J Virol. 1991 Dec;65(12):6931-41. Unique Identifier : AIDSLINE
Human immunodeficiency virus type 1 (HIV-1) isolates display differences
in a variety of in vitro biological properties, including the ability to
infect different cell types, the kinetics of replication, and
cytopathicity in the infected cells. Studies with isolates obtained from
the same individual over time have shown that these in vitro properties
of the viral isolates correlate with pathogenicity in the host. The
later isolates, recovered when disease has developed, display a wider
cellular host range, replicate rapidly and to high titers in the
infected cells, and induce syncytia in these cells. In the present
studies, the genomic determinants of these biological properties were
defined with recombinant viruses generated between two HIV-1 isolates
recovered sequentially from the same individual. The results show that
the rate of HIV-1 replication in the HUT 78 T-cell line is controlled by
the first coding exon of tat. Infection of T-cell and monocytic cell
lines is determined by two specific regions in the envelope gp120, one
of which also confers the ability of an isolate to induce syncytia.
Amino acid sequence comparison of the regions identified revealed minor
differences between the two viral isolates: 2 amino acids in the tat
gene product and 10 and 12 amino acids in the two regions of envelope
gp120. These data suggest that small changes in the tat and env proteins
can have dramatic effects on the pathogenic potential of HIV-1.
Acquired Immunodeficiency Syndrome/MICROBIOLOGY Amino Acid Sequence
Cell Line Cloning, Molecular Comparative Study DNA,
Recombinant/ISOLATION & PURIF DNA, Viral/GENETICS/ISOLATION & PURIF
Exons Gene Products, tat/*GENETICS *Genes, tat Giant Cells/CYTOLOGY
Human HIV Envelope Protein gp120/*GENETICS
HIV-1/GENETICS/*PHYSIOLOGY/PATHOGENICITY Molecular Sequence Data
Monocytes Recombination, Genetic Restriction Mapping Sarcoma Viruses,
Avian/GENETICS Sequence Homology, Nucleic Acid Support, Non-U.S. Gov't
Support, U.S. Gov't, P.H.S. T-Lymphocytes Virus Integration *Virus
Replication JOURNAL ARTICLE