O Comitê de Imunologia Clínica da IUIS produziu um texto produziu o texto "A dead-end host: is there a way out? A position piece on the Ebola virus outbreak by the International Union of Immunology Societies” publicado no Frontiers of Immunology (27 October 2014 | doi: 10.3389/fimmu.2014.00562), que pode ser visualizado aqui.
Vejam alguns trechos:
"The fact that not everyone with Ebola virus disease (EVD) has died during the ongoing outbreak in West Africa, with an estimated case fatality rate of 70.8% by September 2014 (1), suggests that some kind of immunity to this virus is possible. "
“It is also likely that the increase in pro-inflammatory cytokines, shown experimentally and in plasma samples from patients with Ebola infection (5), contribute to enhancing vasodilation and the resulting cytokine storm (8) causes immune dysfunction and general “shut-down” of all immunity. Additionally, monkey models have shown that Ebola infection causes apoptosis in by-stander CD4 and CD8 lymphocytes and NK cells"
"As with all pathogens, Ebola has evolved to evade innate immunity by hijacking specific anti-viral pathways, resulting in immunosuppression. VP35 and VP24 inhibit type I interferon activity. VP35 inhi“its induction of IFN-beta production by suppressing phosphorylation and dimerization of IFN regulatory factor 3 (IRF-3) and enhancing SUMOylation of IRF-7 (5, 10). Viral P24 inhibits type I and type II IFN signaling by inhibiting nuclear signaling transducer ad activator of transcription 1 (STAT 1)”
Figura (aqui)
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