Key result
Cytomegalovirus infection triggers early cardiac fibrosis progressing to ventricular thickening and elevated heart rate in mice.
Why the study?
Human cytomegalovirus infection is associated with chronic heart and vascular diseases, but the phenotypic and functional cardiac consequences of cytomegalovirus infection remain to be elucidated.
Murine cytomegalovirus infection induces early cardiac fibrosis and subsequent functional abnormalities including tachycardia and hypertrophy, providing a model for HCMV-induced acute myocarditis.
Does not support clinical practice changes; leaves open whether HCMV drives human cardiac fibrosis or hypertrophy.
Human cytomegalovirus (HCMV) is associated with increased risk of chronic diseases of the heart and vasculature, including myocarditis, atherosclerosis, and transplant vasculopathy. To investigate CMV infection of the heart, murine cytomegalovirus (MCMV) was used to evaluate both acute and latent infection and the subsequent phenotypic and functional consequences of infection. Female BALB/c mice were intraperitoneally (i.p.) inoculated with 1 × 10 6 pfu of MCMV and evaluated at 14 and 50 days postinfection (dpi). At each time point, echocardiography was used to evaluate cardiac function and histology was conducted for phenotypic evaluation. MCMV replication in the heart was detected as early as 3 dpi and was no longer detectable at 14 dpi. Infected animals had significant cardiac pathology at 14 and 50 dpi when compared to uninfected controls. Histology revealed fibrosis of the heart as early as 14 dpi and the presence of white fibrous deposits on the surface of the heart. Functional evaluation showed significantly increased heart rate and muscle thickening in the latently infected animals when compared to the control animals. At 50 dpi, latent virus was measured by explant reactivation assay, demonstrating that MCMV establishes latency and is capable of reactivation from the heart, similar to other tissues such as spleen and salivary glands. Collectively, these studies illustrate that MCMV infection results in phenotypic alterations within the heart as early as 14 dpi, which progress to functional abnormalities during latency. These findings are similar to sinus tachycardia and hypertrophy of the heart muscle observed in cases of HCMV-induced acute myocarditis.
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Bonavita et al. (2020) studied Cytomegalovirus infection of the heart. Murine cytomegalovirus (MCMV) infection vs. Uninfected controls was evaluated on Cardiac function and histology (fibrosis, heart rate, muscle thickening). Murine cytomegalovirus infection in mice resulted in cardiac fibrosis as early as 14 days postinfection, progressing to significantly increased heart rate and muscle thickening during latency.
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