Capsid is a dominant determinant of retrovirus infectivity in nondividing cells.
A major difference between lentiviruses such as human immunodeficiency virus (HIV) and most other retroviruses is their ability to productively infect nondividing cells. We present here genetic evidence for involvement of the capsid protein (CA) in the infectious phenotype in nondividing cells. A chimeric HIV type 1 (HIV-1) in which the MA and CA of HIV-1 are replaced with the MA, p12, and CA encoding sequences from murine leukemia virus (MLV) loses the ability to efficiently infect nondividing cells. Analysis of the accumulation of two-long-terminal-repeat circles implies that the impairment of nuclear transport of preintegration complexes is responsible for the restricted infection of this chimeric virus in nondividing cells. Incorporation of MLV MA and MLV p12 into HIV virions alone does not exert any adverse effects on viral infection in interphase cells. These results suggest that CA is the dominant determinant for the difference between HIV and MLV in the ability to transduce nondividing cells.
Yamashita
Masahiro
M
Division of Human Biology, Mail Stop C2-023, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. North, P.O. Box 19024, Seattle, WA 98109-1024, USA.
Emerman
Michael
M
D021581:Active Transport, Cell Nucleus; D002213:Capsid / Q000502:physiology*; D015683:Gene Products, gag / Q000502:physiology; D016325:HIV Long Terminal Repeat; D015497:HIV-1 / Q000502:physiology*; D006367:HeLa Cells; D006801:Humans; D009052:Leukemia Virus, Murine / Q000502:physiology*; D014763:Viral Matrix Proteins / Q000502:physiology
C468293:Gag protein p12, moloney murine leukemia virus; D015683:Gene Products, gag; D014763:Viral Matrix Proteins