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感染脑心肌炎病毒、辛德毕斯森林病毒、甲型流感病毒2型、人疱疹病毒2型或鼠巨细胞病毒的小鼠对干扰素诱导的反应受到抑制。

Suppressed response to interferon inducation in mice infected with encephalomyocarditis virus, Semliki forest virus, influenza A2 virus, Herpesvirus hominis type 2, or murine cytomegalovirus.

作者信息

Stringfellow D A, Kern E R, Kelsey D K, Glasgow L A

出版信息

J Infect Dis. 1977 Apr;135(4):540-51. doi: 10.1093/infdis/135.4.540.

Abstract

Mice infected with encephalomyocarditis virus, Semliki Forest virus, influenza A2 virus, Herpesvirus hominis type 2, or murine cytomegalovirus developed a state of hyporeactivity to interferon induction. In general, the capacity of infected animals to produce interferon in response to inducers became progressively impaired during the course of infection. The severity and time of onset of hyporeactivity, however, were dependent upon the inducer and the nature of the viral infection. During viral infections associated with generalized hyporesponsiveness, a factor that could inhibit interferon production by murine cells in culture was identified in the serum. This serum hyporeactive factor may have mediated the development of hyporeactivity in vivo. Hyporeactivity of the host's interferon response was associated with progression of viral infection and may be partially responsible for the limited effectiveness of interferon inducers in the modification of viral infections, when administered after onset of symptoms.

摘要

感染脑心肌炎病毒、辛德毕斯病毒、甲型流感病毒2型、人疱疹病毒2型或鼠巨细胞病毒的小鼠,会出现对干扰素诱导反应低下的状态。一般来说,受感染动物在感染过程中,对诱导剂产生干扰素的能力会逐渐受损。然而,反应低下的严重程度和出现时间取决于诱导剂以及病毒感染的性质。在与全身反应低下相关的病毒感染期间,在血清中发现了一种可抑制培养的鼠细胞产生干扰素的因子。这种血清反应低下因子可能在体内介导了反应低下的发展。宿主干扰素反应的低下与病毒感染的进展相关,并且当在症状出现后给予干扰素诱导剂时,可能部分导致了其在改变病毒感染方面效果有限。

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