Table 1.

HLA associations with HIV-1 disease

HLA genotype	Epidemiological effect	Suggested mechanism
HLA class I homozygosity	Accelerated disease progression	Narrow CTL response(30, 32). Viral escape from common alleles (33, 34).
B*57	Slow disease progression	Broad reactivity across multiple conserved gag epitopes and reduced viral fitness of escape variants (44, 55, 56, 191).
B*27	Slow disease progression	Presents a conserved immunodominant gag epitope that requires a complex pattern of mutation for escape (46, 64–66).
B*35-Px	Accelerated disease progression	Peptide binding specificity (71). Interaction with ILT4 resulting in dendritic cell dysfunction (78).
Bw4	Slow disease progression	More effective HIV-1-specific responses (84).
B*51	Slow disease progression	Strong CTL response to Gag and Pol epitopes (192)
B*58:01	Slow disease progression	Strong CTL response to Gag epitope (35)
B*58:02	Accelerated disease progression	Ineffective CTL response to Env epitope (90)
B*13	Slow disease progression	Targeting of a conserved nef epitope (86). Broad Gag-specific CD8+ response (87).
B*81:01	Slow disease progression	Lower replication capacity of escape variants (89).
DR13 supertype & DRB1*13- DQB1*06 haplotype	Slow disease progression	Selection of a highly conserved Th1 gag epitope (102)
DRB1*01	Protection against infection	Unknown (98, 99)
DRB1*15:03	Increased susceptibility to infection	Unknown (98, 99)
DRB1*13:03	Reduced viral load levels	Unknown (101)