Advances in Virology / 2012 / Article / Tab 1 / Review Article
Antibody-Dependent Cellular Cytotoxicity and NK Cell-Driven Immune Escape in HIV Infection: Implications for HIV Vaccine Development Table 1 Key escape papers.
Immune response Hypothesis Result Ref. CTL based HLA-B*57/B*5801 CTL escape mutations in Gag impacts viral replication in vivo Reductions in relative replication capacity reduce “viral fitness” [20 ] CTL escape mutations in Env do not result in reduced viral fitness Escape mutations within Env-specific CTL are epitopes evident but no correlation with reduced SIV replication [25 ] Step HIV-1 vaccine trial exerts selective CTL pressure on HIV-1 Extended sequence divergence for vaccine recipients who become infected suggests vaccine-induced CTL imparted significant immune pressure Gag-84 most significant signature site [36 ] Nab based Evolving “glycan shield” mechanism prevents Nab binding Env gene mutations in escape virus sparse Escape mutations did not map to known epitopes Efficient neutralization requires potent, high titres [54 ] Continual selection of Nab escape variants occurs All previous viral isolates, but not concurrent isolate, are recognised by concurrent Nab [7 ] Passive transfer of human neutralizing monoclional antibodies delays HIV-1 rebound post-antiretroviral therapy 2G12 monoclonal was crucial for transient in vivo effect of Nab cocktail but immune escape resulted [55 ] ADCC based Immune pressure from HIV-specific ADCC results in immune-escape variants ADCC causes escape in multiple epitopes and evolves over timeADCC antibodies forcing immune escape can be non-eutralizing [9 ] NK cells apply immunological pressure on HIV-1 through direct killing of infected cells HIV-1 selects KIR2DL2+ virus mutations that result in reduced antiviral activity of NK cells [85 ]