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M9630534.TXT
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1996-02-27
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Document 0534
DOCN M9630534
TI Naturally occurring accessory gene mutations lead to persistent human
immunodeficiency virus type 1 infection of CD4-positive T cells.
DT 9603
AU Kishi M; Zheng YH; Bahmani MK; Tokunaga K; Takahashi H; Kakinuma M; Lai
PK; Nonoyama M; Luftig RB; Ikuta K; Section of Serology, Hokkaido
University, Sapporo, Japan.
SO J Virol. 1995 Dec;69(12):7507-18. Unique Identifier : AIDSLINE
MED/96078994
AB Proviral DNA from cells surviving severe but transient cytopathic
effects, mediated by infection with recombinant human immunodeficiency
virus type 1 (HIV-1) carrying a single gene mutation at vif, vpr, or
vpu, was characterized by use of HIV-1-specific primer pairs in a
two-step PCR. Deletion mutations were detected in a region that spanned
the vif and vpr open reading frames. Cloning and sequencing of the
amplified DNA from this region revealed frequent large deletions in a
limited number of nucleotide positions. Analyses of the deletions
suggested that (i) genetic recombination, (ii) template-primer slippage,
and (iii) misalignment of the growing point during reverse transcription
of the HIV-1 genome might be the mechanisms that generated the
mutations. Apart from the large deletions, smaller deletions that gave
frameshift mutations in vif and/or vpr prevailed. In addition, cells
infected with a triple mutant defective in vif, vpr, and vpu did not
show any cytopathic effect. Thus, mutations generating multiple
accessory gene defects during HIV-1 replication correlate with viral
persistence and loss of cytopathogenicity.
DE Base Sequence Cell Line, Transformed Comparative Study CD4-Positive
T-Lymphocytes/*VIROLOGY Defective Viruses/*GENETICS/IMMUNOLOGY DNA
Primers DNA, Viral/GENETICS Frameshift Mutation *Genes, vif *Genes,
vpr *Genes, vpu Genome, Viral Human
HIV-1/*GENETICS/PHYSIOLOGY/PATHOGENICITY Kinetics Molecular Sequence
Data *Mutation Oligonucleotide Probes Proviruses/GENETICS/IMMUNOLOGY
Sequence Deletion Support, Non-U.S. Gov't T-Lymphocytes Time Factors
Virus Replication/*GENETICS JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).