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]