Table 4.
Genes or products | Population | Phenotypes | References |
---|---|---|---|
KIR 3DL1*h/*h or *004 + HLA-B*57 | More frequent in exposed uninfected individuals | (141) | |
Increased KIR2DL2/L3/S2; Decreased KIR2DL1/S1 | Infected patients | Increased VLs | (142) |
KIR3DL1a | Slow progressor | Lower VLs; Strong NK responses | (22, 143, 144) |
KIR3DS1b+HLA-B Bw4-80I (irrespective of HLA-B*57or HLA-B*27) | Slow progressors | Epistasis NK cell function |
(145) (146) |
KIR3DS1b | Progressors | Rapid to endpoint | (145) |
HLA-C*01:02+KIR2DL2; HLA-C*12:02b+KIR2DL3; HLA-B*46:01+KIR2DL2 | CRF01_AE chronically infected Thais | Higher VLs | (147) |
HLA-C*12:03+KIR2DL2; HLA-C*12:03+KIR2DS2 | CRF01_AE chronically infected Thais | Lower VLs | (147) |
Increased NKp44 (CD56dim) | Clade A/D infected Ugandans | Reduced CD4+ T cells | (148) |
No induction of NKp44 Upon rIL2 stimulation | EC/LTNPs | CD4 maintenance | (149) |
Lower NKp30 upon rIL2 stimulation | ECs and LTNP | (149) | |
NKG2A | Infected population | Higher VLs; Reduced CD4+ T cells; Increased NK inhibition | (9) |
Protective effect deduced from multiple independent studies.
Controversial roles in disease progress.