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Peptide-based Identification of Functional Motifs and their Binding Partners
Published on: June 30, 2013
Attenuation of multiple Nef functions in HIV-1 elite controllers
Philip Mwimanzi1, Tristan J Markle, Eric Martin
1Center for AIDS Research, Kumamoto University, 2-2-1 Honjo, Kumamoto 860-0811, Japan.
Retrovirology
|January 8, 2013
Summary
Elite controllers (EC) show reduced HIV-1 Nef protein function, possibly due to immune pressure. This impaired Nef activity may be a key characteristic of elite control in HIV-1 infection.
Area of Science:
- Virology
- Immunology
- Molecular Biology
Background:
- Elite controllers (EC) spontaneously suppress HIV-1 viremia, but the function of the accessory protein Nef is not fully understood.
- Previous studies noted impaired Gag, Pol, and Env functions in EC.
- Nef plays a crucial role in HIV-1 pathogenesis.
Purpose of the Study:
- To investigate the functional activity of HIV-1 Nef clones from elite controllers (EC) and chronic progressors (CP).
- To compare the abilities of Nef clones in down-regulating HLA class I and CD4, up-regulating CD74, enhancing viral infectivity, and stimulating viral replication.
Main Methods:
- Isolated and analyzed 91 HIV-1 Nef clones from plasma of 45 EC and 46 CP.
- Assessed five key Nef functions: HLA class I and CD4 down-regulation, CD74 up-regulation, viral infectivity enhancement, and viral replication stimulation in peripheral blood mononuclear cells (PBMC).
Main Results:
- HIV-1 Nef clones from EC generally showed reduced function across all five tested activities compared to CP.
- Nef clones from EC expressing HLA-B*57 exhibited poorer CD4 down-regulation.
- A correlation was observed between EC-specific HLA-B*57-associated Nef polymorphisms and reduced Nef function.
Conclusions:
- Decreased HIV-1 Nef function is suggested to be a characteristic of the elite controller phenotype.
- Host immune selection pressures likely contribute to the impaired Nef function observed in EC.
- Further research into Nef's role in elite control is warranted.
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