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11th International AIDS ConferenceVancouver, British Columbia — July 7-12, 1996 |
Int Conf AIDS 1996 Jul 7-12; 11:217 (abstract no. Th.A.383)
Tang XB, Hildreth J, Yu XF; Dept. of Molecular Microbiology and Immunology, Johns Hopkins School of Hygiene and Public Health, Baltimore, MD, USA. Fax: 410-955-0105.
OBJECTIVE: A critical step during HIV-1 assembly is to incorporate viral Env proteins into mature virions. During budding, certain cellular glycoproteins are also incorporated into HIV-1 virions. Viral Env and cellular glycoproteins play important roles in virus infectivity and pathogenesis. We have been interested in determining the mechanism of incorporation of viral and cellular glycoproteins into HIV-1 virions.
METHODS: We have previously identified a region in p17 to be critical for incorporation of Env proteins into mature HIV-1 virions. Mutants containing substitutions of highly conserved amino acids in this region were generated and studied for their effects on virus assembly, release, and the incorporation of viral Env and cellular glucoproteins.
RESULTS: Viral Env proteins as well as several cellular glycoproteins including HLA class I, CD29, CD44, and CD63 were incorporated into wild type HIV-1 virions generated from COS-7 cells. Single amino acid substitutions in p17 abolished incorporation of viral Env proteins without affecting virus assembly and release. The incorporation of cellular glycoproteins, HLA class I, CD29, CD44, and CD63 was not inhibited in p17 mutant virus that failed to incorporate viral Env proteins. Substitutions of hydrophobic amino acids in p17 were more detrimental to the incorporation of viral Env into mature virions than substitutions of positively charged amino acids.
CONCLUSIONS: The matrix protein of HIV-1 plays a critical role in selective incorporation of viral Env proteins but not cellular glycoproteins into mature virions. Selective incorporation of HIV-1 Env and certain cellular glycoproteins into mature virions are mediated via two distinct mechanisms.
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ThA383
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