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
[36]

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
[54]
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]