Appeal No. 2006-0735
Reexamination Control No. 90/006,036
adjacent an inhibitory RNA to colocalize it with an HIV RNA to be destroyed.”
(‘038 at 4: 4-9).
14. Neither the examiner nor the patentee has directed us to a specific definition of the
term “cellular or viral compartment” in the ‘038 specification.
The Hu reference
15. The examiner has rejected claims 1-4, 6-10, 12, and 13 under 35 U.S.C. § 102(e) as
being anticipated by US Patent 6,107,062 to Hu et al. (“Hu”).
16. Hu issued on 22 August 2000 from application 07/921,104, filed 30 July 1992.
17. Hu is directed to antisense viruses and antisense ribozyme viruses used in preventing
and treating viral infections.
18. The examiner points out that one of the objects of the Hu invention is “to provide
therapeutic agents for the treatment and prevention of AIDS having....the ability to
target HIV...” (Answer at 5, citing Hu at 4:19-34).
19. The examiner also directs us to col. 11, lines 40-48, of Hu, which states that
(emphasis added):
An HIV-1 antisense proviral molecular clone is made from a functional
(infectious) HIV-1 molecular clone. It retains all of the natural HIV-1
structures and machinery except a part (or parts) of the genome has been
turned antisense by sequence inversion. The antisense proviral clone is
basically an intact molecular clone but the sequence inversion inactivates some
functionally critical gene(s) and renders the whole clone replication-defective.
(Answer at 6).
20. Hu notes that:
The antisense virus is infectious and has the same “targeting” or “homing”
specificity as the naturally occuring (wild type) virus. The antisense HIV-1 is
able to attach to and enter CD4(+) cells, mediated by its normal envelope protein
(gp 120 and gp41) just as the natural virus. Once inside the cells, the viral
nucleocapsid reverse-transcribes the RNA genome into DNA, then integrates the
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