Human Immunodeficiency Virus Type 1 Capsid Mutation N74D Alters Cyclophilin A Dependence and Impairs Macrophage Infection
Year: 2012
Type: article
Abstract: The antiviral factor CPSF6-358 interferes with the nuclear entry of human immunodeficiency virus type 1 (HIV-1). HIV-1 acquires resistance to CPSF6-358 through the N74D mutation of the capsid (CA), which alters its nuclear entry pathway. Here we show that compared to wild-type (WT) HIV-1, N74D HIV-1 is more sensitive to cyclosporine, has increased sensitivity to nevirapine, and is impaired in macrophage infection prior to reverse transcription. These phenotypes suggest a difference in the N74D reverse transcription complex that manifests early after infection and prior to interaction with the nuclear pore. Overall, our data indicate that N74D HIV-1 replication in transformed cells requires cyclophilin A but is dependent on other interactions in macrophages.
Source: Journal of Virology
DOI: 10.1128/jvi.05887-11
Language: English
Topic: HIV Research and Treatment
Subfield: Virology
Field: Immunology and Microbiology
Domain: Life Sciences
Open Access status: green
Awards: G2123889279, Pittsburgh Center for HIV Protein Interactions (PCHPI), University of Pittsburgh Clinical and Translational Science Institute, Mechanisms of Intrinsic Resistance to HIV Infection in Primary Human T Cells, Immunobiology of Regulatory T Cells in HIV Infection, G6607333669, G8245271607, HIV-1 Preintegration Trafficking and Nuclear Localization, Harvard University Center for AIDS Research
OpenAlex ID: W2044993753