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Derivation and characterization of an efficiently myocarditic reovirus variant
B Sherry1, F J Schoen, E Wenske
1Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115.
Abstract:
A reovirus variant, 8B, was isolated from a neonatal mouse which had been inoculated with a mixture of two reovirus strains: type 1 Lang (T1L) and type 3 Dearing (T3D) (E. A. Wenske, S.J. Chanock, L. Krata, and B. N. Fields, J. Virol. 56:613-616, 1985). 8B is a reassortant containing eight gene segments derived from the T1L parent and two gene segments derived from the T3D parent. Upon infection of neonatal mice, 8B produced a generalized infection characteristic of many reoviruses, but it also efficiently induced numerous macroscopic external cardiac lesions, unlike either of its parents. Microscopic examination of hearts from infected mice revealed myocarditis with necrotic myocytes and both polymorphonuclear and mononuclear cellular infiltration. Electron microscopy revealed viral arrays in necrotic myocytes and dystrophic calcification accompanying late lesions. Determination of viral titers in hearts from T1L-, T3D-, or 8B-infected mice indicated that growth was not the primary determinant of myocardial necrosis. Results from inoculations of athymic mice demonstrated that T cells were not a requirement for the 8B-induced myocarditis. Finally, 8B was more cytopathic than either of the parent viruses in cultured mouse L cells. Together, the data suggest that 8B-induced myocardial necrosis is due to a direct effect of reovirus on myocytes. Reovirus thus provides a useful model for the study of viral myocarditis.
Insights
A novel reovirus variant, 8B, causes significant cardiac lesions and myocarditis in neonatal mice. This suggests reovirus directly impacts heart cells, offering a model for viral myocarditis research.
Area of Science:
- Virology
- Cardiovascular Pathology
- Infectious Diseases
Background:
- Reovirus infections can cause generalized disease in neonatal mice.
- Specific reovirus strains have varying pathogenic potentials.
- Understanding viral mechanisms in cardiac tissue is crucial for disease management.
Purpose of the Study:
- To characterize a novel reovirus reassortant (8B) derived from type 1 Lang (T1L) and type 3 Dearing (T3D) strains.
- To investigate the pathogenic mechanisms of reovirus variant 8B in neonatal mice, focusing on cardiac effects.
- To determine if reovirus variant 8B serves as a useful model for studying viral myocarditis.
Main Methods:
- Isolation and characterization of reovirus variant 8B from infected neonatal mice.
- Inoculation of neonatal mice with reovirus strains (T1L, T3D, 8B) and assessment of clinical signs and cardiac pathology.
- Microscopic and electron microscopic examination of heart tissues to identify cellular changes and viral presence.
- Viral titration in heart tissues and inoculation of athymic mice to evaluate the role of viral load and T cells in myocarditis.
Main Results:
- Reovirus variant 8B induced generalized infection and prominent cardiac lesions, including myocarditis with myocyte necrosis and cellular infiltration, unlike its parent strains.
- Viral growth in the heart was not directly correlated with the severity of myocardial necrosis.
- T cells were not essential for the development of 8B-induced myocarditis.
- Reovirus 8B exhibited higher cytopathic effects in cultured mouse L cells compared to parent strains.
Conclusions:
- Reovirus variant 8B causes significant myocardial necrosis, likely through a direct cytopathic effect on myocytes.
- The data support the use of reovirus 8B as a model for studying viral myocarditis.
- Further research into the specific viral factors and host interactions driving reovirus-induced myocarditis is warranted.