Type I interferon gene therapy using IFNA6, A9, and B inhibited acute cytomegalovirus-induced myocarditis, with IFNA6 also reducing chronic cardiac inflammation and virus replication.
Does type I interferon gene therapy reduce virus titre and myocarditis in MCMV-infected mice?
Specific type I interferon subtypes, particularly IFNA6, administered via DNA gene therapy can effectively reduce viral replication and cardiac inflammation in cytomegalovirus-induced myocarditis.
Summary Type I interferons (IFNs) are produced early in response to viral infection and modulate adaptive immunity. Previously we demonstrated localized protection against murine cytomegalovirus (MCMV) infection in IFN DNA‐inoculated mice. Here we examine the effect of seven IFN subtypes ( IFNA1 , A2 , A4 , A5 , A6 , A9 and B ), administered by DNA inoculation, on systemic MCMV infection and myocarditis. IFN transgene expression altered the pathogenesis of MCMV infection with regard to virus titre and myocarditis. IFNA6 treatment reduced MCMV replication whilst IFNA5 and A2 enhanced virus replication. IFNA6 , A9 , and B treatment inhibited acute myocarditis. A T helper type 1‐like, antibody and cytokine, response correlated with decreased virus titre and myocarditis. In addition, IFNA6 was able to reduce chronic cardiac inflammation. This research into the effectiveness of seven type I IFNs, using DNA gene therapy, highlights the need for correct subtype usage in the treatment of disease. We demonstrate effective subtypes for treatment in both the acute and chronic phases of MCMV infection and the resultant development of myocarditis.
Cull et al. (Thu,) conducted a other in Cytomegalovirus-induced myocarditis. Type I interferon gene therapy (IFNA1, A2, A4, A5, A6, A9, B) was evaluated on Systemic MCMV infection (virus titre) and myocarditis. Type I interferon gene therapy using IFNA6, A9, and B inhibited acute cytomegalovirus-induced myocarditis, with IFNA6 also reducing chronic cardiac inflammation and virus replication.
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