Innate and adaptive immunity in viral infections

The defense against viruses requires collaboration of both arms of immunity, innate and adaptive one. Factors of the former may sense viruses early on the principle self/non self and mount fast reaction of the host. Early recognition of intracellular viral invasion is mainly done by pattern recognition receptors (PRRs). It results in the induction of complex inflammatory process composed of proinflammatory agents, collectively named inflammasome. Its formation has a pivotal role in the formation of adaptive response. Infected cells may be also eliminated by natural killer (NK) cells, able to recognize such cells as non-self. Adaptive immunity, both humoral and cellular, is formed later than innate one. Antibodies have a neutralizing effect on viruses, while they are still outside target cells. Cytotoxic T lymphocytes (CTLs) may recognize infected cells and kill them by apoptosis. They are, however, usually too few, to totally eliminate viral infection. Resistance to the progression of HIV/AIDS infection in some individuals is due to the presence of particular HLA alleles, which influence the induction of CTLs directed versus dominant epitope (p24 Gag) of virus. Besides, most viruses possess various escape mechanisms from immune response. Thus, efficient battle with viral infections still remains a formidable challenge.