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Viral resistance v0.28 | KIR3DL1 |
Ivone Leong Added comment: Comment on list classification: KIR3DL1 and KIR3DS1 are highly homologous (both exon and intron) and are considered to be alleles of the same gene PMID: 12134147 found that activation of KIR3DS1 in combination of HLA-B (HLA-B Bw4-80Ile), is associated with delayed progression of AIDS in people infected with HIV-1. If KIR3DS1 is missing then HLA-B Bw4-80Ile is not associated with any AIDS outcomes; however, if HLA-B Bw4-80Ile is missing then KIR3DS1 is associated with more rapid AIDS progression. PMID: 18317000 found that there is an increased proportion of KIR3DS1 in HIV-exposed uninfected individuals compared with individuals who have primary HIV infections. This suggest that KIR3DS1 may contribute to more active natural killer cell function seen in HIV-exposed uninfected individuals. PMID: 16933987 showed that KIR3DS1 in combination with HLA-B Bw4-80Ile confers early direct containment of HIV viral load and protection against development of AIDS defining opportunistic infections (such as pneumocystis carinii pneumonia, CMV retinitis and mycobacterium avium complex). PMID: 31288555 is a meta-analysis based on 25 studies that looked at KIR genes in HIV-1 control or susceptibility. This study found that KIR3DS1 may be associated to protection against HIV-1 infection. KIR3DS1/S1 individuals were significantly slower in getting HIV infection than KIR3DL1/S1 individuals. Therefore, there is enough evidence to promote this gene to Green status. |
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Viral resistance v0.8 | HLA-B |
Rebecca Foulger gene: HLA-B was added gene: HLA-B was added to Viral resistance. Sources: Literature Mode of inheritance for gene: HLA-B was set to Unknown Publications for gene: HLA-B were set to 32303592 Phenotypes for gene: HLA-B were set to immunity to COVID-19 Added comment: PMID:32303592 (Nguyen et al., 2020) performed in-silico analysis of viral-binding affinity across HLA genotypes for SARS-CoV-2 peptides. Based on in-silico results, they suggest that individuals with HLA-B*46:01 may be vulnerable to COVID-19. Conversely, HLA-B*15:03 may enable greater immunity. Sources: Literature |