Key result
Coxsackie B virus-induced inflammatory responses are mediated primarily through Toll-like receptor (TLR) 8 and to a lesser extent through TLR7.
Coxsackie B virus-induced cardiac inflammation is primarily mediated by TLR8, providing a mechanistic understanding of viral myocarditis and chronic inflammatory cardiomyopathy.
Hypothesis-generating for TLR8 blockade in viral myocarditis; requires human validation before any clinical consideration.
The group B coxsackieviruses are single-stranded RNA viruses that have been implicated in viral myocarditis. Viral infection of the myocardium, as well as the associated inflammatory response are important determinants of the virus-associated myocardial damage. Although these viruses are known as cytopathic viruses that cause death of the host cell, their viral RNA has been shown to persist in cardiac muscle contributing to a chronic inflammatory cardiomyopathy. Thus, it is essential that we understand the mechanism by which Coxasckie B viruses (CBVs) trigger this inflammatory response. In this study we investigated the involvement of Toll-like receptors (TLRs) in the recognition of CBV virions as well as CBV single-stranded RNA. Here we report that the CBV-induced inflammatory response is mediated through TLR8 and to a lesser extent through TLR7.
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Triantafilou et al. (2005) studied Viral myocarditis. Coxsackie B viruses (CBVs) was evaluated on Involvement of Toll-like receptors (TLRs) in the recognition of CBV virions and single-stranded RNA. Coxsackie B virus-induced inflammatory responses are mediated primarily through Toll-like receptor (TLR) 8 and to a lesser extent through TLR7.
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