Decline in the mRNA expression of HLA-DQB1 and CD4 corresponds to a higher expression of IFNγ in HIV-1/TB infection

The co-infection of tuberculosis (TB) and human immunodeficiency virus (HIV) poses a major global health challenge. Human leukocyte antigen (HLA) plays a significant role in influencing the outcome of the disease. Several studies have revealed that HLA class II genes, specifically HLA-DRB1 and HLA-DQB1, are linked to TB and HIV infections. Only a few studies have investigated the genotype or allelic frequencies of HLA genes in the co-infection of HIV/TB. In this study, the mRNA expression of DRB1*15:01:01, DQB1*06:02:01:01, CD4, and IFNγ was determined in participants with mono-infection of HIV-1 (n = 28), mono-infection of TB (n = 31), and co-infection of HIV-1/TB (n = 21) and compared with healthy controls (n = 20). The relative quantification of the transcripts was determined using an RT2-Profiler PCR array. The findings revealed a significantly higher expression of the HLA-DRB1 gene, with a fold change of 3.7 (p = 0.005), in individuals with TB infection alone. In contrast, expression of the HLA-DQB1 gene was significantly decreased by 1.3-fold change (p = 0.008) in individuals with HIV-1/TB co-infection. Additionally, the mRNA expression of CD4 was elevated (fc: 1.2, p = 0.94) in the TB group, whereas in the HIV-1 and HIV-1/TB groups, there was a decrease in CD4 mRNA expression (HIV: fc −1.3, p = 0.045) (HIV-1/TB: fc −1.15, p = 0.191). In contrast, IFNγ mRNA expression was decreased in TB but relatively higher in individuals with HIV-1 and HIV-1/TB co-infection. We further evaluated the correlation between CD4 and IFNγ mRNA expression in all three groups. We found a significant negative correlation (TB: r = −0.386, HIV-1: r = −0.498, p < 0.05) between CD4 and IFNγ in the TB and HIV-1 groups, while a positive correlation was observed in the HIV-1/TB group (r = 0.330, p > 0.05). A decrease in HLA-DQB1 and CD4 mRNA expression and an increase in IFNγ in HIV/TB co-infection suggests that these markers are involved in the immunopathogenesis and progression of the disease.