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1 Pediatrics, Baylor College of Medicine, Houston, Texas, United States
2 Centre d'Immunologie de Marseille-Luminy, France
3 Immunobilogy, Yale University School of Medicine, New Haven, Connecticut, United States
4 Pediatrics - Infectious Diseases, Baylor College of Medicine, 6621 Fannin, MC 430.09, Houston, 77030, United States; Pediatrics, Baylor College of Medicine, Houston, United States
* To whom correspondence should be addressed. E-mail: jvallejo{at}bcm.tmc.edu.
Enteroviral-induced myocardial injury can lead to severe heart failure. To date, little is known about the early innate stress response that contributes to host defense in the heart. Toll-like receptor 3 (TLR3) is important in the initiation of the innate antiviral response. We investigated the involvement of TLR3, which recognizes viral double-stranded (ds) RNA, on encephalomyocarditis virus (EMCV) infection. To examine the contribution of TLR3 in protection from EMCV infection, mice deficient in TLR3 were infected with 50 plaque-forming units of EMCV. TLR3-deficient (TLR3-/-) mice were more susceptible to EMCV infection and had a significantly higher viral load in the heart when compared to TLR3+/+ mice. Histopathological examination showed that the inflammatory changes of the myocardium were less marked in TLR3-/- than in TLR3+/+ mice. TLR3-/- mice had impaired proinflammatory cytokine and chemokine expression in the heart following EMCV infection. However, the expression of interferon-beta was not impaired in EMCV-infected TLR3-/- mice. EMCV infection leads to a TLR3-dependent innate stress response, which is involved in mediating protection against virus-induced myocardial injury.
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