Role of interferon in the pathogenesis of virus diseases in mice as demonstrated by the use of anti-interferon serum. II. Studies with herpes simplex, Moloney sarcoma, vesicular stomatitis, Newcastle disease, and influenza viruses.

Abstract

The effect of potent sheep anti-mouse interferon globulin was investigated in several different experimental virus diseases of mice. In anti-interferon globulin-treated mice infected intraperitoneally with herpes simplex virus (HSV) type I, the latent period was shortened, and the overall LD50 was increased several hundredfold compared to virus-infected control mice. When HSV was inoculated subcutaneously all anti-interferon globulin-treated mice died, whereas only 5% of virus-infected control mice died. Subsequent treatment with anti-interferon globulin of previously HSV-infected mice did not result in reactivation of HSV. Treatment of adult mice with anti-interferon globulin resulted in an earlier appearance of MSV-induced tumors, a greater number of mice bearing tumors, an increase in tumor size, and an increase in the duration of tumors. All tumors eventually regressed despite reinjection of anti-interferon globulin. Anti-interferon globulin treatment resulted in a rapid onset of disease and death in adult mice inoculated (intranasal) with VSV and in newborn mice infected with NDV. Anti-interferon globulin exerted no effect on the course of influenza virus infection of mice. We conclude that the early production of interferon is an importane element in the response of the mouse to several viruses exhibiting different pathogeneses.

Viral Infection Causes Rapid Sensitization to Lipopolysaccharide: Central Role of IFN-αβ

“…Together, these findings suggest that although T cell-dependent IFN-␥ production is important, it is not the only mechanism through which viruses may prime for TNF-␣ production. IFN-␣␤ is a likely candidate in this respect, because most viral infections including LCMV and VSV are known to induce substantial production of IFN-␣␤ (21)(22)(23)(24)(25). In virus-infected immunocompetent mice, production of IFN-␣␤ generally reaches peak levels 1-3 days post infection (p.i.…”

IFN-α-Expressing Tumor Cells Enhance Generation and Promote Survival of Tumor-Specific CTLs

“…I. Gresser (Institut Gustav Roussy, Paris, France) (10,11). Sheep IgG and rat IgG (Sigma, St. Louis, MO) were used as a control for sheep polyclonal anti-mouse IFN-␣-neutralizing Ab and rat anti-mouse CD8a Ab, respectively.…”

Type I Interferons Mediate the Innate Cytokine Response to Recombinant Fowlpox Virus but Not the Induction of Plasmacytoid Dendritic Cell-Dependent Adaptive Immunity

“…The creation of mice deficient in the type I IFN receptor (IFNAR Ϫ/Ϫ ) (36) has accelerated the understanding of the many important and often differential roles for type I IFNs in the antiviral response while concurrently illustrating their role as a contributing factor modulating many other pathologies (19,30,57). Mice deficient in IFNAR are defective in their ability to mount a normal innate and subsequent adaptive immune response to many viruses, including avian H5N1 influenza virus (49), vesicular stomatitis virus (VSV), herpes simplex virus (HSV), Newcastle disease virus (NDV) (20), Semliki Forest virus (SFV), lymphocytic choriomeningitis virus (LCMV), and vaccinia virus (VV) (36).…”