Role of CXCR5⁺CD8⁺ T cells in human hepatitis B virus infection

Abstract

Human hepatitis B virus (HBV) infection, a primary cause of cirrhosis and liver cancer worldwide, remains a global public health concern due to the associated high morbidity and mortality rates. 1,2 Generally, HBV infection can be controlled by reverse-transcriptase inhibitors (nucleos (t) ide analogs [NAs]) and interferon (IFN) therapy. However, both these medications are available in limited quantities for eliminating HBV. Although antiviral therapy can efficaciously inhibit viral replication and significantly delay disease progression in patients infected with HBV, it is not curative and must be taken for a long period or even a lifetime. 3 Furthermore, once antiviral therapy is discontinued, new intact virus particles can be resynthesized, resulting from the covalently closed circular DNA (cccDNA). 4 Another major cause of the long-term existence of HBV is the dysfunction of the adaptive immune response, and the principal mechanism at play here is the immune tolerance induced by multiple viral antigens (e.g. HBV surface antigen, e antigen, core antigen). 5 Consequently,