Activation of complement system during viral infections: Prospects and future challenges

Abstract

The complement system is homeostatic system evolved to remain constant check on pathogen but as per the recent knowledge it is involved in many biological processes including complementing adaptive immunity. It gets activated in most of the viral infections and leads to neutralization of virus via opsonization of C3b, aggregation, phagocytosis, membrane attack complex (MAC) mediated lysis of virus or virus-infected cells. Primary work of complement in viral diseases clears the virus by MAC or by opsonization nonetheless it offers favorable milieu locally during localized infection. It increases vascular permeability, generates edema, recruits phagocytes by chemotaxis, mediates release of cytokines depending on the cell type. This acute inflammation generated due to local activation of complement in initial stage of infection is crucial. C3a and C5a anaphylatoxins modulate adaptive immunity generation via modulating priming of T cells and enhancing Th1 immunity. In the absence of certain complement components and its receptors, some viruses become more pathogenic than in general, denote complement functions at more than one step in different viruses of their pathogenesis.