Previous Article | Next Article ![]()
J. Virol., Apr 1995, 2068-2074, Vol 69, No. 4
M Courcoul, C Patience, F Rey, D Blanc, A Harmache, J Sire, R Vigne and B Spire
Previous studies have demonstrated the absence of viral replication of Vif-
mutants in stimulated primary blood mononuclear cells (PBMC). Human
immunodeficiency virus type 1 strain NDK Vif- mutants were propagated on
the semipermissive CEM cell line, and the viral stock obtained was compared
with the wild-type virus during a single cycle in PBMC. The Vif- virus was
able to enter PBMC with the same efficiency as the wild type, as
demonstrated by quantification of the strong-stop cDNA, and
retrotranscription was observed for both viruses within 4 h postinfection.
Using a PCR assay with an Alu-long terminal repeat pair of primers, we
detected integration for both the wild-type and Vif- viruses. We then used
qualitative and quantitative reverse transcription-mediated PCR techniques
to study the steady-state level of intracellular and extracellular viral
RNAs. All mRNA species were detected in PBMC infected with the wild-type
virus or with the Vif- virus 36 h postinfection. Furthermore,
quantification of viral RNA released from infected cells demonstrated
similar levels of virus produced after a unique cycle of replication.
However, the Vif- virus obtained after one replication cycle in PBMC was
unable to initiate retrotranscription in permissive target cells. These
data strongly suggest that the failure to infect target cells is due to a
defect in the formation of the viral particle in PBMC.
Copyright © 1995, American Society for Microbiology
Peripheral blood mononuclear cells produce normal amounts of defective Vif- human immunodeficiency virus type 1 particles which are restricted for the preretrotranscription steps
INSERM U372, 13276 Marseille, France.
This article has been cited by other articles:
| J. Bacteriol. | Mol. Cell. Biol. | Microbiol. Mol. Biol. Rev. |
|---|
| Clin. Vaccine Immunol. | ALL ASM JOURNALS |
|---|