This is supported by: (i) the temporal association that exists between the increase in virus-specific CD8+ T cell responses and the post-peak decline in plasma viremia9,10; (ii) the CD8+ CTLs ability to suppress new infections in vitro11,12; (iii) the virus escape mutations that consistently arise in response to the host CD8+ T cell response during all stages of infection1,2,13,14; (iv) the strong association between specific host MHC-I alleles and HIV/SIV disease progression15; and (v) the association of circulating escape mutants with the prevalence of specific HLAs in the population16,17. This evidence concerns the gene CD8A and infection.