Cells with high cyclophilin A content support replication of human immunodeficiency virus type 1 Gag mutants with decreased ability to incorporate cyclophilin A
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Ackerson, B
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UNIV CALIF LOS ANGELES, DEPT PEDIAT, DIV PEDIAT INFECT DIS, LOS ANGELES, CA 90095 USAUNIV CALIF LOS ANGELES, DEPT PEDIAT, DIV PEDIAT INFECT DIS, LOS ANGELES, CA 90095 USA
Ackerson, B
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Rey, O
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UNIV CALIF LOS ANGELES, DEPT PEDIAT, DIV PEDIAT INFECT DIS, LOS ANGELES, CA 90095 USAUNIV CALIF LOS ANGELES, DEPT PEDIAT, DIV PEDIAT INFECT DIS, LOS ANGELES, CA 90095 USA
Rey, O
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Canon, J
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UNIV CALIF LOS ANGELES, DEPT PEDIAT, DIV PEDIAT INFECT DIS, LOS ANGELES, CA 90095 USAUNIV CALIF LOS ANGELES, DEPT PEDIAT, DIV PEDIAT INFECT DIS, LOS ANGELES, CA 90095 USA
Canon, J
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Krogstad, P
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UNIV CALIF LOS ANGELES, DEPT PEDIAT, DIV PEDIAT INFECT DIS, LOS ANGELES, CA 90095 USAUNIV CALIF LOS ANGELES, DEPT PEDIAT, DIV PEDIAT INFECT DIS, LOS ANGELES, CA 90095 USA
Krogstad, P
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[1] UNIV CALIF LOS ANGELES, DEPT PEDIAT, DIV PEDIAT INFECT DIS, LOS ANGELES, CA 90095 USA
Gag polyprotein-mediated incorporation of cellular cyclophilin A (CyPA) into virions is essential for the formation of infectious human immunodeficiency virus type 1 (HIV-1) virions. Either a point mutation in Gag (P222A) or drugs which bind CyPA decrease virion incorporation of CyPA and interfere with HIV-1 replication. We have found that lymphoid cells varied greatly in their CyPA content and that cells with high CyPA content supported the replication of P222A HIV-1 Gag mutants. These experiments demonstrated that a higher cellular CyPA content of some cells was able to compensate for the decreased binding affinity of P222A mutant Gag for CyPA, allowing virus replication to occur.