Reovirus pathogenesis and the identity of REO3MH

Bennette (1960) isolated an oncolytic virus (reo3MH) which was later (Bennette, Bush and Steele, 1967 a,b ) claimed to be a strain of reovirus type 3. This has now been shown to be a strain of reovirus type 1, which could explain the discrepancies in the clinical symptoms and pathology between their infected mice and those infected with reovirus type 3 (Stanley, Dorman and Ponsford, 1953). The pathological effects in mice of an oncolytic virus, isolated from a mouse ascites tumour undergoing spontaneous degeneration (Bennette, 1960), were reported in detail by Bennette et al. (1967 a,b ). They claimed that the virus was a strain of reovirus type 3 and gave it the designation reo3MH (Middlesex Hospital). However they commented that the pathological data showed important differences between the pattern of the acute disease in newborn mice of several strains (Schofield, CB, ARC, Compton and C3H) produced by reo3MH and that produced by the reovirus type 3 strain studied by Walters et al. (1963) in Prince Henry (PH) mice. The absence of the classical “oily hair effect” (OHE) always associated with acute reovirus type 3 infections of mice (Stanley et al. , 1953; Walters et al. , 1963; Stanley and Keast, 1967) led Bennette et al. (1967 a,b ) to suggest that the host commensal microbial population and/or normally latent viruses may also have contributed to the pathology attributed to reovirus type 3/or 3MH infections. The absence of the classical OHE and the extensive myocarditis produced by reo3MH were in fact strongly reminiscent of reovirus type 1 infection of mice (Hassan, Rabin and Melnick, 1965). Reo3MH (the Middlesex Hospital isolate) had not been unequivocally shown to be a strain of reovirus type 3, and attempts were therefore made to characterize this virus.