Does Coxsackievirus B3 infection induce the release of inflammatory cytokines from human monocytes?
Coxsackievirus B3 infection activates human monocytes to produce large amounts of inflammatory cytokines, which may contribute to tissue damage in viral myocarditis.
Coxsackievirus B3 (CVB3) infections produce an inflammatory and immune response that suggests the involvement of cytokines. In this in vitro study, we exposed purified human monocytes to CVB3 and determined the release of interferon (IFN), interleukin 1 beta (IL-1 beta) and tumour necrosis factor-alpha (TNF-alpha). Exposure to CVB3 did not alter the viability of monocytes, however, it induced an increased adherence. After 12 and 24 h of CVB3 exposure, monocytes released large amounts of IFN, IL-1 beta and TNF-alpha. These data show that CVB3 strongly affects human monocytes and activates them to production of biologically active cytokines, particularly IL-1 beta and TNF-alpha. It is suggested that both cytokines, when released in large amounts and for a prolonged period, may contribute to a strong inflammatory response and eventual tissue damage in afflicted organs such as the myocardium.
Henke et al. (Fri,) studied this question.