Journal
JOURNAL OF VIROLOGY
Volume 78, Issue 11, Pages 5670-5678Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.78.11.5670-5678.2004
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Funding
- NIAID NIH HHS [R01 AI51153, R37 AI30927, R01 AI051153, R37 AI030927] Funding Source: Medline
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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 or 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.
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