Inflammation during virus infection: Swings and roundabouts

Abstract

Inflammation constitutes a concerted series of cellular and molecular responses that follow disturbance of systemic homeostasis, by either toxins or infectious organisms. Leukocytes modulate inflammation through production of secretory mediators, like cytokines and chemokines, which work in an autocrine and/or paracrine manner. These mediators can either promote or attenuate the inflammatory response and depending on differential temporal and spatial expression play a crucial role in the outcome of infection. Even though the objective is clearance of the pathogen with minimum damage to host, the pathogenesis of multiple human pathogenic viruses has been suggested to emanate from a dysregulation of the inflammatory response, sometimes with fatal consequences. This review discusses the nature and the outcome of inflammatory response, which is triggered in the human host subsequent to infection by single-sense plus-strand RNA viruses. In view of such harmful effects of a dysregulated inflammatory response, an exogenous regulation of these reactions by either interference or supplementation of critical regulators has been suggested. Currently multiple such factors are being tested for their beneficial and adverse effects. A successful use of such an approach in diseases of viral etiology can potentially protect the affected individual without directly affecting the virus life cycle. Further, such approaches whenever applicable would be useful in mitigating death and/or debility that is caused by the infection of those viruses which have proven particularly difficult to control by either prophylactic vaccines and/or therapeutic strategies using specific antiviral drugs.