Phenotypic and immunologic changes in SIVMne variants that emerge in association with progression to AIDS are determined by multiple changes in gag and env.

Important note: Information in this article was accurate in 1997. The state of the art may have changed since the publication date.

Phenotypic and immunologic changes in SIVMne variants that emerge in association with progression to AIDS are determined by multiple changes in gag and env.

Conf Adv AIDS Vaccine Dev. 1997 May 4-7;:33. Unique Identifier : AIDSLINE MED/97927021
Kimata JT; Chackerian B; Rudensey L; Overbaugh J; Department of Microbiology, University of Washington, Seattle, WA.; Fax: (206) 543-8297.

Abstract: In infected macaques, SIVMne evolves from a M-tropic, slowly replicating, minimally cytopathic, nonsyncytium-inducing virus slow-low/NSI) to a T-tropic, rapidly replicating, highly cytopathic, syncytium-inducing virus population (rapid-high/SI) in association with the progression to AIDS. During the course of infection, virus variants with mutations encoding Ser and Thr residues in the V1 of Env SU are also selected. Biochemical analyses directly demonstrate that the V1 Ser and Thr amino acid changes are sites for O- and N-linked glycosylation. These V1 carbohydrate changes alter neutralizing antibody recognition, and mutational studies suggest that V1 is a part of a conformational domain of the principal neutralizing determinant for SIVMne. However, the SU changes in the late variant viruses are not the primary viral determinant for the switch from slow-low/NSI to rapid-hi/SI during the course of SIVMne infection, and they do not alter CCR-5 coreceptor recognition. To examine the cytopathic and replication determinants, two full-length proviruses were cloned from late in SIVMne infection. One variant is a prototype rapid-hi/SI variant, and we have mapped the determinants for SI phenotype to Env TM and the primary replication and cytopathic determinant to Gag. A second variant obtained from the lymph node of a macaque with AIDS was slow-low/NSI in T-cell lines, but was rapidly replicating in both stimulated and unstimulated PBMCs cultures.

Keywords: *Acquired Immunodeficiency Syndrome/GENETICS *Gene Products, env/GENETICS *Gene Products, gag/GENETICS *SIV/IMMUNOLOGY
971130
M97B1197

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