Abstract:
BACKGROUND:The mechanism by which HIV infection leads to a selective depletion of CD4 cells leading to immunodeficiency remains highly debated. Whether the loss of CD4 cells is a direct consequence of virus infection or bystander apoptosis of uninfected cells is also uncertain. RESULTS:We have addressed this issue in the humanized mouse model of HIV infection using a HIV variant with a point mutation in the gp41 region of the Env glycoprotein that alters its fusogenic activity. We demonstrate here that a single amino acid change (V38E) altering the cell-to-cell fusion activity of the Env minimizes CD4 loss in humanized mice without altering viral replication. This differential pathogenesis was associated with a lack of bystander apoptosis induction by V38E virus even in the presence of similar levels of infected cells. Interestingly, immune activation was observed with both WT and V38E infection suggesting that the two phenomena are likely not interdependent in the mouse model. CONCLUSIONS:We conclude that Env fusion activity is one of the determinants of HIV pathogenesis and it may be possible to attenuate HIV by targeting gp41.
journal_name
Virol Jjournal_title
Virology journalauthors
Garg H,Joshi A,Ye C,Shankar P,Manjunath Ndoi
10.1186/1743-422X-8-34subject
Has Abstractpub_date
2011-01-21 00:00:00pages
34issn
1743-422Xpii
1743-422X-8-34journal_volume
8pub_type
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