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Sensitivity to pyrexial temperatures: a factor contributing to virulence differences between two clones of influenza virus.

机译:对热解温度的敏感性:这是两个流感病毒克隆之间毒力差异的一个因素。

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摘要

The influence of pyrexia on the differential persistence of a virulent and an attenuated clone of influenza virus in the respiratory tract of ferrets has been further studied. Clone 64d, an attenuated clone of a recombinant virus (A/PR/8/34-A/England/939/69 (H3N2)) grown in organ cultures of ferret nasal turbinates, was inactivated at pyrexial temperatures more readily than a virulent Clone 7a. In addition, replication of Clone 64d was restricted at pyrexial temperatures to a greater extent than that of Clone 7a in organ cultures of both ferret nasal turbinate and lung tissue. The greater adverse effects of pyrexial temperatures on Clone 64d appears to explain the earlier reduction of upper respiratory tract infection seen in ferrets infected with this attenuated clone. Also, the differential influence of pyrexial temperatures may be the reason for the virtual lack of lung infection with Clone 64d in vivo in contrast to the consistent infection found with Clone 7a. The relevance of these findings to human infection and to markers of attenuation of influenza virus is discussed.
机译:发热对雪貂呼吸道中流感病毒弱毒和减毒克隆的持续存留的影响已得到进一步研究。克隆64d是在雪貂鼻甲的器官培养物中生长的重组病毒(A / PR / 8 / 34-A / England / 939/69(H3N2))的减毒克隆,在炎热温度下比强力克隆更容易失活7a。此外,在白鼬鼻甲和肺组织的器官培养物中,发烧温度下克隆64d的复制受到的限制比克隆7a更大。发热温度对克隆64d的更大不利影响似乎可以解释在用这种减毒克隆感染的雪貂中上呼吸道感染的早期减少。另外,与克隆7a持续感染相比,发烧温度的差异影响可能是克隆64d在体内实际上缺乏肺部感染的原因。讨论了这些发现与人类感染以及流感病毒减毒标志物的相关性。

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