PLoS Pathogens ：温度和湿度对于流感传播的影响被揭示

生物谷

    今年的流感季节又要来了，现在正是思考一个问题的好时候：为什么流感最容易在冬天侵袭我们？一项新研究表明，病毒似乎在较低的温度和湿度下更容易传染。该发现可以帮助研究人员找到减少流感传染的策略。

   过去，科学家已经提出关于流感季节性暴发的许多解释。一些传染病专家把季节性暴发的原因归结于人们在冬天交往更多，因为冷的时候人们很少出门；其他人怀疑人的免疫系统在冬天比较脆弱。但到目前为止还没有支持这些说法的充分证据。所以，由纽约Mount  Sinai医学院病毒学家Peter  Palese领导的研究小组测试了温度和湿度对于流感传播的影响。

    在一系列实验中，研究人员把4只感染了人类流感病毒的豚鼠养在4只健康豚鼠的隔壁。通过不断调整温度和湿度，研究人员发现，在湿度较低（约20%～35%）时传染率最大，大约75%～100%的健康豚鼠被传染上了流感。当湿度达到50%时，仅有1只豚鼠感染了病毒，而当湿度达到80%以上时，所有豚鼠都不会被传染——似乎传染的通道被堵塞了。研究人员在10月份的《Plos病原学》上报告了这一结果。

    对于温度，5℃时传染最严重——所有的动物都被感染了。而温度一旦达到30℃，传染就不再发生。

    “这就很好地解释了为什么我们在冬天更容易得流感了，因为冷的时候更容易被病毒感染。”Palese说。但这个结论还需要通过人体试验进行确认。Palese认为，传染增加的一个可能原因是流感病毒在低温、低湿度的情况下更稳定，而我们身体阻挡病原体的屏障如鼻黏膜等在这种情况下可能会削弱。

    加拿大多伦多儿童医院的分子生物学家Raymond  Tellier表示，该发现说明提升建筑物里的湿度将有助于预防流感的传染，但同时这也是一个矛盾的策略，因为高湿度会催生导致其他疾病的病原体。“你不会想要减少一种传染病而同时却增加了其他疾病。”Tellier说。（科学时报）

原始出处:

PLoS Pathogens

Received: June 7, 2007; Accepted: August 10, 2007; Published: October 5, 2007

A Single Mutation in the PB1-F2 of H5N1 (HK/97) and 1918 Influenza A Viruses Contributes to Increased Virulence

Gina M. Conenello1, Dmitriy Zamarin1, Lucy A. Perrone2, Terrence Tumpey2, Peter Palese1,3*

1 Department of Microbiology, Mount Sinai School of Medicine, New York, New York, United States of America, 2 Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, United States of America, 3 Department of Medicine, Mount Sinai School of Medicine, New York, New York, United States of America

The proapoptotic PB1-F2 protein of influenza A viruses has been shown to contribute to pathogenesis in the mouse model. Expression of full-length PB1-F2 increases the pathogenesis of the influenza A virus, causing weight loss, slower viral clearance, and increased viral titers in the lungs. After comparing viruses from the Hong Kong 1997 H5N1 outbreak, one amino acid change (N66S) was found in the PB1-F2 sequence at position 66 that correlated with pathogenicity. This same amino acid change (N66S) was also found in the PB1-F2 protein of the 1918 pandemic A/Brevig Mission/18 virus. Two isogenic recombinant chimeric viruses were created with an influenza A/WSN/33 virus background containing the PB1 segment from the HK/156/97: WH and WH N66S. In mice infected with WH N66S virus there was increased pathogenicity as measured by weight loss and decreased survival, and a 100-fold increase in virus replication when compared to mice infected with the WH virus. The 1918 pandemic strain A/Brevig Mission/18 was reconstructed with a pathogenicity-reducing mutation in PB1-F2 (S66N). The resultant 1918 S66N virus was attenuated in mice having a 3-log lower 50% lethal dose and caused less morbidity and mortality in mice than the wild-type virus. Viral lung titers were also decreased in 1918 S66N–infected mice compared with wild-type 1918 virus–infected mice. In addition, both viruses with an S at position 66 (WH N66S and wt 1918) induced elevated levels of cytokines in the lungs of infected mice. Together, these data show that a single amino acid substitution in PB1-F2 can result in increased viral pathogenicity and could be one of the factors contributing to the high lethality seen with the 1918 pandemic virus.

相关报道:

美国科学家发现人蛋白片断可阻断流感病毒传播

副流感病毒的传播途径及防治措施

Science：血凝素是人类流感传播的关键