Figure 2.

Immune response to viral infection. Viral infections elicit an immune response by first activating the innate immune system. Infected cells release IFN and pro-inflammatory cytokines that activate natural killer cells to destroy the viral infection. Simultaneously, infected cells express viral antigens on the cell surface, activating professional APCs such as dendritic cells (DCs). DCs interact with viral antigens through pattern recognition receptors for their maturation and in turn switch naïve T-cells into mature T-cells (Th1, Th17, Th2, and Tregs) that regulate both the innate and adaptive immune system. The innate response regulates a Th1 driven pro-inflammatory cascade, resulting in the recruitment of immune cells for rapid eradication of the infection (1). The adaptive immune system stimulates the differentiation and expansion of T lymphocytes into specific subsets, better known as cytotoxic T-cells (CTLs, CD8+) and T helper cells (CD4+). CTLs are responsible for the direct killing and eradication of viral particles and infected cells (2), whilst T helper cells recruit immune cells and stimulate the differentiation of B lymphocytes. B lymphocytes are responsible for the viral specific rapid response and long lasting immunological memory against recurring infection through the production of two subsets known as plasma cells and memory B-cells. Differentiation into plasma cell results in the production of virus specific antibodies for the neutralisation of viral progeny, the activation of the complement cascade, and antibody mediated opsonisation (3). Upon re-infection, memory B-cells stored within lymph nodes differentiate into active plasma cells, generating antibodies and the rapid activation of the adaptive immune system to provide effective relief faster than the first initial infection, usually leaving the individual asymptomatic. NK = natural killer cell. IFN = interferon.