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Inhibition of HIV and SIV infectivity by blockade of alpha-glucosidase activity.

作者信息

Ratner L, vander Heyden N, Dedera D

机构信息

Department of Medicine, Washington University, St. Louis, Missouri 63110.

出版信息

Virology. 1991 Mar;181(1):180-92. doi: 10.1016/0042-6822(91)90483-r.

DOI:10.1016/0042-6822(91)90483-r
PMID:1704656
Abstract

Processing of HIV and SIV envelope oligosaccharides is critical for proper intracellular trafficking and function. An inhibitor of alpha-glucosidases I and II, N-butyl deoxynojirimycin (N-BuDNJ), retards HIV-1 and SIVmac spread in lymphocytes and monocytes by diminishing virus infectivity, and also causes a reduction in syncytia formation between infected cells and uninfected lymphocytes. N-BuDNJ retards envelope processing from the precursor form to the mature surface (SU) and transmembrane proteins in HIV-1- and SIVmac-infected cells, as well as in cells infected with vaccinia-HIV-1 envelope recombinant virus. However, no significant reduction is seen in the amount of SU in released virus particles, though the virus particle-associated SU from N-BuDNJ-treated cells has an altered electrophoretic mobility. In contrast, N-BuDNJ had no effect on GAG protein synthesis and processing. These findings demonstrate a critical requirement for oligosaccharide processing by alpha-glucosidases I and II for HIV-1 and SIVmac envelope processing and fusogenicity.

摘要

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