Sensitivity to inhibition by beta-chemokines correlates with biological phenotypes of primary HIV-1 isolates - PubMed (original) (raw)
Comparative Study
Sensitivity to inhibition by beta-chemokines correlates with biological phenotypes of primary HIV-1 isolates
M Jansson et al. Proc Natl Acad Sci U S A. 1996.
Abstract
Primary HIV-1 isolates were evaluated for their sensitivity to inhibition by beta-chemokines RANTES (regulated upon activation, normal T-cell expressed and secreted), macrophage inflammatory protein 1 alpha (MIP-1 alpha), and MIP-1 beta. Virus isolates of both nonsyncytium-inducing (NSI) and syncytium-inducing (SI) biological phenotypes recovered from patients at various stages of HIV-1 infection were assessed, and the results indicated that only the isolates with the NSI phenotype were substantially inhibited by the beta-chemokines. More important to note, these data demonstrate that resistance to inhibition by beta-chemokines RANTES, MIP-1 alpha, and MIP-1 beta is not restricted to T cell line-adapted SI isolates but is also a consistent property among primary SI isolates. Analysis of isolates obtained sequentially from infected individuals in whom viruses shifted from NSI to SI phenotype during clinical progression exhibited a parallel loss of sensitivity to beta-chemokines. Loss of virus sensitivity to inhibition by beta-chemokines RANTES, MIP-1 alpha, and MIP-1 beta was furthermore associated with changes in the third variable (V3) region amino acid residues previously described to correlate with a shift of virus phenotype from NSI to SI. Of interest, an intermediate V3 genotype correlated with a partial inhibition by the beta-chemokines. In addition, we also identified viruses sensitive to RANTES, MIP-1 alpha, and MIP-1 beta of NSI phenotype that were isolated from individuals with AIDS manifestations, indicating that loss of sensitivity to beta-chemokine inhibition and shift in viral phenotype are not necessarily prerequisites for the pathogenesis of HIV-1 infection.
Figures
Figure 1
Sensitivity to β-chemokines of primary HIV-1 isolates with either NSI or SI biological phenotype. Percentage of HIV-1 p24 release, in relation to controls, of β-chemokine-exposed virus cultures of (a) NSI phenotype or (b) SI phenotype.
Figure 2
Sensitivity to β-chemokine-mediated replication inhibition of primary HIV-1 isolates with different biological phenotypes obtained sequentially from individual patients. Percentage of p24 release, in relation to controls, of β-chemokine-exposed virus cultures with (a) NSI phenotype or after switch with (b) SI phenotype.
Figure 3
V3 region amino acid sequences obtained from viruses losing β-chemokine sensitivity simultaneously with a switch from NSI to SI phenotype in infected individuals. V3 amino acid residues are numbered according to the HIV-1MN sequence presented in the Los Alamos data base (35). A dash (-) indicates an amino acid identical to that present in the V3 sequence of the early isolate obtained from a corresponding individual, and a gap was introduced to align the sequences and is pointed out by a dot (.). Sequence heterogeneity is indicated by assigning two amino acids at the same position.
Figure 4
Sensitivity to chemokine-mediated replication inhibition of primary HIV-1 isolates with NSI phenotype obtained sequentially from three individual patients with AIDS. Percentage of p24 release, in relation to controls, of chemokine-exposed virus isolates obtained from patients F (a), G (b), and H (c).
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