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. 2018 Nov 26;9:2735. doi: 10.3389/fimmu.2018.02735

Table 4.

The influence of cell surface proteins of NK cells on the outcome of HIV-1 infection.

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)
a

Protective effect deduced from multiple independent studies.

b

Controversial roles in disease progress.