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Institution

Aaron Diamond AIDS Research Center

FacilityNew York, New York, United States
About: Aaron Diamond AIDS Research Center is a facility organization based out in New York, New York, United States. It is known for research contribution in the topics: Virus & Simian immunodeficiency virus. The organization has 563 authors who have published 966 publications receiving 118392 citations.


Papers
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Journal ArticleDOI
12 Jan 1995-Nature
TL;DR: Treatment of infected patients with ABT-538 causes plasma HIV-1 levels to decrease exponentially and CD4 lymphocyte counts to rise substantially, indicating that replication of HIV- 1 in vivo is continuous and highly productive, driving the rapid turnover ofCD4 lymphocytes.
Abstract: Treatment of infected patients with ABT-538, an inhibitor of the protease of human immunodeficiency virus type 1 (HIV-1), causes plasma HIV-1 levels to decrease exponentially (mean half-life, 2.1 +/- 0.4 days) and CD4 lymphocyte counts to rise substantially. Minimum estimates of HIV-1 production and clearance and of CD4 lymphocyte turnover indicate that replication of HIV-1 in vivo is continuous and highly productive, driving the rapid turnover of CD4 lymphocytes.

4,306 citations

Journal ArticleDOI
20 Jun 1996-Nature
TL;DR: The principal cofactor for entry mediated by the envelope glycoproteins of primary macrophage-tropic strains of HIV-1 is CC-CKR-5, a receptor for the β-chemokines RANTES, Mip-1α and MIP-1β.
Abstract: Entry of HIV-1 into target cells requires cell-surface CD4 and additional host cell cofactors. A cofactor required for infection with virus adapted for growth in transformed T-cell lines was recently identified and named fusin. However, fusin does not promote entry of macrophage-tropic viruses, which are believed to be the key pathogenic strains in vivo. The principal cofactor for entry mediated by the envelope glycoproteins of primary macrophage-tropic strains of HIV-1 is CC-CKR-5, a receptor for the β-chemokines RANTES, MIP-1α and MIP-1β.

3,802 citations

Journal ArticleDOI
15 Mar 1996-Science
TL;DR: A new mathematical model was used to analyze a detailed set of human immunodeficiency virus-type 1 (HIV-1) viral load data collected from five infected individuals after the administration of a potent inhibitor of HIV-1 protease, providing not only a kinetic picture ofAIDS pathogenesis, but also theoretical principles to guide the development of treatment strategies.
Abstract: A new mathematical model was used to analyze a detailed set of human immunodeficiency virus-type 1 (HIV-1) viral load data collected from five infected individuals after the administration of a potent inhibitor of HIV-1 protease. Productively infected cells were estimated to have, on average, a life-span of 2.2 days (half-life t1/2 = 1.6 days), and plasma virions were estimated to have a mean life-span of 0.3 days (t1/2 = 0.24 days). The estimated average total HIV-1 production was 10.3 × 109 virions per day, which is substantially greater than previous minimum estimates. The results also suggest that the minimum duration of the HIV-1 life cycle in vivo is 1.2 days on average, and that the average HIV-1 generation time—defined as the time from release of a virion until it infects another cell and causes the release of a new generation of viral particles—is 2.6 days. These findings on viral dynamics provide not only a kinetic picture of HIV-1 pathogenesis, but also theoretical principles to guide the development of treatment strategies.

3,519 citations

Journal ArticleDOI
20 Jun 1996-Nature
TL;DR: The β-chemokine receptor CC-CKR-5 as mentioned in this paper is a second receptor for NSI primary viruses, which allows env-mediated cell-cell membrane fusion, but it does not allow the fusion of cells from some HIV-1-exposed uninfected individuals.
Abstract: The β-chemokines MIP-1α, MIP-1β and RANTES inhibit infection of CD4+ cells by primary, non-syncytium-inducing (NSI) HIV-1 strains at the virus entry stage, and also block env-mediated cell–cell membrane fusion. CD4+ T cells from some HIV-1-exposed uninfected individuals cannot fuse with NSI HIV-1 strains and secrete high levels of β-chemokines. Expression of the β-chemokine receptor CC-CKR-5 in CD4+ , non-permissive human and non-human cells renders them susceptible to infection by NSI strains, and allows env-mediated membrane fusion. CC-CKR-5 is a second receptor for NSI primary viruses.

3,304 citations

Journal ArticleDOI
09 Aug 1996-Cell
TL;DR: A CKR-5 allele present in the human population appears to protect homozygous individuals from sexual transmission of HIV-1 and is suggested to provide a means of preventing or slowing disease progression.

3,110 citations


Authors

Showing all 564 results

NameH-indexPapersCitations
Michel C. Nussenzweig16551687665
Douglas D. Richman14263382806
Joseph Sodroski13854277070
John P. Moore13652260331
Chi-Huey Wong129122066349
David D. Ho12438569837
Richard A. Koup12240161738
Alan S. Perelson11863266767
David A. Cooper11790369249
Bette T. Korber11739249526
Carlos F. Barbas11551853545
Robert W. Doms11127939660
Andrew Carr11184254974
Charles R. Mackay10627250300
Jay A. Levy10445137920
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20231
20222
202166
202043
201920
201828