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M9630103.TXT
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1996-02-27
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Document 0103
DOCN M9630103
TI Single amino acid substitution in constant region 1 or 4 of gp120 causes
the phenotype of a human immunodeficiency virus type 1 variant with
mutations in hypervariable regions 1 and 2 to revert.
DT 9603
AU Wang WK; Essex M; Lee TH; Department of Cancer Biology, Harvard School
of Public Health,; Boston, Massachusetts 02115, USA.
SO J Virol. 1996 Jan;70(1):607-11. Unique Identifier : AIDSLINE
MED/96099479
AB The second major cysteine loop of human immunodeficiency virus type 1
envelope glycoprotein gp120 contains 5 to 11 consensus N-linked
glycosylation sites, which is disproportionately higher than the number
of such sites found in other regions of gp120. Amino acid substitutions
introduced at three of six N-linked glycosylation sites in this region
of an infectious molecular clone, HXB2, resulted in severe impairment of
virus infectivity. Isolation and genetic characterization of a revertant
of this mutant revealed an isoleucine-for-valine substitution at
position 84 in constant region 1 and an isoleucine-for-methionine
substitution at position 434 in constant region 4. Further mutational
analysis indicated that either isoleucine substitution was sufficient to
confer the revertant phenotype. These findings demonstrate that V1/V2
not only functionally interacts with C4, as previously reported, but
also interacts with C1. The observation that compensatory changes do not
involve regeneration of N-linked glycosylation sites in the second major
cysteine loop suggests that replication of human immunodeficiency virus
type 1 in vitro is independent of the presence of a disproportionate
number of N-linked glycosylation sites within this loop.
DE Amino Acid Sequence Animal Base Sequence Binding Sites Cell Line
Cloning, Molecular DNA Primers Glycosylation Human HIV Envelope
Protein gp120/*GENETICS/METABOLISM HIV-1/*GENETICS/METABOLISM
Molecular Sequence Data Mutagenesis, Site-Directed *Mutation
Phenotype Support, U.S. Gov't, Non-P.H.S. Support, U.S. Gov't, P.H.S.
Variation (Genetics) JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).