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【bio-news】流感变为超级流感的罪魁
From Flu to Superflu
By Steve Mitchell
ScienceNOW Daily News
11 October 2007
Just in time for flu season comes the discovery that a single protein may largely explain the unprecedented deadliness of the 1918 influenza epidemic. The finding should help infectious disease experts spot future flu viruses that pose the most risk of causing another global pandemic.
The 1918 outbreak--also known as the Spanish flu--was the deadliest strain of flu virus the world has ever seen (ScienceNOW, 17 January). Estimates of fatalities range from 40 million to 100 million. Some people fell victim to the flu virus itself, but many of the deaths were due to the pneumonia that people developed as a result of damage to their lungs. Why was the virus so deadly? Scientists suspect that a recently discovered protein called PB1-F2, which is found in many flu viruses, including the H5N1 bird flu strain that has killed 202 people, may hold some answers.
To get a better handle on the role of PB1-F2 in the 1918 epidemic, a team led by Jonathan McCullers, a virologist at St. Jude Children's Research Hospital in Memphis, Tennessee, genetically modified a mouse strain of flu virus to produce a PB1-F2 protein identical to that in the 1918 strain. When the researchers dripped high doses of the modified virus into the noses of mice, all of the animals died within 8 days and had more lung inflammation than animals receiving similar doses of the same flu virus with unaltered PB1-F2.
In a separate experiment, the researchers gave mice nonlethal doses of the modified flu virus and then infected them with the pneumonia-causing bacterium, Streptococcus pneumoniae. All of the animals died within 4 days and showed evidence of severe pneumonia, the team reports in the October issue of Cell Host & Microbe. In contrast, 80% of the mice that received the unmodified virus were alive 4 days after exposure to the pneumonia bacterium and 20% were still alive when the study ended at 14 days.
"This is one of the big reasons 1918 was so bad, because PB1-F2 allowed bacteria to cause more problems due to lung inflammation and damage," McCullers says. How PB1-F2 amplifies flu virulence remains uncertain, but he says the protein could be a potential target for flu drugs, with the goal being to suppress it to help reduce lung damage and subsequent pneumonia.
Terrence Tumpey, a microbiologist with the Centers for Disease Control and Prevention in Atlanta, Georgia, says monitoring the PB1-F2 protein in flu viruses could help determine which ones pose the most threat to public health. "It could help us recognize if a particular virus is something we have to watch out for," Tumpey says 本人已认领该文编译，48小时后若未提交译文，请其他战友自由认领。 每次进入深秋，流感流行的时候，总是会让人想起恐怖的1918西班牙流感大爆发。近日从美国科学家传来好消息，他们发现某种蛋白在空前致死性的1918年流感中起了重要作用。这一发现将有助于传染病专家更好地监测流感病毒，以防再一次的流感大爆发。相关论文发表在10月11日的《细胞－宿主与微生物》（Cell Host & Microbe）上。
导致1918年西班牙流感的是一种空前致命性的流感病毒，死亡人数据估计在4千万到1亿之间。有些人是死于流感病毒本身，但更多的是死于由流感造成的肺炎。为什么此次流感如此致命？很多科学家认为，近来发现的在很多种流感病毒中都存在的PB1-F2蛋白可能与此有关。
为了更深入地研究PB1-F2在1918年流感中扮演的角色，美国孟菲斯圣•裘德儿童研究医院（）的病毒学家Jonathan McCullers和研究小组改造了小鼠的一种流感病毒基因，使其产生与1918年流感中相同的PB1-F2蛋白。研究人员随后将这种改造病毒注射进小鼠的鼻子，发现所有的小鼠在8天之内全部死亡，并且产生的肺部炎症要比那些注射了同等剂量含有普通PB1-F2流感病毒的小鼠要多。
在另外一个独立实验中，研究人员向小鼠注射了非致命量的改造流感病毒，并紧接着让它们感染肺炎病菌。结果发现，所有的小鼠在4天之内全部死亡，并表现出严重的肺炎症状。与此相对照，注射了同等剂量普通流感病毒的小鼠在暴露于肺炎病菌4天后，由80％仍然存活，而当14天后实验结束时，还有20％存活。
McCullers说，PB1-F2会使流感病毒的破坏能力加强，导致更多问题，这是1918年流感如此致命的重要原因之一。他表示，虽然PB1-F2的具体作用机制还不清楚，但此蛋白可作为流感药物的潜在药靶，通过抑制它的功能减少肺部损伤和并发炎症。
美国亚特兰大疾病预防与控制中心的微生物学家Terrence Tumpey认为，通过监测PB1-F2可以帮助我们确定哪一种流感会对公众健康造成最大危害。他说：“PB1-F2能帮助我们确定是否需要小心提防某种病毒 这个在年初德国黑尔姆霍尔茨传染病研究中心和埃朗根-纽伦堡大学的专家就发现了!已在美国《生物化学杂志》上发表。 From Flu to Superflu
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作者:admin@医学,生命科学 2011-06-17 05:11
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