See, Burmakina et al 2016 and Rodríguez et al 1993) and for commercial success. Having knowledge in the art that there is no effective vaccine or treatment available for ASFV infection in pigs. One of the ordinary skills in the art would have a reasonable expectation of success to arrive at the invention of claim 11 given the prior teachings as applied to the claim as recited supra. This is analogous to some teaching, suggestion, or motivation in the prior art that would have led one of ordinary skill to modify the prior art reference or to combine prior art reference teachings to arrive at the invention as claimed in claim 11. See KSR Int'l Co. v. Teleflex Inc., 550 U.S. 398, 415-421, 82 USPQ2d 1385, 1395-97 (2007) (see MPEP § 2143, example of rationales, A-G).
17: Claims 12-13 and 15-16 are rejected under 35 U.S.C. 103 as being unpatentable over combined teachings of Guelen et al 2019 (US20170056492A1 published 03/02/2017), Salsas et al 2013 (Virus Research 173 (2013) 29– 41), Rath et al 2008 (US20080131449A1 published 06/05/2008), Neilan et al 2004 (Virology 319 (2004) 337– 342), Pérez-Núñez et al 2019 (Veterinary Immunology and Immunopathology 208 (2019) 34–43), Gaudreault et al 2019 (Vaccines 2019, 7, 56), Netherton et al 2019 (Frontiers in Immunology, vol 10, article 1318), Jia et al 2017 (J Vet Res. 2017 Dec 6;61(2):135-143), Sánchez et al 2012 (PLoS Pathog. 2012;8(6): e1002754), Sánchez et al 2017 (Vaccines (Basel). 2017 Nov 8;5(4):42), Yang et al 2021 (Drug Delivery, Vol. 28, No. 1, 957–962), Galindo et al 2015 (Virus Research, 200 (2015) 45–55).
as applied to claim 9 above, and further in view of Andrés et al 2001 (J Virol. 2001 Aug;75(15):6758-68) and Wang et al 2019 (Science. 2019 Nov 1;366(6465):640-644).
Claims 12-13 and 15-16: The combined teachings Guelen et al 2019, and other additional prior arts as applied to claims 9-10 and 16 teaches method of claims 9 as recited supra. However, does not teach added limitations of instant claims 12-13, and 15-16. The prior arts recited below teaches the added limitations of claims 9-10 and 16.
Rath et al 2008 (US20080131449A1) teaches an invention directed to administration of polypeptides from African Swine Fever virus infection as vaccines for preventive and therapeutic use (See, US20080131449A1, abstract, claim 24, para [0005]- [0006], [0009], [0012]). The protein p12 of the African Swine Virus (para [0048]), the protein p72 of the African Swine Virus (para [0054]).
Salsas et al 2013 teaches outer envelope proteins pE402R (CD2v), p24 and p12, and capsid proteins B646L (p72) (See, Salsas et al 2013, Fig 1-C).
Neilan et al 2004 teaches induction of neutralizing antibodies (induction B-cell response, claim 16 limitation) to African swine fever virus protein p30, an inner envelope protein p54, and a capsid protein p72 are not sufficient for antibody-mediated protection in pigs. The administering steps for pr the protein antigens are performed with a single injection or separate injections by disclosing the intra-muscular ASFV protein immunization experiments in pigs (See, Neilan et al 2004, abstract, page 341 col 2 para 2; entire article).
Andrés et al 2001 teaches that protein pE120R protein is essential for the microtubule-mediated transport of ASFV particles from the viral factories to the plasma membrane – virus budding (See, title and abstract, page 6761-6762 Fig 1 and 3, entire article).
Wang et al 2019 teaches that using an optimized image reconstruction strategy, we solved the ASFV capsid structure up to 4.1 angstroms, which is built from 17,280 proteins, including one major (p72) and four minor (M1249L, p17, p49, and H240R) capsid proteins organized into pentasymmetrons and trisymmetrons.
It would have been obvious to one of ordinary skills in the art before the effective filing date of the claimed invention to modify the combined prior art teachings on p72 as applied to claim 9 (Rath et al, Salsas et al and Neilan et al) with additional teachings of prior arts by Andrés et al 2001 on pE120R protein and Wang et al 2019 on p49 protein to arrive at the invention of claims 12-13 and 15-16. One of ordinary skills in the art would have been motivated to incorporate the teachings of Andrés et al 2001 on pE120R protein and Wang et al 2019 on p49 protein to develop an effective method of treatment by incorporating pE120R protein and p49 protein to prevent virus budding to cell surface and assembly of the capsid, respectively by inducing antibodies that bind to pE120R protein and p49 protein to develop the claimed methods for commercial success, having knowledge in the art that there is no effective vaccine or treatment available for ASFV infection in pigs. One of the ordinary skills in the art would have a reasonable expectation of success to arrive at the invention of claims 12-13 and 15-16 given the prior teachings as applied to the claims as recited supra. This is analogous to some teaching, suggestion, or motivation in the prior art that would have led one of ordinary skill to modify the prior art reference or to combine prior art reference teachings to arrive at the invention as claimed in claim 12-13, and 15-16. See KSR Int'l Co. v. Teleflex Inc., 550 U.S. 398, 415-421, 82 USPQ2d 1385, 1395-97 (2007) (see MPEP § 2143, example of rationales, A-G).
Response to Arguments
18. Applicant’s arguments with respect to amended claims 9-13, and 15-16 filed on 01/02/2026 have been considered but are moot because the new ground of rejection does not rely on any reference applied in the prior rejection of record for any teaching or matter specifically challenged in the argument.
Applicant’s Argument:
Claims 9-10 stand rejected under 35 USC §103 as being unpatentable over Guelen, et al. in combination with Salsas, et al., Rath, et al., Neilan, et al., Perez-Nunez, et al., Gaudreault, et al., and Netherton, et al. Specifically, the Office Action holds that Guelen, et al. discloses the method as above, and Rath, et al. teaches administering polypeptides from ASFV as vaccines (p12 and p72), Salsas, et al. teaches outer envelope proteins pE402R, p24 and p12, and capsid proteins B646L (p72), Neilan, et al. teaches neutralizing antibodies to African swine fever virus protein p30, an inner envelope protein p54, and a capsid protein p72 are not sufficient for antibody-mediated protection in pigs, Perez-Nunez, et al. teaches immunization of pigs against ASFV with combinations of viral proteins CD2v-E and p72, Gaudreault, et al. teaches that ASFV structural proteins p30, p54, p72, pp62, and CD2v encoded by genes CP204L, E183L, B646L, CP530R, and EP402R, have been the main targets of subunit and DNA vaccine strategies for ASFV, and Netherton, et al. teaches a method for identification and assessing immunogenicity of ASFV antigens by screening >150 ASFV viral proteins for peptides. The Office Action holds it would have been obvious to modify the method of Guelen, et al. with these references to develop an effective treatment for ASFV as claimed. Reconsideration of the rejection under 35 USC §103 as being unpatentable is respectfully requested.
“Any need or problem known in the field of endeavor at the time of invention and addressed by the patent can provide a reason for combining the elements in the manner claimed” however, that reason must be present for the combination to be obvious. KSR Intern Co. v. Teleflex, 127 S Ct 1727, 1742, US (2007). This requirement was confirmed in Takeda Chem. Industr., et al. v. Alphapharm, No. 06-1329 (Fed Cir 2007).
“The key to supporting any rejection under 35 USC 103 is the clear articulation of the reason(s) why the claimed invention would have been obvious. The Supreme Court in KSR International Co. v. Teleflex Inc., 82 USPQ 2d 1385, 1396 (2007) noted that the analysis supporting a rejection under 35 USC 103 should be made explicit.” MPEP §2143.
“The rationale to support a conclusion that the claim would have been obvious is that all the claimed elements were known in the prior art and one skilled in the art could have combined the elements as claimed by known methods with no change in their respective functions, and the combination yielded nothing more than predictable results to one of ordinary skill in the art.” KSR International Co. v. Teleflex, Inc., 83 USPQ2d 1385, 1395 (2007)
and MPEP §2143.
As stated above, Guelen, et al. does not disclose or suggest the claimed invention. Adding Salsas, et al., Rath, et al., Neilan, et al., Perez-Nunez, et al., Gaudreault, et al., and Netherton, et al. does not make up for these deficiencies.
Since neither the cited references alone or in combination with knowledge in the art suggest the currently claimed invention, it is consequently respectfully submitted that the claims are clearly patentable over the combination, even if the combination were to be applied in opposition to applicable law, and reconsideration of the rejection is respectfully requested.
Claim 11 stands rejected under 35 USC §103 as being unpatentable over Guelen, et al. in combination with Salsas, et al., Rath, et al., Neilan, et al., Perez-Nunez, et al., Gaudreault, et al., Netherton, et al., Burmakina, et al. and Rodriguez, et al. The Office Action holds that Burmakina, et al. teaches ASFV protein CD2v (EP402R or pE402R) is ASFV serotype-specific proteins are significant protective antigens for ASFV, and Rodriguez, et al. teaches that pEP402R gene encoded protein is required for the attachment/binding of red blood cells to infected macrophages and is directly involved in hemadsorption phenomenon induced by the infection of susceptible cells with ASFV and contribute to ASFV pathogenesis and progression of pathogenicity through circulation to different organ system of red blood cells to which the ASFV is bound. Therefore, one skilled in the art would have combined the references to arrive at the invention of claim 11. Reconsideration of the rejection under 35 USC §103 as being unpatentable is respectfully requested.
As stated above, Guelen, et al. does not disclose or suggest the claimed invention. Adding Salsas, et al., Rath, et al., Neilan, et al., Perez-Nunez, et al., Gaudreault, et al., Netherton, et al., Burmakina, et al. and Rodriguez, et al. does not make up for these deficiencies.
Since neither the cited references alone or in combination with knowledge in the art suggest the currently claimed invention, it is consequently respectfully submitted that the claims are clearly patentable over the combination, even if the combination were to be applied in opposition to applicable law, and reconsideration of the rejection is respectfully requested.
Claims 12-13 and 15-16 stand rejected under 35 USC §103 as being unpatentable over Guelen, et al. in combination with Salsas, et al., Rath, et al., Neilan, et al., Perez-Nunez, et al., Gaudreault, et al., Netherton, et al., Andres, et al, and Wang, et al. The Office Action holds that
Andres, et al. teaches that protein pE120R protein is essential for the microtubule-mediated transport of ASFV particles from the viral factories to the plasma membrane - virus budding, and that Wang, et al. teaches capsid protein p49. Therefore, one skilled in the art would have combined the references to arrive at the invention of claims 12-13 and 15-16. Reconsideration of the rejection under 35 USC §103 as being unpatentable is respectfully requested.
As stated above, Guelen, et al. does not disclose or suggest the claimed invention. Adding Salsas, et al., Rath, et al., Neilan, et al., Perez-Nunez, et al., Gaudreault, et al., Netherton, et al., Andres, et al, and Wang, et al. does not make up for these deficiencies.
Since neither the cited references alone or in combination with knowledge in the art suggest the currently claimed invention, it is consequently respectfully submitted that the claims are clearly patentable over the combination, even if the combination were to be applied in opposition to applicable law, and reconsideration of the rejection is respectfully requested.
Claim 14 stands rejected under 35 USC §103 as being unpatentable over Guelen, et al. in combination with Salsas, et al., Rath, et al., Neilan, et al., Perez-Nunez, et al., Gaudreault, et al., Netherton, et al., Andres, et al, and Wang, et al. The Office Action holds that Andres, et al. teaches that protein pE120R protein is essential for the microtubule-mediated transport of ASFV particles from the viral factories to the plasma membrane - virus budding, and that Wang, et al. teaches capsid protein p49. Therefore, one skilled in the art would have combined the references to arrive at the invention of claim 14. Reconsideration of the rejection under 35 USC §103 as being unpatentable is respectfully requested.
As stated above, Guelen, et al. does not disclose or suggest the claimed invention. Adding Salsas, et al., Rath, et al., Neilan, et al., Perez-Nunez, et al., Gaudreault, et al., Netherton, et al., Andres, et al, and Wang, et al. does not make up for these deficiencies.
Since neither the cited references alone or in combination with knowledge in the art suggest the currently claimed invention, it is consequently respectfully submitted that the claims are clearly patentable over the combination, even if the combination were to be applied in opposition to applicable law, and reconsideration of the rejection is respectfully requested.
In Response: Applicant’s arguments regarding rejection of claims 9-13 and 15-16 (applicant cancelled claim 14) under 35 U.S.C. 103 have been considered and are not persuasive in view of the modified rejection under 35 U.S.C. 103 in response to the amended claim 9 that affected dependent claims. In response to the amendment additional teachings from the previously cited prior arts have been applied and additional prior arts were introduced as recited in the rejection. The obviousness rejection under 35 U.S.C. 103 as recited supra renders obvious the instant amended claims 9-13, and 15-16, and thus the rejection is maintained.
Double Patenting
19. 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.
20. Claims 9-13, and 15-16 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 9-17 of co-pending Application No. 18/072,783 (reference application). Although the claims at issue are not identical, they are not patentably distinct from each other because the instant claims 9-13, and 15-16 and reference claims 9-17 of the co-pending Application No. 18/072,783 (reference application) are directed to a method of treating a ASFV infection in an individual (animal/subject) with an ASFV virus proteins (viral antigens) are derived from both lysogenic (the ASFV viral envelope) and Iytic (the ASFV viral capsid) including the steps of: administering the viral antigens that targets protein on an outer membrane (viral envelope) of the ASFV released by “budding” (lysogenic phase of the virus); administering a viral antigen that targets protein on a capsid of a lytic phase of the virus (ASFV without envelope that is released by cell burst without ASFV budding mechanism); and treating the ASFV viral infection, inter alia, wherein the viral infection is ASFV and wherein the individual is a swine, wherein said administering a viral antigen that targets protein CD2v (EP402R) and / or, EP153R and / or, 1177L and / or p12 (061R), CD2v (EP402R), EP153R, 1177L, p54 (E183L), p14.5 (E120R), p72 (B646L), p30 (CP204L), p49 (B438L), p12 (061 R), p11.5 (A137R) and combinations thereof.
The claims at issue are almost identical, and the instant claims and reference claims are not patentably distinct from each other.
This is a provisional nonstatutory double patenting rejection because the patentably indistinct claims have not in fact been patented.
Applicant’s Argument as filed on 01/02/2026:
Claims 9-10 and 14-16: The claims of this application have further been rejected as unpatentable based on provisional non-statutory obviousness-type double patenting over co-pending Application No. 18/072,783. As noted in the Office Action, these rejections can be readily overcome by the filing of a terminal disclaimer in compliance with 37 CFR 1.321(c) or (d). Applicants stand ready to provide the appropriate terminal disclaimer upon the indication of the allowance of the pending claims.
In Response: Applicant’s argument is not persuasive in view of the USPTO compact prosecution requirement and therefore a terminal disclaimer in compliance with 37 CFR 1.321(c) or (d) is required.
Conclusion
21. No claim is allowed.
22. Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
23. A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to SAMADHAN J JADHAO whose telephone number is (703)756-1223. The examiner can normally be reached M-F 8:00-5:00.
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/SAMADHAN JAISING JADHAO/Examiner, Art Unit 1672
/BENNETT M CELSA/Primary Examiner, Art Unit 1600