Why the study?
Does recombinant hybrid human leukocyte interferon-alpha A/D reduce mortality and clinical illness in mice with experimental Ross River virus polymyositis?
Does recombinant hybrid human leukocyte interferon-alpha A/D reduce mortality and clinical illness in mice with experimental Ross River virus polymyositis?
Recombinant interferon-alpha A/D reduces mortality and viral replication in a mouse model of Ross River virus polymyositis.
Preclinical efficacy in Ross River virus myositis supports further antiviral development; leaves open human translation.
Ross River virus (RRV), an alpha togavirus, causes an inflammatory myopathy in mice, which probably results from direct lytic effects of virus or viral products on myofibers. Administration of recombinant hybrid human leukocyte interferon-alpha A/D (rIFN-alpha A/D) ameliorates clinical illness and reduces mortality from 86 to 42%. Peak concentrations of virus are reduced by 1,000-fold in serum and by 30-fold in muscle, but anti-RRV antibody production is not altered. Treatment with rIFN-alpha A/D dramatically reduces inflammation and necrosis in muscle. Beneficial effects of rIFN-alpha A/D on experimental, RRV-induced polymyositis result in part from inhibition of viral replication and spread, though immunomodulation might also play an important role.
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Seay et al. (1987) studied this question.
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