Why the study?
The mechanisms that cathelicidin antimicrobial peptides use to influence nonenveloped virus infection were unclear.
Cathelicidin antimicrobial peptides restrict coxsackievirus B3 infection by targeting exosomal HSP60 and reducing cardiomyocyte apoptosis, providing new mechanistic insights into antiviral defenses in the heart.
Hypothesis-generating for exosome-targeted antivirals in myocarditis; leaves open cathelicidin mechanisms in cardiomyocytes.
The relative mechanisms that cathelicidin antimicrobial peptides use to influence nonenveloped virus infection are unclear. We show here that cathelicidin antimicrobial peptides (CRAMP and LL-37) directly target exosomal HSP60 to destroy exosomes, which in turn block the diffusion of exosomes to recipient cardiomyocytes and reduced HSP60-induced apoptosis, thus restricting coxsackievirus B3 infection. Our results provide new insights into the mechanisms cathelicidin antimicrobial peptides use against viral infection.
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Yang et al. (2023) studied this question.
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