Viral (hepatitis C virus, hepatitis B virus, HIV) persistence and immune homeostasis

Abstract

Immune homeostasis is a host characteristic that maintains biological balance within a host. Humans have evolved many host defence mechanisms that ensure the survival of individuals upon encountering a pathogenic infection, with recovery or persistence from a viral infection being determined by both viral factors and host immunity. Chronic viral infections, such as hepatitis B virus, hepatitis C virus and HIV, often result in chronic fluctuating viraemia in the face of host cellular and humoral immune responses, which are dysregulated by multi-faceted mechanisms that are incompletely understood. This review attempts to illuminate the mechanisms involved in this process, focusing on immune homeostasis in the setting of persistent viral infection from the aspects of host defence mechanism, including interferon-stimulated genes, apolipoprotein B mRNA editing enzyme catalytic polypeptide 3 (APOBEC3), autophagy and interactions of various immune cells, cytokines and regulatory molecules.

Keywords: HIV; hepatitis C virus; immune homeostasis; viral persistence.

Figure 1

Viral persistence and immune homeostasis. With high viral load infection, virus may evade host immunity, leading to death (a) or illness (b) of the host. With anti-viral treatment, viral load may be reduced, leading to viral clearance or latency. Meanwhile, anti-viral treatment may cause mutation in the virus and drug-resistance (b). When immune homeostasis is maintained, the host exhibits asymptomatic persistent infection, whereby the immune system fight against the virus; and viral load fluctuates during chronic infection (c). Under a strong host immune response, viral infection may become latent (d) or be cleared (e).