Abstract
We have undertaken a genetic strategy to map Vpu regions necessary for BST-2 antagonism and viral egress. This approach is based on our identification of an egress-defective Vpu variant encoded by an HIV-1 subtype C strain. We constructed a series of chimeric Vpu molecules made from the Vpu C variant and Vpu B from a standard laboratory strain. The TM domain from the inactive Vpu C, which contains multiple non-conserved residues, was responsible for a significant decrease in egress activity and BST-2 downregulation, confirming the functional importance of the Vpu TM domain. However, for complete inactivation, both the N-terminus and TM domain from the inactive Vpu C molecule were required, suggesting a new role for the Vpu N-terminus. In addition, determinants in the C-terminus of Vpu B that may be involved in efficient TGN accumulation were also necessary for enhanced viral egress but are missing or non-functional in Vpu C.
Original language | English (US) |
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Pages (from-to) | 182-196 |
Number of pages | 15 |
Journal | Virology |
Volume | 441 |
Issue number | 2 |
DOIs | |
State | Published - Jul 5 2013 |
Keywords
- BST-2
- HIV-1
- Immune evasion
- Innate immunity
- Tetherin
- Viral egress
- Vpu
ASJC Scopus subject areas
- Virology