Inhibition of coxsackievirus infection in cardiomyocytes by small dsRNA targeting its cognate coxsackievirus adenovirus receptor

Figures

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  Fig. 1. Relative coxsackievirus adenovirus receptor (CAR) messenger RNA expression in coxsackievirus B-infected H9c2 cells harvested after different time intervals. The CT values of CAR and β-actin/18S were compared and relative quotient (RQ) was calculated (grey bars). The CAR expression was observed to increase relative to uninfected H9c2.

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  Fig. 2. Flow cytometry histograms showing H9c2 cell population transfected with fluorescein isothiocyanate (FITC)-labelled control small dsRNA. (A) Untransfected cell control; (B) cells transfected with 20 pmol small dsRNA; (C) cells transfected with 40 pmol small dsRNA; (D) cells transfected with 60 pmol small dsRNA; (E) cells transfected with 80 pmol small dsRNA; (F) cells transfected with 100 pmol small dsRNA.

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  Fig. 3. (A) Cell viability in H9c2 cell line after transfection with 20, 40, 60, 80 and 100 pmol of coxsackievirus adenovirus receptor (CAR) small dsRNA; (B) CAR messenger RNA inhibition in H9c2 cells transfected with 20, 40 and 60 pmol CAR small dsRNA relative to untransfected cells. The CT values of CAR and β-actin/18S were compared and relative quotient (RQ) was calculated (grey bars).

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  Fig. 4. Coxsackievirus adenovirus receptor messenger RNA (CAR mRNA) expression in H9c2 cells transfected with 60 pmol coxsackievirus adenovirus receptor small dsRNA and after 18 h of transfection infected with coxsackievirus B and harvested after 24, 48 and 72 h post-infection. The CT values of CAR and β-actin/18S were compared and relative quotient (RQ) was calculated (grey bars). It was observed that relative to untransfected and uninfected cells the CAR mRNA expression was decreased.

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  Fig. 5. Viral load in H9c2 cells transfected with 60 pmol coxsackievirus adenovirus receptor small dsRNA and after 18 h of transfection infected with coxsackievirus B and harvested after 24, 48 and 72 h post-infection (p.i.).

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  Fig. 6. RNA interference against coxsackievirus adenovirus receptor (CAR) and coxsackievirus B (CVB) can be a new therapeutic approach for the treatment of viral myocarditis and prevent its progression to dilated cardiomyopathy (DCM).