z-logo
open-access-imgOpen Access
Mechanistic Studies of a T20-Dependent Human Immunodeficiency Virus Type 1 Variant
Author(s) -
Christopher E. Baldwin,
Ben Berkhout
Publication year - 2008
Publication title -
journal of virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.617
H-Index - 292
eISSN - 1070-6321
pISSN - 0022-538X
DOI - 10.1128/jvi.02524-07
Subject(s) - biology , gp41 , virology , virus , infectivity , viral replication , mutation , human immunodeficiency virus (hiv) , viral envelope , antibody , lipid bilayer fusion , genetics , microbiology and biotechnology , epitope , gene
We previously described a T20-dependent human immunodeficiency virus type 1 variant from a patient on T20 therapy. This virus carries two mutations in the gp41 domain of the envelope protein (Env) that was proposed to undergo a premature conformational switch to the 6-helix bundle structure. The T20 peptide can rescue this hyperfusogenic Env protein by preventing the premature switch and preserving an earlier prefusion conformation, thus restoring virus infectivity and replication. In this study, we set out to critically test this mechanistic explanation with alternative effectors that may control the Env switch, including other fusion inhibitors and antibodies that target gp41.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here