The systematic inflammation resulting from HIV infection may induce fibrosis via a number of mechanisms, including oxidative stress and mitochondrial dysfunction as a result of ER stress. CD4/CD8 imbalances seen in HIV can lead to underexpression of IFN-gamma (an antifibrotic cytokine), thus favoring induction of apoptosis of activated HSCs, and hepatic progression into a profibrotic state. The gene discussed is CD4; the disease is HIV infectious disease.