Human Immunodeficiency Virus Type 1 Capsid Mutation N74D Alters Cyclophilin A Dependence and Impairs Macrophage Infection

被引：79

作者：

Ambrose, Zandrea ^{[1
]}

Lee, KyeongEun ^{[2
]}

Ndjomou, Jean ^{[1
]}

Xu, Hongzhan ^{[1
]}

Oztop, Ilker ^{[3
]}

Matous, James ^{[1
]}

Takemura, Taichiro ^{[2
]}

Unutmaz, Derya ^{[4
]}

Engelman, Alan ^{[3
]}

Hughes, Stephen H. ^{[2
]}

KewalRamani, Vineet N. ^{[2
]}

机构：

[1] Univ Pittsburgh, Sch Med, Div Infect Dis, Pittsburgh, PA 15260 USA

[2] NCI, HIV Drug Resistance Program, Frederick, MD 21701 USA

[3] Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA

[4] NYU, Sch Med, Dept Pathol & Microbiol, New York, NY USA

来源：

JOURNAL OF VIROLOGY | 2012年 / 86卷 / 08期

基金：

美国国家卫生研究院;

关键词：

HIV-1; INFECTION; DENDRITIC CELLS; NUCLEAR IMPORT; RESTRICTION; COMPLEX; PROTEIN; REPLICATION; RESISTANCE; PARTICLES; SAMHD1;

D O I：

10.1128/JVI.05887-11

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

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.

引用

页码：4708 / 4714

页数：7

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