Ectromelia virus: the causative agent of mousepox

Esteban, David J.; Buller, R. Mark

doi:10.1099/vir.0.81090-0

Cited by 152 publications

(179 citation statements)

References 146 publications

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“…1). 4 Uncontrolled viral replication leading to liver tissue destruction, necrosis, and apoptosis is a hallmark of mousepox (19,20,41).…”

Section: Discussionmentioning

confidence: 99%

“…Liver damage and liver failure, as a result of uncontrolled ECTV replication within the organ, are major reasons for mortality (19,20,41). In addition to effective activation of ECTV-specific CD8 ϩ effector T cells, recruitment of those cells into the sites of viral replication is also critical for limiting infection and disease.…”

Section: Reduced Cd8 ϩ T Cell Numbers In Foci Of Infection In the Absmentioning

confidence: 99%

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IL-12p40 and IL-18 Play Pivotal Roles in Orchestrating the Cell-Mediated Immune Response to a Poxvirus Infection

Wang

Chaudhri

Jackson

et al. 2009

The Journal of Immunology

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A strong cell-mediated immune response is critical for controlling viral infections and is regulated by a number of cytokines, including IL-12 and IL-18. Indeed, some viruses have evolved to specifically target these pathways to counter the host immune response. Orthopoxviruses, including ectromelia virus, encode immune evasion molecules that specifically target IL-18 and IFN-γ. We hypothesized that IL-12 and IL-18 are pivotal for induction of IFN-γ production and subsequent generation of an effective host response to ectromelia virus infection. In this study, we demonstrate that absence of both IL-12p40 and IL-18 resulted in increased susceptibility to infection that was associated with skewing of the cytokine response to Th2 and a reduction in NK and CTL responses. The decrease in CTL response correlated with a defect in CD8+ T cell proliferation and lower numbers of virus-specific CD8+ T cells. Lack of either IL-12p40 and/or IL-18 was also associated with reduced numbers of CD8+ T cells at sites of infection and with an increase in the numbers of splenic T regulatory cells. Taken together, our data indicate that IL-12p40 and IL-18 act in concert and play an important antiviral role through the up-regulation of IFN-γ production and cell-mediated immune responses.

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“…1). 4 Uncontrolled viral replication leading to liver tissue destruction, necrosis, and apoptosis is a hallmark of mousepox (19,20,41).…”

Section: Discussionmentioning

confidence: 99%

Section: Reduced Cd8 ϩ T Cell Numbers In Foci Of Infection In the Absmentioning

confidence: 99%

IL-12p40 and IL-18 Play Pivotal Roles in Orchestrating the Cell-Mediated Immune Response to a Poxvirus Infection

Wang

Chaudhri

Jackson

et al. 2009

The Journal of Immunology

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“…In contrast, susceptible A, BALB/c, DBA and C3H mice often succumb to disease due to necrosis of the spleen and liver. Resistance to mousepox is associated with rmp (resistance to mousepox) genes and recovery from infection requires mobilization of cell-mediated and innate immune responses (Esteban and Buller 2005). Krzyżowska and colleagues (2002) showed that infection of BALB/c mice with a highly virulent Moscow strain of ECTV (ECTV-MOS) leads to DEVDase-(caspase-3-and caspase-7-) dependent apoptosis in the liver, spleen, conjunctivae and lymph nodes which, presumably, regulates the resolution of viral infection.…”

Section: Introductionmentioning

confidence: 99%

In vivo induction of autophagy in splenocytes of C57BL/6 and BALB/c mice infected with ectromelia orthopoxvirus

Martyniszyn

Szulc-Dąbrowska

Boratyńska-Jasińska

et al. 2013

Polish Journal of Veterinary Sciences

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Autophagy is a self-degradation process of cellular components. It plays both antiviral and pro-viral roles in the life cycle of different viruses and the pathogenesis of different viral diseases. In this study, we evaluated autophagy induction in splenocytes of ectromelia virus (ECTV)-resistant C57BL/6 and ECTV-susceptible BALB/c mice during infection with the Moscow strain of the ectromelia virus (ECTV-MOS). Autophagy was analyzed using the Western blot method by assessing type II microtubule-associated protein 1 (MAP1) light chain 3 (LC3) and Beclin 1 expression levels relative to β-actin. Results indicated an increased ratio of LC3-II to β-actin in splenocytes of C57BL/6 mice only at 7 day post infection (d.p.i.) compared to uninfected animals. LC3-II/β-actin and Beclin 1/β-actin ratios in splenocytes of BALB/c mice increased at 5 d.p.i. and remained high until day 14 and 7 p.i., respectively. We confirmed the formation of autophagosome structures in the spleen of BALB/c mice by transmission electron microscopy (TEM). Moreover, autophagy accompanied necrosis in the splenocytes of infected animals. Results suggest that ECTV-MOS induced autophagy, especially in the spleen of the susceptible mouse strain, may support viral replication and promote cell necrosis.

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“…108). Importantly, in comparison to the VACV-based mouse challenge model, ECTV infection of BALB/c or C57BL/6 mice is characterized by an extended asymptomatic incubation period.…”

Section: Animal Modelsmentioning

confidence: 99%