April 24, 2026
View Full PaperCoxsackievirus B3murine myocarditis: A pathologic spectrum of myocarditis in genetically defined inbred strains
Key Result
Genetic susceptibility to early and late phase coxsackievirus B3 myocarditis differs markedly among mouse strains, with four of six strains showing late ongoing myocardial inflammation after day 9.
Key Points
- This research investigates how genetic factors influence the severity and progression of coxsackievirus B3-induced myocarditis in mice.
- Examined six different inbred strains of mice for 45 days post coxsackievirus B3 infection.
- Analyzed histopathological changes including myocyte necrosis and inflammation phases over time.
- Monitored the emergence of heart-specific autoantibodies in relation to myocardial inflammation.
- Dramatic differences in the prevalence and severity of myocarditis were observed among mouse strains during the first 7 days.
- Four strains exhibited persistent myocardial inflammation beyond day 9, indicating ongoing immune response.
- Histological changes included focal necrosis with polymorphonuclear leukocytes early on, followed by mononuclear cell infiltration and diffuse interstitial patterns later.
Structured PICO
Does genetic background influence the histopathologic features and susceptibility to early and late phase coxsackievirus B3 myocarditis in mice?
P
Population
Six different inbred strains of mice differing in major histocompatibility complex haplotypes or background genome
I
Intervention
Coxsackievirus B3 infection
O
Outcome
Histopathology of myocarditis (prevalence, severity, cellular infiltrate, and autoantibody production)surrogate
Genetic background significantly influences the susceptibility, severity, and histopathologic progression of coxsackievirus B3-induced myocarditis in mice.
Abstract
Group B coxsackieviruses are the most frequent causative agents in human viral myocarditis. Susceptibility to viral infections varies widely among individuals. In the mouse, coxsackievirus B3 also causes myocarditis. The differential susceptibility of different inbred strains of mice to coxsackie B3-induced myocarditis also appears to be under genetic control. This study details the histopathology of coxsackie B3 myocarditis in six different inbred strains of mice for the first 45 days after coxsackie B3 infection. These strains differ either in the haplotypes of their major histocompatibility complex or in their background genome. During the first 7 days after coxsackie B3 infection, there are dramatic differences among strains with respect to prevalence and severity of myocarditis. Focal zones of myocyte necrosis involving polymorphonuclear leukocytes as well as contraction band injury appear to be the early manifestations of direct viral injury. Four of the six strains, though, continue to show myocardial inflammation after day 9. This late phase myocarditis is characterized by the emergence of mononuclear cells within healing foci of myocyte necrosis as well as a distinctive diffuse interstitial pattern of myocarditis. The strains that develop this late ongoing myocardial inflammation frequently produce heart-specific autoantibodies. Thus the pathologic features of murine coxsackie B3 myocarditis change over the course of the illness, and genetic susceptibility to both early and late phase myocarditis differs markedly among various mouse strains.