The roles of programmed death ligand 1 in virus-associated cancers

Abstract

Programmed death ligand 1 (PD-L1) is a surface glycoprotein that induces T-cell anergy or apoptosis by binding to PD-1 on activated T and B cells. It is also known as a cluster of differentiation 274 (CD274) or B7 homolog 1 (B7-H1). Suppressing the adaptive arm of the immune system is the critical role of PD-L1.so it prohibits the proliferation of activated T cells and reduces apoptosis in regulatory T cells. When PD-L1 binds to PD-1, it prevents T cells from killing other cells such as cancer cells. Viruses have various strategies to evade from the immune system such as modifying host gene expression or deregulating proteins function. So they can directly or indirectly change the expression of PD-L1. This study proposed to evaluate the effect of viruses on the expression of PD-L1 which leading to uncontrolled cell growth and tumor formation. We have studied serious tumorigenic viruses, including Human Papillomaviruses (HPV), Epstein-Barr viruses (EBV), Human T-cell leukemia viruses type 1 (HTLV-1), Hepatitis B viruses (HBV) and Hepatitis C viruses (HCV). So we surveyed the correlation between the presence of viruses and expression of PD-L1. Most studies showed the PD-L1 overexpression due to viral functions; however, further studies are needed to better understand the role of the PD-1/PD-L1 pathway in virus-associated cancers as a candidate of anti- PD-L1 therapy.