Association of CD209 promoter variants and tuberculosis infection susceptibility, AIDS development, and treatment response outcomes among the HIV-1 Moroccan population

The DC-SIGN (Dendritic Cell-Specific Intercellular adhesion molecule-3-Grabbing Non-integrin) molecules located on the surface of Dendritic Cell subsets showed high-affinity binding to HIV-1 and Mycobacterium tuberculosis (Mtb) . It is exploited by HIV-1 and Mtb as a part of their immune evasion strategy. In this study, we explored how variations in the CD209 gene, which encodes for DC-SIGN, may be linked to the development of tuberculosis (TB) in individuals with HIV-1 infection. Additionally, we examined their potential association with the progression of AIDS and the treatment response outcome in the Moroccan population.Two single nucleotide polymorphisms in the CD209 promoter − 336A>G (rs4804803) and − 139G>A (rs2287886) were investigated. Two hundred eighteen Moroccan patients living with HIV-1 were genotyped using direct DNA sequencing. Among the 218 patients, 90 were found to have a co-infection with Mtb. We categorized the patients based on their TB status into two groups: those with HIV-1 infection and without TB (HIV-1 + /TB − ) and those with both HIV-1 infection and TB (HIV-1 + /TB + ). We further classified them based on their AIDS status into two groups: AIDS and Non-AIDS patients.Our results revealed that genotype and allele frequencies of the − 336A>G and − 139G>A polymorphisms were not significantly different between HIV-1 + /TB − and HIV-1 + /TB + patients ( p > 0.05). Likewise, the development of AIDS does not appear to be affected by these two SNPs either ( p > 0.05). Haplotype analysis showed that none of the 4 possible haplotypes is associated with HIV-1 and TB co-infection ( p > 0.05). Interestingly, the analysis of the − 139G>A genotype distribution according to the HIV-1 viral load showed an improvement in patients with AG and GG genotypes, after antiretroviral therapy, compared to AA patients ( p = 0.0069 and p = 0.0476; respectively). Overall, − 336A>G and − 139G>A polymorphisms do not influence the susceptibility of HIV-1-infected individuals to develop TB and AIDS. However, − 139G>A polymorphism may affect the response to treatment as measured by RNA viral load levels.