Background: Chronic immune activation is one of the most widely recognized hallmarks
of HIV infection. T-cells that express CD38+ and HLA-DR+ show poor proliferative potential,
signal transduction, and increased apoptotic potential. This affects HIV pathogenesis and its
outcome and further complicates with a coinfection like HBV.
Methods: Study Design: cross-sectional. Blood samples were collected and analyzed for virological
markers using ELISA for HBeAg and RT-PCR for HIV&HBV Viral load. Chronic immune activation
markers of CD8+ and CD4+ T cells were measured by Flow cytometry for both HIV and
Results: There was a significant increase in HBV replication shown by higher HBV DNA
(p=0.002), a higher proportion of HBeAg (p=0.0049), and lower CD4 counts (p=0.04) among
HIV/HBV coinfected individuals, compared to the monoinfected groups. The frequencies of CD4+
CD38+ HLA-DR+ and CD8+ CD38+ HLA-DR+ in the HIV/HBV coinfection were significantly
higher than HBV monoinfected group (P< 0.0001) and in the HIV monoinfected group (P <
0.0001). The Liver fibrosis score APRI and FIB-4, were higher in the coinfected group compared
with HBV monoinfected group (0.67 vs. 0.25, p = 0.0085; 3.48 vs. 0.98, p = 0.0026) respectively.
The cytokine levels of IL-17, Fas-L,TNF -α, IL-10, IL-2 and Granzyme B were also measured and
compared among the study groups.
Conclusion: Our data suggest that HIV probably influences immune activation of CD4+ and
CD8+ T cells and this may play a significant role in accelerating the disease outcome among
HIV/HBV coinfected individuals.