Early immune response to viral infection may contribute to sex-based differences in viral myocarditis 

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Presentation Time: 11:30 AM - 12:45 PM
Poster Board Number: B237
Abstract ID: 4109

Presenting Author:
Justin D Callahan , PhD Student at Univ. of Toronto, Toronto Gen. Hosp. Res. Inst.

Abstract:

Viral infection is a common trigger for myocarditis, prompting immune cell trafficking to the myocardium, and causing irreversible cardiac injury when unresolved. Interestingly, young males are the most susceptible demographic to viral myocarditis, suggesting that sex-based differences could contribute to myocarditis development though the mechanisms involved have not been elucidated.  

We show that in an adolescent mouse model of viral myocarditis, infection with encephalomyocarditis virus recapitulates the phenotype of male susceptibility observed in humans. At 4 days post infection (dpi), males have elevated viral titers compared to females, despite subsequent recruitment of antigen specific CD8+ T cells at 7dpi, suggesting a sex-based difference in ability to control early viral replication was independent of CD8+ T cell trafficking. Importantly, spatially segregated fibrotic injury and cardiomyocyte loss was markedly enhanced in adolescent males during viral infection, which is a hallmark of cardiac pathology 

We then sought to identify sex-based differences in the early immune response. At 1dpi, males displayed exaggerated levels of type I interferons (IFN-Is) in serum, but no differences were observed in expression of interferon-stimulated genes in the heart. Since no viral titers were detected at 1dpi, current studies are focused on understanding the relationship between early IFN-Is, viral titers, and cardiac injury at late timepoints.