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 .
Claims 1-61 have been canceled. Claims 62-79 have been added.
Claim Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 62-79 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
A) The specification lacks written description for any cell with any genetically modified GGTA1, CMAH, or B4GALNT2 gene that has “enhanced” resistance to African swine fever virus (ASFV) as broadly encompassed by claim 62 other than a genetically modified pig cell whose genome comprises inactivated GTTA1, CMAH, and B4GALNT2 genes.
Claim 62 is drawn to a cell with a genetic modification of any GGTA1, CMAH, or B4GALNT2 gene that renders enhanced resistance to viral infection by African swine fever virus (ASFV). The claim encompasses any cell in vivo or in vitro. The cell may be from an invertebrate, insect, fish, amphibian, reptile, bird or mammal. Despite the fact that ASFV only infects pig cells, the claims encompass any rat, beaver, squirrel, whale, porpoise, groundhog, muskrat, hamster, capybara, chinchilla, porcupine, gerbil, dog, cat, pig, sheep, horse, cow, deer, rabbit, elephant, giraffe, skunk, or other mammal. Claims 77, 78 encompass any non-human mammalian cell or artiodactyl cell. Artiodactyls encompass hippos, moose, okapi, pronghorn, sheep, antelope, camel, boar, deer, warthogs, cattle, bison, reindeer, ox, llama, wildebeest, etc.
Claim 62 encompasses any single nucleotide or amino acid genetic mutation of any GGTA1, CMAH, or B4GALNT2 gene as well as any insertion or deletion. The genetic mutation may still allow expression of a mutant or variant GGTA1, CMAH, or B4GALNT2 or it may completely inactivate expression of GGTA1, CMAH, or B4GALNT2.
Claims 72 and 73 encompass genetically modifying a GGTA1, CMAH, or B4GALNT2 in the genome of the cell or in a transcript.
Dai (“Targeted Disruption of the alpha1 ,3-galactosyltransferase Gene in Cloned Pigs”, Nature Biotechnology, Mar. 2002, vol. 20, No. 3, pp. 251-255) taught a genetically modified pig cell whose genome comprises an inactivated GGTA1 gene (Title, abstract, Methods, Results). Tector (20240196872) taught a genetically modified pig cell whose genome comprises inactivated GT and CMAH genes (Title, abstract, Examples). “GT” in Tector is GGTA1 as required in claim 62. Tector (20170311579) taught a genetically modified pig cell whose genome comprises inactivated GTTA1, CMAH, and B4GALNT2 genes (Fig. 3, para 32). These cells inherently MUST exhibit “enhanced resistance to viral infection by [ASFV]” as required in claim 62 because they have the genetic modification claimed (claims 65, 74) and described by applicants as being part of the invention.
The specification contemplates the breadth claimed, but the examples are limited to a genetically modified pig cell whose genome comprises inactivated GTTA1, CMAH, and B4GALNT2 genes (pg 81, Example 1).
The specification does not correlate a genetically modified pig cell whose genome comprises inactivated GTTA1, CMAH, or B4GALNT2 genes to any invertebrate, insect, fish, amphibian, reptile, bird, rat, beaver, squirrel, whale, porpoise, groundhog, muskrat, hamster, capybara, chinchilla, porcupine, gerbil, dog, cat, sheep, horse, cow, deer, rabbit, elephant, giraffe, skunk, hippos, moose, okapi, pronghorn, sheep, antelope, camel, boar, deer, warthogs, cattle, bison, reindeer, ox, llama, wildebeest, etc. cell. The specification does not teach any single nucleotide or amino acid genetic mutation of any GGTA1, CMAH, or B4GALNT2 gene or any insertion or deletion of any GGTA1, CMAH, or B4GALNT2 gene capable of rendering the cell resistant to ASFV infection. The specification does not teach any mutant or variant GGTA1, CMAH, or B4GALNT2 that renders the cell resistant to ASFV infection other than inactivation of a GGTA1, CMAH, or B4GALNT2 gene. The specification does not teach inactivation of any one of GGTA1, CMAH, or B4GALNT2 renders the cell resistant to ASFV as claimed without inactivating all three genes. The specification does not correlate a cell whose genome comprises an inactivated GGTA1, CMAH, or B4GALNT2 gene to a gene with an inactivated transcript of a gene as required in claim 73.
Accordingly, the specification lacks written description for the cell claimed other than a genetically modified pig cell whose genome comprises inactivated GTTA1, CMAH, and B4GALNT2 genes.
B) Claims 69-71 are similarly rejected. The claims are drawn to a cell with a genetic modification of any CD163, ANPEP, or RELA gene. The claim encompasses any cell in vivo or in vitro. The cell may be from an invertebrate, insect, fish, amphibian, reptile, bird or mammal. Despite the fact that ASFV only infects pig cells, the claims encompass any rat, beaver, squirrel, whale, porpoise, groundhog, muskrat, hamster, capybara, chinchilla, porcupine, gerbil, dog, cat, pig, sheep, horse, cow, deer, rabbit, elephant, giraffe, skunk, or other mammal. Claims 77, 78 encompass any non-human mammalian cell or artiodactyl cell. Artiodactyls encompass hippos, moose, okapi, pronghorn, sheep, antelope, camel, boar, deer, warthogs, cattle, bison, reindeer, ox, llama, wildebeest, etc. Claim 62 encompasses any single nucleotide or amino acid genetic mutation of any CD163, ANPEP, or RELA gene as well as any insertion or deletion. The genetic mutation may still allow expression of a mutant or variant CD163, ANPEP, or RELA or it may completely inactivate expression of CD163, ANPEP, or RELA.
Prather (WO 2017023570), Prather (WO 2019210175), and Whitelaw (WO 2014041327) taught genetically modified pig cells whose genomes comprise inactivated CD163, ANPEP, or RELA genes. The specification does not correlate a genetically modified pig cell whose genome comprises inactivated CD163, ANPEP, or RELA genes to any invertebrate, insect, fish, amphibian, reptile, bird, rat, beaver, squirrel, whale, porpoise, groundhog, muskrat, hamster, capybara, chinchilla, porcupine, gerbil, dog, cat, sheep, horse, cow, deer, rabbit, elephant, giraffe, skunk, hippos, moose, okapi, pronghorn, sheep, antelope, camel, boar, deer, warthogs, cattle, bison, reindeer, ox, llama, wildebeest, etc. cell. The specification does not teach any single nucleotide or amino acid genetic mutation of any CD163, ANPEP, or RELA gene or any insertion or deletion of any CD163, ANPEP, or RELA gene capable of rendering the cell resistant to ASFV infection. The specification does not teach any mutant or variant CD163, ANPEP, or RELA that renders the cell resistant to ASFV infection other than inactivation of a CD163, ANPEP, or RELA gene. Accordingly, the specification lacks written description for the cell claimed other than a genetically modified pig cell whose genome comprises inactivated CD163, ANPEP, or RELA gene.
C) The specification lacks written description for rendering resistance to any “additional genus of virus” as required in claim 75 specifically any PRRSV or TEGV as required in claim 76. The specification does not teach inactivation of GGTA1, CMAH, or B4GALNT2 alone or any combination thereof will cause resistance to PRRSV, TEGV, or any “additional genus of virus”. Accordingly, the specification lacks written description for the cell having the features of claims 75 and 76.
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 62-79 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 62 is indefinite because it is unclear when resistant to ASFV infection is “enhanced”. While resistance to ASFV infection can be measured compared to a wild-type cell without a modification of a GGTA1, CMAH, or B4GALNT2 gene, the specification and the art do not teach when resistance to ASFV infection is “enhanced”. The phrase appears to infer that a certain level of resistance is required to be considered “enhanced” resistance, but that level of resistance to ASFV is not defined by applicants or the art. If the term “enhanced” does not further limit the term “resistance”, i.e. if “enhanced resistance” encompasses any resistance to ASFV, then take the term “enhanced” out. If the term “enhanced” does further limit the amount of resistance to ASFV, then please point to a place in the specification that defines the level at which resistance to ASFV is “enhanced”.
Claim 73 is indefinite because it says “wherein the at least one endogenous gene is a transcript of a chromosomal gene” while parent claim 62 requires “genetic modification of at least one endogenous gene selected from the group consisting of GGTA1, CMAH, and B4GALNT2”. A transcript of a gene is not a “gene” so the “endogenous gene” cannot be a “transcript” as required in claim 73. The phraseology is scientifically and logically unsound which makes the claim indefinite.
Claims 75 and 76 are indefinite because it is unclear when resistant to viral infection is “enhanced”. While resistance to an “additional genus of virus”, specifically ASFV, PRRSV, or TGEV, infection can be measured compared to a wild-type cell without a modification of a GGTA1, CMAH, or B4GALNT2 gene, the specification and the art do not teach when resistance to an “additional genus of virus”, specifically ASFV, PRRSV, or TGEV infection is “enhanced”. The phrase appears to infer that a certain level of resistance is required to be considered “enhanced” resistance, but that level of resistance to an “additional genus of virus”, specifically ASFV, PRRSV, or TGEV is not defined by applicants or the art. If the term “enhanced” does not further limit the term “resistance”, i.e. if “enhanced resistance” encompasses any resistance to an “additional genus of virus”, specifically ASFV, PRRSV, or TGEV, then take the term “enhanced” out. If the term “enhanced” does further limit the amount of resistance to an “additional genus of virus”, specifically ASFV, PRRSV, or TGEV, then please point to a place in the specification that defines the level at which resistance to an “additional genus of virus”, specifically ASFV, PRRSV, or TGEV is “enhanced”.
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.
Claims 62, 63, 72-79 are rejected under 35 U.S.C. 102a1 as being anticipated by Dai (“Targeted Disruption of the alpha1 ,3-galactosyltransferase Gene in Cloned Pigs”, Nature Biotechnology, Mar. 2002, vol. 20, No. 3, pp. 251-255).
Dai taught a genetically modified pig cell whose genome comprises an inactivated GGTA1 gene (Title, abstract, Methods, Results). The cell inherently MUST exhibit “enhanced resistance to viral infection by [ASFV]” as required in claim 62 because it has the genetic modification claimed (claim 74) and described by applicants as being part of the invention.
The cell inherently MUST exhibit “enhanced resistance to viral infection by [ASFV]” “characterized by having reduced viral titer upon incubation with the ASFV as compared to that of the control lacking the genetic modification” as required in claim 63 because it has the genetic modification claimed (claim 74) and described by applicants as being part of the invention.
The GGTA1 gene inactivated by Dai is “chromosomal” as required in claim 72.
The GGTA1 gene inactivated by Dai has a “transcript of a chromosomal gene” as required in claim 73.
The GGTA1 gene inactivated by Dai is “a knockout” as required in claim 74.
The GGTA1 gene inactivated by Dai renders “enhanced resistance to viral infection by ASFV and an additional genus of virus” as required in claim 75 because it has the genetic modification claimed (claim 74) and described by applicants as being part of the invention.
The GGTA1 gene inactivated by Dai renders “enhanced resistance to viral infection by ASFV, PRRSV, and TGEV” as required in claim 76 because it has the genetic modification claimed (claim 74) and described by applicants as being part of the invention.
The pig cell of Dai is non-human mammalian as required in claim 77.
The pig cell of Dai is within the genus of artiodactyl as required in claim 78.
The pig cell of Dai is a pig cell as required in claim 79.
Claims 62-65, 72-79 are rejected under 35 U.S.C. 102a1 as being anticipated by Tector (20240196872).
Tector has priority to March 14, 2013.
Tector taught a genetically modified pig cell whose genome comprises inactivated GT and CMAH genes (Title, abstract, Examples). “GT” in Tector is GGTA1 as required in claim 62. The cell inherently MUST exhibit “enhanced resistance to viral infection by [ASFV]” as required in claim 62 because it has the genetic modification claimed (claims 65, 74) and described by applicants as being part of the invention.
The cell inherently MUST exhibit “enhanced resistance to viral infection by [ASFV]” “characterized by having reduced viral titer upon incubation with the ASFV as compared to that of the control lacking the genetic modification” as required in claim 63 because it has the genetic modification claimed (claims 65, 74) and described by applicants as being part of the invention.
Tector inactivated GGTA1 and CMAH which is at least two of GGTA1, CMAH, and B4GALNT2 as required in claim 64.
Tector inactivated GGTA1 and CMAH as required in claim 65.
The GGTA1 and CMAH genes inactivated by Tector are “chromosomal” as required in claim 72.
The GGTA1 and CMAH genes inactivated by Tector have a “transcript of a chromosomal gene” as required in claim 73.
The GGTA1 and CMAH genes inactivated by Tector are “knocked out” as required in claim 74.
The GGTA1 and CMAH genes inactivated by Tector render “enhanced resistance to viral infection by ASFV and an additional genus of virus” as required in claim 75 because it has the genetic modification claimed (claims 65, 74) and described by applicants as being part of the invention.
The GGTA1 and CMAH genes inactivated by Tector render “enhanced resistance to viral infection by ASFV, PRRSV, and TGEV” as required in claim 76 because it has the genetic modification claimed (claims 65, 74) and described by applicants as being part of the invention.
The pig cell of Tector is non-human mammalian as required in claim 77.
The pig cell of Tector is within the genus of artiodactyl as required in claim 78.
The pig cell of Tector is a pig cell as required in claim 79.
Claims 62-68, 72-79 are rejected under 35 U.S.C. 102a1 as being anticipated by Tector (20170311579).
Tector taught a genetically modified pig cell whose genome comprises inactivated GTTA1, CMAH, and B4GALNT2 genes (Fig. 3, para 32). The cell inherently MUST exhibit “enhanced resistance to viral infection by [ASFV]” as required in claim 62 because it has the genetic modification claimed (claims 68, 74) and described by applicants as being part of the invention.
The cell inherently MUST exhibit “enhanced resistance to viral infection by [ASFV]” “characterized by having reduced viral titer upon incubation with the ASFV as compared to that of the control lacking the genetic modification” as required in claim 63 because it has the genetic modification claimed (claims 68, 74) and described by applicants as being part of the invention.
Tector inactivated GGTA1, CMAH, and B4GALNT2 which is at least two of GGTA1, CMAH, and B4GALNT2 as required in claim 64.
Tector inactivated GGTA1 and CMAH as required in claim 65.
Tector inactivated GGTA1 and B4GALNT2 as required in claim 66.
Tector inactivated CMAH and B4GALNT2 as required in claim 67.
Tector inactivated GGTA1, CMAH, and B4GALNT2 as required in claim 68.
The GGTA1, CMAH, and B4GALNT2 genes inactivated by Tector are “chromosomal” as required in claim 72.
The GGTA1, CMAH, and B4GALNT2 genes inactivated by Tector have a “transcript of a chromosomal gene” as required in claim 73.
The GGTA1, CMAH, and B4GALNT2 genes inactivated by Tector are “knocked out” as required in claim 74.
The GGTA1, CMAH, and B4GALNT2 genes inactivated by Tector render “enhanced resistance to viral infection by ASFV and an additional genus of virus” as required in claim 75 because it has the genetic modification claimed (claims 68, 74) and described by applicants as being part of the invention.
The GGTA1, CMAH, and B4GALNT2 genes inactivated by Tector render “enhanced resistance to viral infection by ASFV, PRRSV, and TGEV” as required in claim 76 because it has the genetic modification claimed (claim 68, 74) and described by applicants as being part of the invention.
The pig cell of Tector is non-human mammalian as required in claim 77.
The pig cell of Tector is within the genus of artiodactyl as required in claim 78.
The pig cell of Tector is a pig cell as required in claim 79.
Claims 62-68, 72-79 are rejected under 35 U.S.C. 102a1 as being anticipated by Wang (Transplantation, 2016, Vol. 100, pg 533-537).
Wang taught a genetically modified pig cell whose genome comprises inactivated GTTA1, CMAH, and B4GALNT2 genes (pg 534, Materials and Methods). The cell inherently MUST exhibit “enhanced resistance to viral infection by [ASFV]” as required in claim 62 because it has the genetic modification claimed (claims 68, 74) and described by applicants as being part of the invention.
The cell inherently MUST exhibit “enhanced resistance to viral infection by [ASFV]” “characterized by having reduced viral titer upon incubation with the ASFV as compared to that of the control lacking the genetic modification” as required in claim 63 because it has the genetic modification claimed (claims 68, 74) and described by applicants as being part of the invention.
Wang inactivated GGTA1, CMAH, and B4GALNT2 which is at least two of GGTA1, CMAH, and B4GALNT2 as required in claim 64.
Wang inactivated GGTA1 and CMAH as required in claim 65.
Wang inactivated GGTA1 and B4GALNT2 as required in claim 66.
Wang inactivated CMAH and B4GALNT2 as required in claim 67.
Wang inactivated GGTA1, CMAH, and B4GALNT2 as required in claim 68.
The GGTA1, CMAH, and B4GALNT2 genes inactivated by Wang are “chromosomal” as required in claim 72.
The GGTA1, CMAH, and B4GALNT2 genes inactivated by Wang have a “transcript of a chromosomal gene” as required in claim 73.
The GGTA1, CMAH, and B4GALNT2 genes inactivated by Wang are “knocked out” as required in claim 74.
The GGTA1, CMAH, and B4GALNT2 genes inactivated by Wang render “enhanced resistance to viral infection by ASFV and an additional genus of virus” as required in claim 75 because it has the genetic modification claimed (claims 68, 74) and described by applicants as being part of the invention.
The GGTA1, CMAH, and B4GALNT2 genes inactivated by Wang render “enhanced resistance to viral infection by ASFV, PRRSV, and TGEV” as required in claim 76 because it has the genetic modification claimed (claim 68, 74) and described by applicants as being part of the invention.
The pig cell of Wang is non-human mammalian as required in claim 77.
The pig cell of Wang is within the genus of artiodactyl as required in claim 78.
The pig cell of Wang is a pig cell as required in claim 79.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
A) Claims 62-69, 72-79 are rejected under 35 U.S.C. 103 as being unpatentable over Tector (20170311579) in view of Prather (WO 2017023570).
Tector taught a genetically modified pig cell whose genome comprises inactivated GTTA1, CMAH, and B4GALNT2 genes (Fig. 3, para 32). The cell inherently MUST exhibit “enhanced resistance to viral infection by [ASFV]” as required in claim 62 because it has the genetic modification claimed (claims 68, 74) and described by applicants as being part of the invention.
Tector did not teach inactivating an endogenous CD163 gene as required in claim 69.
However, Prather taught inactivating an endogenous CD163 gene in pig cells (abstract, Example 1).
Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to make a genetically modified pig cell whose genome comprises inactivated GTTA, CMAH, and B4GALNT2 genes as described by Tector further comprising an inactivated CD163 gene as described by Prather. Those of ordinary skill in the art at the time of filing would have been motivated to inactivate the CD163 gene in the cells of Tector to make the cell more resistant to other viral infection.
The cell inherently MUST exhibit “enhanced resistance to viral infection by [ASFV]” “characterized by having reduced viral titer upon incubation with the ASFV as compared to that of the control lacking the genetic modification” as required in claim 63 because it has the genetic modification claimed (claims 69, 74) and described by applicants as being part of the invention.
Tector inactivated GGTA1, CMAH, and B4GALNT2 which is at least two of GGTA1, CMAH, and B4GALNT2 as required in claim 64.
Tector inactivated GGTA1 and CMAH as required in claim 65.
Tector inactivated GGTA1 and B4GALNT2 as required in claim 66.
Tector inactivated CMAH and B4GALNT2 as required in claim 67.
Tector inactivated GGTA1, CMAH, and B4GALNT2 as required in claim 68.
The GGTA1, CMAH, and B4GALNT2 genes inactivated by Tector and the CD163 gene inactivated by Prather are “chromosomal” as required in claim 72.
The GGTA1, CMAH, and B4GALNT2 genes inactivated by Tector and the CD163 gene inactivated by Prather have a “transcript of a chromosomal gene” as required in claim 73.
The GGTA1, CMAH, and B4GALNT2 genes inactivated by Tector and the CD163 gene inactivated by Prather are “knocked out” as required in claim 74.
The GGTA1, CMAH, and B4GALNT2 genes inactivated by Tector and the CD163 gene inactivated by Prather render “enhanced resistance to viral infection by ASFV and an additional genus of virus” as required in claim 75 because it has the genetic modification claimed (claims 69, 74) and described by applicants as being part of the invention.
The GGTA1, CMAH, and B4GALNT2 genes inactivated by Tector render “enhanced resistance to viral infection by ASFV, PRRSV, and TGEV” as required in claim 76 because it has the genetic modification claimed (claim 69, 74) and described by applicants as being part of the invention.
The pig cell of Tector and Prather is non-human mammalian as required in claim 77.
The pig cell of Tector and Prather is within the genus of artiodactyl as required in claim 78.
The pig cell of Tector and Prather is a pig cell as required in claim 79.
Thus, Applicants' claimed invention as a whole is prima facie obvious in the absence of evidence to the contrary.
B) Claims 62-68, 70, 72-79 are rejected under 35 U.S.C. 103 as being unpatentable over Tector (20170311579) in view of Prather (WO 2019210175).
Tector taught a genetically modified pig cell whose genome comprises inactivated GTTA1, CMAH, and B4GALNT2 genes (Fig. 3, para 32). The cell inherently MUST exhibit “enhanced resistance to viral infection by [ASFV]” as required in claim 62 because it has the genetic modification claimed (claims 68, 74) and described by applicants as being part of the invention.
Tector did not teach inactivating an endogenous ANPEP gene as required in claim 70.
However, Prather taught inactivating an endogenous ANPEP gene in pig cells (abstract, Example 1).
Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to make a genetically modified pig cell whose genome comprises inactivated GTTA, CMAH, and B4GALNT2 genes as described by Tector further comprising an inactivated ANPEP gene as described by Prather. Those of ordinary skill in the art at the time of filing would have been motivated to inactivate the ANPEP gene in the cells of Tector to make the cell more resistant to other viral infection.
The cell inherently MUST exhibit “enhanced resistance to viral infection by [ASFV]” “characterized by having reduced viral titer upon incubation with the ASFV as compared to that of the control lacking the genetic modification” as required in claim 63 because it has the genetic modification claimed (claims 70, 74) and described by applicants as being part of the invention.
Tector inactivated GGTA1, CMAH, and B4GALNT2 which is at least two of GGTA1, CMAH, and B4GALNT2 as required in claim 64.
Tector inactivated GGTA1 and CMAH as required in claim 65.
Tector inactivated GGTA1 and B4GALNT2 as required in claim 66.
Tector inactivated CMAH and B4GALNT2 as required in claim 67.
Tector inactivated GGTA1, CMAH, and B4GALNT2 as required in claim 68.
The GGTA1, CMAH, and B4GALNT2 genes inactivated by Tector and the ANPEP gene inactivated by Prather are “chromosomal” as required in claim 72.
The GGTA1, CMAH, and B4GALNT2 genes inactivated by Tector and the ANPEP gene inactivated by Prather have a “transcript of a chromosomal gene” as required in claim 73.
The GGTA1, CMAH, and B4GALNT2 genes inactivated by Tector and the ANPEP gene inactivated by Prather are “knocked out” as required in claim 74.
The GGTA1, CMAH, and B4GALNT2 genes inactivated by Tector and the ANPEP gene inactivated by Prather render “enhanced resistance to viral infection by ASFV and an additional genus of virus” as required in claim 75 because it has the genetic modification claimed (claims 70, 74) and described by applicants as being part of the invention.
The GGTA1, CMAH, and B4GALNT2 genes inactivated by Tector and the ANPEP gene inactivated by Prather render “enhanced resistance to viral infection by ASFV, PRRSV, and TGEV” as required in claim 76 because it has the genetic modification claimed (claim 70, 74) and described by applicants as being part of the invention.
The pig cell of Tector and Prather is non-human mammalian as required in claim 77.
The pig cell of Tector and Prather is within the genus of artiodactyl as required in claim 78.
The pig cell of Tector and Prather is a pig cell as required in claim 79.
Thus, Applicants' claimed invention as a whole is prima facie obvious in the absence of evidence to the contrary.
C) Claims 62-68, 71-79 are rejected under 35 U.S.C. 103 as being unpatentable over Tector (20170311579) in view of Whitelaw (WO 2014041327).
Tector taught a genetically modified pig cell whose genome comprises inactivated GTTA1, CMAH, and B4GALNT2 genes (Fig. 3, para 32). The cell inherently MUST exhibit “enhanced resistance to viral infection by [ASFV]” as required in claim 62 because it has the genetic modification claimed (claims 68, 74) and described by applicants as being part of the invention.
Tector did not teach inactivating an endogenous RELA gene as required in claim 71.
However, Whitelaw taught genetically modifying an endogenous RELA gene in pig cells (Examples, claim 3).
Thus, it would have been obvious to those of ordinary skill in the art at the time of filing to make a genetically modified pig cell whose genome comprises inactivated GTTA, CMAH, and B4GALNT2 genes as described by Tector further comprising an inactivated RELA gene as described by Whitelaw. Those of ordinary skill in the art at the time of filing would have been motivated to inactivate the RELA gene in the cells of Tector to make the cell more resistant to other viral infection.
The cell inherently MUST exhibit “enhanced resistance to viral infection by [ASFV]” “characterized by having reduced viral titer upon incubation with the ASFV as compared to that of the control lacking the genetic modification” as required in claim 63 because it has the genetic modification claimed (claims 71, 74) and described by applicants as being part of the invention.
Tector inactivated GGTA1, CMAH, and B4GALNT2 which is at least two of GGTA1, CMAH, and B4GALNT2 as required in claim 64.
Tector inactivated GGTA1 and CMAH as required in claim 65.
Tector inactivated GGTA1 and B4GALNT2 as required in claim 66.
Tector inactivated CMAH and B4GALNT2 as required in claim 67.
Tector inactivated GGTA1, CMAH, and B4GALNT2 as required in claim 68.
The GGTA1, CMAH, and B4GALNT2 genes inactivated by Tector and the RELA gene inactivated by Whitelaw are “chromosomal” as required in claim 72.
The GGTA1, CMAH, and B4GALNT2 genes inactivated by Tector and the RELA gene modified by Whitelaw have a “transcript of a chromosomal gene” as required in claim 73.
The GGTA1, CMAH, and B4GALNT2 genes inactivated by Tector and the RELA gene inactivated by Whitelaw are “knocked out” as required in claim 74.
The GGTA1, CMAH, and B4GALNT2 genes inactivated by Tector and the RELA gene modified by Whitelaw render “enhanced resistance to viral infection by ASFV and an additional genus of virus” as required in claim 75 because it has the genetic modification claimed (claims 71, 74) and described by applicants as being part of the invention.
The GGTA1, CMAH, and B4GALNT2 genes inactivated by Tector and the RELA gene modified by Whitelaw render “enhanced resistance to viral infection by ASFV, PRRSV, and TGEV” as required in claim 76 because it has the genetic modification claimed (claim 71, 74) and described by applicants as being part of the invention.
The pig cell of Tector and Whitelaw is non-human mammalian as required in claim 77.
The pig cell of Tector and Whitelaw is within the genus of artiodactyl as required in claim 78.
The pig cell of Tector and Whitelaw is a pig cell as required in claim 79.
Thus, Applicants' claimed invention as a whole is prima facie obvious in the absence of evidence to the contrary.
Conclusion
No claim is allowed.
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Michael C. Wilson
/MICHAEL C WILSON/
Primary Examiner, Art Unit 1638