Lentiviral nucleic acids and uses thereof

Details Lentiviral nucleic acids and uses thereof Lentiviral nucleic acids and uses thereof

2001-04-17

2003-04-29

Guzo, David (Department: 1636)

Drug, bio-affecting and body treating compositions

Whole live micro-organism, cell, or virus containing

Genetically modified micro-organism, cell, or virus

C435S320100, C435S325000, C435S366000, C435S235100, C435S455000, C435S456000, C435S457000, C536S023100, C536S023720, C536S024100, C536S024500, C424S093100, C424S093200, C424S093600

Reexamination Certificate

active

06555107

ABSTRACT:

BACKGROUND OF THE INVENTION
Gene therapy provides methods for combating chronic infectious diseases (e.g., HIV infection), as well as non-infectious diseases including cancer and some forms of congenital defects such as enzyme deficiencies. Several approaches for introducing nucleic acids into cells in vivo, ex vivo and in vitro have been used. These include liposome based gene delivery (Debs and Zhu (1993) WO 93/24640 and U.S. Pat. No. 5,641,662); Mannino and Gould-Fogerite (1988)
BioTechniques
6(7): 682-691; Rose U.S. Pat No. 5,279,833; Brigham (1991) WO 91/06309; and Felgner et al. (1987)
Proc. Natl. Acad. Sci. USA
84: 7413-7414) and adenoviral vector mediated gene delivery, e.g., to treat cancer (see, e.g., Chen et al. (1994)
Proc. Nat'l. Acad. Sci. USA
91: 3054-3057; Tong et al. (1996)
Gynecol. Oncol.
61: 175-179; Clayman et al. (1995)
Cancer Res.
5: 1-6; O'Malley et al. (1995)
Cancer Res.
55: 1080-1085; Hwang et al. (1995)
Am. J. Respir. Cell Mol. Biol.
13: 7-16; Haddada et al. (1995)
Curr. Top. Microbiol. Immunol.
199 (Pt. 3): 297-306; Addison et al. (1995)
Proc. Nat'l. Acad. Sci. USA
92: 8522-8526; Colak et al. (1995)
Brain Res.
691: 76-82; Crystal (1995)
Science
270: 404-410; Elshami et al. (1996)
Human Gene Ther.
7: 141-148; Vincent et al. (1996)
J. Neurosurg.
85: 648-654). Replication-defective retroviral vectors harboring a therapeutic polynucleotide sequence as part of the retroviral genome have also been used, particularly with regard to simple MuLV vectors. See, e.g., Miller et al. (1990)
Mol. Cell. Biol.
10:4239 (1990); Kolberg (1992)
J. NIH Res.
4:43, and Cornetta et al.
Hum. Gene Ther.
2:215 (1991)).
One of the most attractive targets for gene therapy is HIV infection. The pandemic spread of HIV has driven an intense world-wide effort to unravel the molecular mechanisms and life cycle of these viruses. It is now clear that the life cycle of HIVs provide many potential targets for inhibition by gene therapy, including cellular expression of transdominant mutant gag and env nucleic acids to interfere with virus entry, TAR (the binding site for tat, which is typically required for transactivation) decoys to inhibit transcription and trans activation, and RRE (the binding site for Rev; i.e., the Rev Response Element) decoys and transdominant Rev mutants to inhibit RNA processing. See, Rosenburg and Fauci (1993) in
Fundamental Immunology, Third Edition
Paul (ed) Raven Press, Ltd., New York and the references therein for an overview of HIV infection and the HIV life cycle. Gene therapy vectors encoding ribozymes, antisense molecules, decoy genes, transdominant genes and suicide genes, including retroviruses are described in Yu et al.,
Gene Therapy
(1994) 1:13-26. Antisense and ribozyme therapeutic agents are of increasing importance in the treatment and prevention of HIV infection.
Despite the various gene therapeutic approaches now underway for treating cancer, HIV and the like, there are a variety of limitations of the delivery systems currently used in gene therapy. For instance, with regard to HIV treatment, the extensively used murine retroviral vectors transduce (transfer nucleic acids into) human peripheral blood lymphocytes poorly, and fail to transduce non-dividing cells such as monocytes/macrophages, which are known to be reservoirs for HIV. New safer vectors for the delivery of viral inhibitors, particularly to non-dividing hematopoietic stem cells for the treatment of HIV infection, are desirable.
Non-primate lentiviruses provide a possible system for the development of new vector systems; however, relatively little is known about these viruses. Although their biology has received considerably less scrutiny than that of the primate lentiviruses (e.g., HIV-1, HIV-2 and SIV), non-primate lentiviruses are of interest for comparative lentivirus biology and as potential sources of safer lentiviral vectors. HIV-based retroviral vectors have recently shown promise for therapeutic gene transfer because they display the lentiretrovirus-specific property of permanently infecting non-dividing cells (see, Naldini et al. (1996)
Science
272, 263-267). In contrast, retroviral vectors derived from simpler retroviruses (e.g., the Oncovirinae) require breakdown of the nuclear envelope during mitosis to complete reverse transcription and integration. Consequently, these vectors transduce non-dividing cells poorly, which may limit usefulness for gene transfer to quiescent or post-mitotic cellular targets. However, HIV vectors present complex safety problems (see, Emerman (1996)
Nature Biotechnology
14, 943).
The non-primate lentiviruses include the ungulate lentiviruses, including visna/maedi virus, caprine arthritis encephalitis virus (CAEV), equine infectious anemia virus (EIAV), and bovine immunodeficiency virus (BIV). These lentiviruses only infect hoofed animals (ungulates) and generally only infect particular species of ungulates.
The non-primate lentiviruses also include feline immunodeficiency virus (FIV) (see, Clements & Zink (1996)
Clinical Microbiology Reviews
9, 100-117), which only infects felines. Numerous strains of FIV have been identified.
Non-primate (e.g., feline and ungulate) lentiviruses may provide a safer alternative than primate lentiviral vectors, but their use is complicated by a relative lack of knowledge about their molecular properties, especially their adaptability to non-host animal cells (Emerman, id). All lentiviruses display highly restricted tropisms (see, Clements & Zink (1996), supra, and Haase (1994)
Annals of the New York Academy of Sciences
724, 75-86).
FIV was discovered in 1986 as a cause of acquired immune deficiency and neurological disease in, and only in, domestic cats (Felis catus) Pedersen et al. (1987)
Science
235, 790-793 (1987); Elder & Phillips (1993)
Infectious Agents and Disease
2, 361-374; Pedersen (1993) “The feline immunodeficiency virus” in The Retroviridae (ed. Levy, J. A.) 181-228 (Plenum Press, New York Bendinelli et al. (1995)
Clinical Microbiology Reviews
8, 87-112; and, Sparger (1993)
Veterinary Clinics of North America, Small Animal Practice
23, 173-191). In the great cats, FIV is widely dispersed geographically and appears to be commensal: 18 of 37 species of free-roaming, non-domestic Felidae are known to be infected world-wide, but none develop disease (Elder & Phillips (1993), supra; Olmsted et al. (1992)
Journal of Virology
66, 6008-6018; Barr et al. (1995)
Journal of Virology
69, 7371-7374; Courchamp & Pontier (1994) “Feline immunodeficiency virus: an epidemiological review.”
Comptes Rendus de L Academie des Sciences. Serie III, Sciences de la Vie
317, 1123-1134). The virus is prevalent, infecting 2-20% of domestic cat populations in North America, Europe and Japan; higher rates are seen in cats brought to veterinary attention (Pedersen (1993), supra and Courchamp, F. & Pontier (1994), supra). The worldwide prevalence of FIV in diverse Felidae and the observation that
Felis catus
sera dating to the 1960's show similar high rates of positivity, suggest that FIV has not been recently introduced into domestic cats (Bendinelli et al. (1995), supra, Olmsted et al. (1992), supra; Courchamp, F. & Pontier (1994) supra; Shelton et al. (1990)
Journal of Acquired Immune Deficiency Syndromes
3, 623-630; Bennett & Smyth (1992)
British Veterinary Journal
148, 399-412; Brown et al. (1993)
Journal of Zoo and Wildlife Medicine
24, 357-364; Carpenter & O'Brien (1995)
Current Opinion in Genetics and Development
5, 739-745.
There is no evidence for FIV infection of non-felids. Cross-infection by any of the ungulate or feline lentiviruses has never been observed in non-ungulates, or non-felids respectively. HIV and FIV differ notably in their modes of transmission since FIV is spread principally by biting (Pederson (1993), supra). Despite frequent exposure of humans to FIV through bites by domestic cats, this plausibly efficient means of inoculation does not result in human seroconversion or any other detectable evidence of human i

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