Importance of interferons in recovery from mousepox

Abstract

Gamma interferon is shown to be critical in recovery of C57BLU6 mice from mousepox. Anti-gamma interferon treatment of mice infected in the footpad with ectromelia virus resulted in enhanced spread to and efficient virus replication in the spleen, lungs, ovaries, and, especially, liver. All treated, infected mice died within a mean of 7 days, 2.5 days earlier than mice with severe combined immunodeficiency that were given a comparable infection. On the other hand, alpha interferon appeared not to have a major role in controlling virus replication in tissues examined, and beta interferon was important for virus clearance in the liver and ovaries but not the spleen. Either anti-alpha, beta interferon or anti-beta interferon antibody therapy resulted in only 25% mortality. Infected control mice survived but showed persistence of ectromelia virus at the site of infection (the footpad) and transient presence of the virus in the spleen, liver, lungs, and ovaries and in the fibroreticular but not lymphoid cells of the draining popliteal lymph node. Depletion of gamma interferon but not alpha and/or beta interferon resulted in a significant reduction in the numbers of splenic T (especially 'y8-TCR+), B, and Mac-l+ cells, although the proportion of Mac-l+ cells in the spleen increased compared with control values. Depletion of alpha, beta, or gamma interferons did not severely affect the generation of virus-specific cytotoxic T-lymphocyte responses or natural killer cell cytolytic activity. This study, in which a natural virus disease model was used, underscores the crucial importance of gamma interferon in virus clearance at all stages of infection and in all tissues tested except the primary site of infection, where virus clearance appears to be delayed.

Association between nitric oxide synthesis and vaccination-acquired resistance to murine hepatitis virus by spf mice

“…Also, previous studies have associated an early and strong iNOS expression with genetic and acquired resistance after vaccination against Marek disease herpesvirus in chicken [28]. Moreover, our results confirm previous suggestions that a specific humoral immune response, albeit important, is not enough to neutralize virus infections [43][44][45]. Because it has been shown that development of resistance to MHV-3 infection in mice is not exclusively dependent on antibodies or T cells [9], our results suggest that nitric oxide may be the additional protective factor against MHV-3 infection.…”

The role of IL-12, IL-23 and IFN-γ in immunity to viruses

“…f An abnormal immune defense refers to a more severe disease or in vitro immune response in mice with impaired IFN␥-or IL-12/IL-23-mediated response; GKO: and IFN-␥R1KO mice; aG: anti-IFN␥ antibody treated-mice; 12KO: IL-12p40 and IL-12R␤1 KO mice; a12: anti-IL-12 antibody-treated mice. Infection routes: intravenous [112,117,126,131,142]; intraperitoneal [113,114,125,126,[139][140][141]; intradermal [112,125,135,136]; intracerebral [115,123,127,128]; intranasal [116,121]; milk [147]. References for each of the experimental infection are indicated.…”

“…References for each of the experimental infection are indicated. Genetic backgrounds were: IFN-␥KO mice: Balb/C [112,125,127,128,141,149]; C57BL/6 [114,116,117,123,127,128,145,147]; IFN-␥R1KO mice: 129/SV/E [112,115,122,126,[136][137][138][139][140]; Balb/C [147]; anti-IFN␥ antibody-treated mice: Balb/C [113,132,142]; C57BL/6 [112,119,135,143,144]; 129/SV/E [113]; CBA/Ht [140]; IL-12p40KO mice: C57BL/6 [118,121,145]; anti-IL-12-antibody treated mice: Balb/C [143]. and anti-IFN-␥ Ab-treated [119,130,131] mice become more susceptible or succumb to LCMV infection.…”

“…Experimental infection with rare murine-specific tropic viruses was considered ( Table 3). GKO and anti-IFN-␥ Ab-treated mice succumbed to infection with mousepox virus, and ecromelia virus (EV) [135,136]. Inhibition of EV replication is due to the ability of IFN-␥ to induce nitric oxide synthases [137,138].…”

Cloning, expression and immunoassay detection of ferret IFN-γ

“…Moreover, high levels of IFN-g bias the polarity of CD4 + T helper cells towards a Th1 phenotype, characterized by production of IL-2 and IFN-g [16,17]. A Th1-type immune response is fundamental to the development of host immunity against many pathogens, including influenza A virus [18][19][20]. IFN-g is also necessary for T cell-mediated viral clearance and limitation of latent viral infections [21].…”