Cells with high cyclophilin A content support replication of human immunodeficiency virus type 1 Gag mutants with decreased ability to incorporate cyclophilin A.
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.
Ackerson
B
B
Department of Pediatrics, University of California, Los Angeles 90095, USA.
Rey
O
O
Canon
J
J
Krogstad
P
P
D000818:Animals; D001483:Base Sequence; D002460:Cell Line; D004279:DNA, Viral / Q000096:biosynthesis / Q000235:genetics; D015750:Genes, gag; D015497:HIV-1 / Q000235:genetics* / Q000502:physiology*; D006801:Humans; D066298:In Vitro Techniques; D008214:Lymphocytes / Q000378:metabolism / Q000821:virology; D019696:Peptidylprolyl Isomerase / Q000378:metabolism*; D017354:Point Mutation; D014779:Virus Replication / Q000235:genetics* / Q000502:physiology*
D004279:DNA, Viral; D019696:Peptidylprolyl Isomerase