Abstract
Background Understanding of the autologous neutralizing antibody (Nab) targets during HIV-1 infection remains fragmentary and warrants further investigation in order to be incorporated during development of a successfully protective vaccine. In subtype C infection, the eighteen amino acid amphipathic alpha2 helix, encoded immediately downstream of gp120's V3 domain, undergoes strong positive selection where mutations track with the neutralization resistant phenotype; such characteristics would seem to make the alpha2 helix an attractive potential site for Nab targeting and escape.
Highlights
Understanding of the autologous neutralizing antibody (Nab) targets during HIV-1 infection remains fragmentary and warrants further investigation in order to be incorporated during development of a successfully protective vaccine
In subtype C infection, the eighteen amino acid amphipathic alpha2 helix, encoded immediately downstream of gp120's V3 domain, undergoes strong positive selection where mutations track with the neutralization resistant phenotype; such characteristics would seem to make the alpha2 helix an attractive potential site for Nab targeting and escape
Utilizing longitudinal samples from subtype C-infected Zambian patients, we identified autologous Nab escape variants
Summary
HIV-1 infection fails to alter neutralization sensitivity or efficiency of in vitro replication. MK Murphy*1, R Rong, B Li1, J Mulenga, SA Allen, S Gnanakaran and CA Derdeyn. Address: 1Immunology and Molecular Pathogenesis, Emory University, Atlanta, GA, USA, 2Zambia Blood Transfusion Service, Lusaka, Zambia and 3Los Alamos National Laboratory, Los Alamos, NM, USA. Published: 22 October 2009 Retrovirology 2009, 6(Suppl 3):P114 doi:10.1186/1742-4690-6-S3-P114. AIDS Vaccine 2009 Anna Laura Ross Meeting abstracts – A single PDF containing all abstracts in this Supplement is available here. http://www.biomedcentral.com/content/pdf/1471-2105-10-S12-info.pdf
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