Despite several decades of research, HIV infection is still incurable and demands commitment to lifelong antiretroviral therapy (ART) to suppress the virus and prevent AIDS. The challenges to HIV cure is mainly due to the reservoir of memory CD4+ T cells that harbor transcriptionally silent latent proviruses which produces virus during treatment interruption. Virus-specific CD8+ T cell responses is elicited during HIV infection, resulting in the secretion of Interferon-γ (IFNγ), cytokines and other effector molecules to control the infection. Similarly, during chronic hepatitis B infection, HBV-specific CD8+ T cell exhaustion and altered CD4+ T cell responses occur. Therefore, hepatitis co-infection with HIV is likely to alter T cell responses even more which may result in increased immune activation. The role of HBV co-infection on T cell responses and the reservoir size has not been well studied, hence a critical gap that needs to be filled. 

We hypothesize that compared to HIV-only patients, those who are co-infected with HIV/HBV will have T cells that are more exhausted and will respond poorly to latency reversing agents and have larger reservoir size than those with mono-infections.