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Publication

Nuclear pore heterogeneity influences HIV-1 infection and the antiviral activity of MX2.

eLife | 2018

HIV-1 accesses the nuclear DNA of interphase cells via a poorly defined process involving functional interactions between the capsid protein (CA) and nucleoporins (Nups). Here, we show that HIV-1 CA can bind multiple Nups, and that both natural and manipulated variation in Nup levels impacts HIV-1 infection in a manner that is strikingly dependent on cell-type, cell-cycle, and cyclophilin A (CypA). We also show that Nups mediate the function of the antiviral protein MX2, and that MX2 can variably inhibit non-viral NLS function. Remarkably, both enhancing and inhibiting effects of cyclophilin A and MX2 on various HIV-1 CA mutants could be induced or abolished by manipulating levels of the Nup93 subcomplex, the Nup62 subcomplex, NUP88, NUP214, RANBP2, or NUP153. Our findings suggest that several Nup-dependent 'pathways' are variably exploited by HIV-1 to target host DNA in a cell-type, cell-cycle, CypA and CA-sequence dependent manner, and are differentially inhibited by MX2.

Pubmed ID: 30084827 RIS Download

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Associated grants

Agency: National Institute of Allergy and Infectious Diseases, International
Id: R01AI062520
Agency: National Institute of Allergy and Infectious Diseases, International
Id: F32AI116263
Agency: NIAID NIH HHS, United States
Id: R01 AI062520
Agency: National Institute of Allergy and Infectious Diseases, International
Id: R3764003
Agency: NIAID NIH HHS, United States
Id: R37 AI064003
Agency: National Institute of Allergy and Infectious Diseases, International
Id: R01AI100720
Agency: NIAID NIH HHS, United States
Id: R01 AI100720
Agency: Howard Hughes Medical Institute, United States
Id: Investigator Award

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