From Federal Register notice submitted by NIH for publication on Nov. 21, 1996

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Cells Expressing Both Human CD4 and a Human Fusion Accessory Factor Associated with HIV Infection

Description of Invention:
HIV-1 infects target cells by first binding to CD4, a receptor on the target cell membrane. The virus and target cell membranes then fuse, allowing the virus to enter the target cell. It has previously been determined that CD4 alone is not sufficient to allow entry, but that another factor specific to human cells is also required. The current invention embodies the identification of a cDNA encoding a protein, designated "fusin," which demonstrates properties expected of a fusion co-factor for T-cell line tropic HIV-1 isolates. Fusin is a member of the 7-transmembrane segment (7-TMS) superfamily of G-protein-coupled receptors. While this cDNA has previously been cloned, its potential role as an accessory protein necessary for HIV infection is novel to the current invention. The invention, therefore, should represent a valuable tool to be used in the production of transgenic mice and of cell lines for the study of HIV infection. In addition, the invention may itself represent a potential therapeutic agent against HIV or target for agents acting to block entry of HIV into target cells. This technology was reported in Science 272:809-810 (1996); Chemical and Engineering News, p. 7 (May 13, 1996); BioWorld Today, pp. 1-2 (May 13, 1996); Biotechnology News, 16(13):1-2 (1996); and BioWorld Today, pp. 1,3 (June 21, 1996).

Inventors:
EA Berger, Y Feng, CC Broder, PE Kennedy (NIAID)

Relevant Publications:
• Nussbaum, O, et al., J. Virol., 68(9):5411-5422 (1994)
• Broder, C, et al., PNAS 92:9004-9008 (1995)
• Fent, Y, et al., Science 272:872-877 (1996)

Patent Status:
Serial No. 60/010,854 filed 30 Jan 96

Portfolios:
Infectious Diseases - Research Materials
Infectious Diseases - Other
Infectious Diseases - Therapeutics, anti-virals, AIDS

Licensing Status:
Available for exclusive or non-exclusive licensing

For additional information, please contact:
Cindy K. Fuchs, J.D.
Office of Technology Transfer
National Institutes of Health
6011 Executive Boulevard, Suite 325
Rockville, MD 20852-3804
Phone: 301/496-7735 ext 232
Fax: 301/402-0220

CC Chemokine Receptor 5 DNA, New Animal Models and Therapeutic Agents for HIV Infection

Description of Invention:
This invention concerns a novel macrophage-selective CC chemokine receptor, designated "CC CKR5," which is a necessary cofactor for the infection of target cells by macrophage-tropic HIV isolates. Macrophage-tropic HIV isolates represent the predominant type of isolates from infected persons and appear to be preferentially transmitted between individuals. The invention embodies the CC CKR5 genetic sequence, cell lines and transgenic mice, the cells of which coexpress human CD4 and CC CKR5, and which may represent valuable tools for the study of HIV infection and for screening anti-HIV agents. The invention also embodies anti-CC CKR5 agents that block HIV env-mediated membrane fusion associated with HIV entry into human CD4-positive target cells or between HIV-infected cells and uninfected human CD4-positive target cells. This technology was reported in Science 272:1955-1958 (1996); BioWorld Today, pp. 1 and 3 (June 21, 1996); and Chemical and Engineering News, p. 8 (June 24, 1996) and p. 46 (July 29, 1996).

Inventors:
C Combadiere, Y Feng, EA Berger, G Alkahatib, PM Murphy, CC Broder (NIAID)

Patent Status:
Serial No. 60/018,508 filed 28 May 1996

Portfolios:
Infectious Diseases - Therapeutics, anti-virals, AIDS
Infectious Diseases - Research Materials

Licensing Status:
Available for exclusive or non-exclusive licensing

For additional information, please contact:
Cindy K. Fuchs, J.D.
Office of Technology Transfer
National Institutes of Health
6011 Executive Boulevard, Suite 325
Rockville, MD 20852-3804
Phone: 301/496-7735 ext 232
Fax: 301/402-0220
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