Emerging role of mitochondria in response to HBV infection

Hepatitis B is a major global health problem that potentially life-threatening liver infection caused by the hepatitis B virus (HBV), which can lead to death due to liver cirrhosis and hepatocellular carcinoma (HCC). A considerable of research has demonstrated that mitochondrial dysfunction exists in patients with HBV infection, indicating that there is clinical relation between HBV infection and mitochondrial alterations. To explore the complex interplay between the functions of mitochondria and HBV infection in greater depth, we systematically summarized these mitochondrial alterations due to HBV infection in recent years. The liver is the central organ of metabolism that is a mitochondria-rich tissue and represents strong defense and regeneration capabilities in the body. Infested cells and their microenvironment must upregulate energy production for proliferation, growth, and effector functions to restrain the damage imposed by HBV. The changes in metabolic pathways caused by HBV infection are nothing more than those in the cytoplasm and mitochondria. Thus, this article brings into focus the effects of novel reprogramming of inner and outer mitochondria on HBV infection and then derives novel insights and new approaches for HBV diagnosis and therapy.