Table 1: Key escape papers.

Immune responseHypothesisResultRef.

CTL basedHLA-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 fitnessEscape 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-1Extended sequence divergence for vaccine recipients who become infected suggests vaccine-induced CTL imparted significant immune pressure
Gag-84 most significant signature site

Nab basedEvolving “glycan shield” mechanism prevents Nab bindingEnv gene mutations in escape virus sparse
Escape mutations did not map to known epitopes
Efficient neutralization requires potent, high titres
Continual selection of Nab escape variants occursAll 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 therapy2G12 monoclonal was crucial for transient in vivo effect of Nab cocktail but immune escape resulted[55]

ADCC basedImmune pressure from HIV-specific ADCC results in immune-escape variantsADCC 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 cellsHIV-1 selects KIR2DL2+ virus mutations that result in reduced antiviral activity of NK cells[85]