Abstract
Human Cytomegalovirus (HCMV) is a widespread pathogen that causes lifelong latent infection and is associated with the exacerbation of chronic inflammatory diseases in seropositive individuals. Of particular impact, HCMV infection is known to worsen many cardiovascular diseases including myocarditis, atherosclerosis, hypertension, and transplant vasculopathy. Due to its similarity to HCMV, murine CMV (MCMV) is an appropriate model to understand HCMV-induced pathogenesis in the heart and vasculature. MCMV shares similar sequence homology and recapitulates much of the HCMV pathogenesis, including HCMV-induced cardiovascular diseases. This review provides insight into HCMV-associated cardiovascular diseases and the murine model of MCMV infection, which has been used to study the viral pathogenesis and mechanisms contributing to cardiovascular diseases. Our new functional studies using echocardiography demonstrate tachycardia and hypertrophy in the mouse, similar to HCMV-induced myocarditis in humans. For the first time, we show long term heart dysfunction and that MCMV reactivates from latency in the heart, which raises the intriguing idea that HCMV latency and frequent virus reactivation perturbs long term cardiovascular function.
Highlights
Lemmermann and Vanda JuranicHuman cytomegalovirus (HCMV) is a ubiquitous pathogen that infects 50–90% of the world’s population and causes lifelong infection which, similar to other herpesviruses, can reactivate to produce infectious virus
This review will focus on the cardiovascular diseases associated with Human Cytomegalovirus (HCMV) infection and will discuss the murine model used to study HCMV-induced cardiovascular pathogenesis
HCMV-associated cardiac dysfunction has clearly been shown in patients with myocarditis, which can present with sinus tachycardia, ventricular overload, and cardiomegaly [18]
Summary
Human cytomegalovirus (HCMV) is a ubiquitous pathogen that infects 50–90% of the world’s population and causes lifelong infection which, similar to other herpesviruses, can reactivate to produce infectious virus. Despite the lack of symptoms during acute infection, studies point to an association between HCMV seropositivity and an exacerbation of chronic inflammatory diseases later in life [5]. HCMV seropositivity was shown to significantly increase in all-cause mortality in individuals age 25–45 and reduce life expectancy by 4 years in elderly participants when compared to HCMV-seronegative control subjects [6,7]. This review will focus on the cardiovascular diseases associated with HCMV infection and will discuss the murine model used to study HCMV-induced cardiovascular pathogenesis. Our lab has recently conducted heart functional studies that demonstrate tachycardia and hypertrophy in MCMV-infected animals during acute and latent infection, further implicating the mouse model of CMV infection with potential to shed new insights on HCMV-induced cardiovascular diseases.
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