The Role of Vitamin D in HBV infection

Hepatitis B virus (HBV) infection, 30 years later since the launch of its vaccine, is still a global health Problem. The infection by HBV is a multiplex process dependent on host immune response involving the genetic milieu of the host for proliferation. In acute self-limiting hepatitis, a broad T-cell immune response occurs that is strong enough to eradicate the virus or suppress viral replication. The role of T-cell in the immunopathogenesis of HBV is to control HBV replication, destroy hepatocytes infected by HBV and ultimately eradicate infection. Vitamin D (1, 25(OH) D3) with its autocrine, intracrine and endocrine functions, is an important regulator of immune function, affecting both innate and adaptive immunity. T cells are richly provided with vitamin D receptor (VDR) and have been shown to play a critical role in the pathogenesis of viruses. The toll like receptors (TLR-2) activated by HBV attack, stimulates CYP27B1 (1α-hydroxylase) enzyme within macrophages to convert vitamin 25(OH)D2 to 1,25(OH)D3 which increases regulatory T cells and enhances the secretion of IL-10, and decreases the IL-2 release from dendritic cells. In addition it transcribes mRNAs for the synthesis of antimicrobial proteins which help in the phagocytosis of the HBV pathogens. This systematic review of the literature focuses on the role of vitamin D on the course of HBV infection. How vitamin D regulates the development and function of the immune complexes and the phagocytic proteins to control the clearing of the HBV infection is assessed and discussed.