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Nathaniel R. Landau

Researcher at Salk Institute for Biological Studies

Publications -  62
Citations -  15508

Nathaniel R. Landau is an academic researcher from Salk Institute for Biological Studies. The author has contributed to research in topics: Medicine & Virus. The author has an hindex of 31, co-authored 45 publications receiving 14968 citations. Previous affiliations of Nathaniel R. Landau include New York University & Aaron Diamond AIDS Research Center.

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Identification of a major co-receptor for primary isolates of HIV-1

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.
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Homozygous Defect in HIV-1 Coreceptor Accounts for Resistance of Some Multiply-Exposed Individuals to HIV-1 Infection

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.
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Change in Coreceptor Use Correlates with Disease Progression in HIV-1–Infected Individuals

TL;DR: The results suggest that HIV-1 evolves during the course of infection to use an expanded range of coreceptors for infection, and that this adaptation is associated with progression to AIDS.
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The role of a mutant CCR5 allele in HIV–1 transmission and disease progression

TL;DR: The CCR5 genotype of 1252 homosexual men enrolled in the Chicago component of the Multicenter AIDS Cohort Study (MACS) was analyzed and no evidence was found to suggest that heterozygotes were protected against HIV–1 infection, but a limited protective role against disease progression was noted.
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Species-Specific Exclusion of APOBEC3G from HIV-1 Virions by Vif

TL;DR: It is reported that HIV-1 Vif forms a complex with human APOBEC3G that prevents its virion encapsidation and suggests that therapeutic intervention that either induced APOBec3G or blocked its interaction with Vif could be clinically beneficial.