2005
DOI: 10.1099/vir.0.81370-0
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Inhibition of host peripheral blood mononuclear cell proliferation ex vivo by Rinderpest virus

Abstract: Rinderpest, or cattle plague, is caused by Rinderpest virus (RPV), which is related most closely to human Measles virus (MV), both being members of the genus Morbillivirus, a group of viruses known to have strong immunosuppressive effects in vitro and in vivo. Here, it was shown that peripheral blood mononuclear cells (PBMCs) isolated from cattle experimentally infected with either wild-type or vaccine strains of RPV impaired the proliferation of PBMCs derived from uninfected animals; however, in contrast to e… Show more

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Cited by 16 publications
(11 citation statements)
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“…Similar immunologic changes have been reported in the early phase of morbillivirus infection in other mammals. Natural infections of MV, CDV and RPV share common features in the acute phase of disease including lymphopenia, a prolonged cytokine imbalance consistent with suppression of cellular immunity leading to secondary infections and decreased in vitro proliferation of T cells in response to mitogens (von Messling et al 2003, Heaney et al 2005, Kerdiles et al 2006, Yanagi et al 2006, Griffin 2007, 2010, Nielsen et al 2009, Schneider-Schaulies & Schneider-Schaulies 2009, Avota et al 2010, Koga et al 2010. The specific ability of some morbilliviruses to impair T cell-dependent immune responses noted more than 100 yr ago continues to be central to the severe generalized immunosuppression caused by morbilliviruses (Gas sert et al 2009).…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Similar immunologic changes have been reported in the early phase of morbillivirus infection in other mammals. Natural infections of MV, CDV and RPV share common features in the acute phase of disease including lymphopenia, a prolonged cytokine imbalance consistent with suppression of cellular immunity leading to secondary infections and decreased in vitro proliferation of T cells in response to mitogens (von Messling et al 2003, Heaney et al 2005, Kerdiles et al 2006, Yanagi et al 2006, Griffin 2007, 2010, Nielsen et al 2009, Schneider-Schaulies & Schneider-Schaulies 2009, Avota et al 2010, Koga et al 2010. The specific ability of some morbilliviruses to impair T cell-dependent immune responses noted more than 100 yr ago continues to be central to the severe generalized immunosuppression caused by morbilliviruses (Gas sert et al 2009).…”
Section: Discussionmentioning
confidence: 99%
“…Morbilliviruses are lymphotrophic and induce multisystemic infections in their highly susceptible natural hosts, causing disease with high morbidity and mortality. In these cases, the pathogenesis of morbillivirus infections shares common features, including transient profound immune suppression which may lead to secondary viral and bacterial infections, and associated cli nicoimmuno pathologic abnormalities (von Mes sling et al 2003, Heaney et al 2005, Yanagi et al 2006, Nielsen et al 2009). Another attribute of morbillivirus infections is the induction of an efficient and often lifelong immunity in hosts that eventually survive and appear to clear the virus (Appel et al 1982, Griffin 2007.…”
Section: Introductionmentioning
confidence: 99%
“…MeV infection has been shown to cause profound immune suppression as a result of lymphopenia, cytokine imbalances and deficient expansion of PBMCs [66]. Immune suppression was also seen in RPV-infected animals, even those exposed only to the vaccine [67]. Research is therefore required to examine whether PPRV similarly causes long-term immune suppression and whether the vaccine strains have any such effect, even if transient, which may impact on the efficacy of co-administered vaccines.…”
Section: Development and Application Of Pprv Vaccinesmentioning
confidence: 99%
“…Thus, accumulating evidence strongly links immunosuppression and lymphopenia not only to direct effects following infection and subsequent destruction of signalling lymphocytic activating molecule (SLAM)-positive immune cells and precursor cells in the acute phase of the infections, but also to indirect effects modulating the host innate and adaptive immune systems (Cruz et al, 2006;Devaux et al, 2008;Heaney et al, 2005;Karp et al, 1996;Schlender et al, 1996;Tatsuo et al, 2001;von Messling et al, 2006). The relative impact on virulence of the different mechanisms modulating the immune system in vivo is, however, not yet clarified.…”
Section: Introductionmentioning
confidence: 99%