2013年6月6日 訊 /生物谷BIOON/ --近日,，刊登在國(guó)際雜志PLoS Neglected Tropical Diseases上的一篇研究報(bào)告中,，來(lái)自弗吉尼亞理工學(xué)院的研究者通過(guò)研究表明,，當(dāng)蚊子處于低溫條件下后,，其機(jī)體免疫力會(huì)變?nèi)?，這就使得其對(duì)危險(xiǎn)的病毒更加易感,，而且有可能將這些易感病毒傳染給人類,。
研究者M(jìn)yles表示,，我們的研究數(shù)據(jù)提出了一種合理的假說(shuō)，就是天氣的變化如何影響疾病的傳播,。隨著全球氣候的變化,，多樣的天氣隨時(shí)都會(huì)發(fā)生。本文的研究者就重點(diǎn)研究了氣候改變和疾病傳播之間的關(guān)系。
研究者說(shuō)道,，蚊子一般在黑暗潮濕的環(huán)境中繁殖產(chǎn)卵,，因?yàn)槠洚a(chǎn)的卵會(huì)在水中生存很久，蚊子不會(huì)在太陽(yáng)光下產(chǎn)卵,，因?yàn)椴焕诼训拇婊?，盡管如此，研究者依然試圖去研究環(huán)境對(duì)蚊子免疫系統(tǒng)的影響,，研究者希望可以通過(guò)本項(xiàng)研究來(lái)建立更好的研究模型從而預(yù)測(cè)疾病的傳播趨勢(shì),。
當(dāng)前的計(jì)算機(jī)疫情模型主要考慮到氣象學(xué)的變化以及人口指數(shù)，但是并沒(méi)有考慮到溫度對(duì)于蚊子免疫力的影響效應(yīng),，研究者就發(fā)現(xiàn)當(dāng)蚊子處于較低溫度下時(shí),，其RNA干擾途徑就會(huì)被損傷，進(jìn)而就會(huì)增加對(duì)某些病毒的易感性,，從而就會(huì)間接地傳染給人類,。
疾病的傳播以及爆發(fā)都會(huì)發(fā)生在意想不到的地方，比如1999年在紐約爆發(fā)的西尼羅河病毒,、2007年和2010年在意大利和法國(guó)爆發(fā)的切昆貢亞病毒等,，因此本項(xiàng)研究對(duì)于預(yù)測(cè)蚊子所攜帶疾病的傳播非常重要。（生物谷Bioon.com）
doi:10.1371/journal.pntd.0002239
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Cooler Temperatures Destabilize RNA Interference and Increase Susceptibility of Disease Vector Mosquitoes to Viral Infection
Adelman ZN, Anderson MAE, Wiley MR, Murreddu MG, Samuel GH, et al.
Background The impact of global climate change on the transmission dynamics of infectious diseases is the subject of extensive debate. The transmission of mosquito-borne viral diseases is particularly complex, with climatic variables directly affecting many parameters associated with the prevalence of disease vectors. While evidence shows that warmer temperatures often decrease the extrinsic incubation period of an arthropod-borne virus (arbovirus), exposure to cooler temperatures often predisposes disease vector mosquitoes to higher infection rates. RNA interference (RNAi) pathways are essential to antiviral immunity in the mosquito; however, few experiments have explored the effects of temperature on the RNAi machinery. Methodology/Principal Findings We utilized transgenic “sensor” strains of Aedes aegypti to examine the role of temperature on RNA silencing. These “sensor” strains express EGFP only when RNAi is inhibited; for example, after knockdown of the effector proteins Dicer-2 (DCR-2) or Argonaute-2 (AGO-2). We observed an increase in EGFP expression in transgenic sensor mosquitoes reared at 18°C as compared with 28°C. Changes in expression were dependent on the presence of an inverted repeat with homology to a portion of the EGFP sequence, as transgenic strains lacking this sequence, the double stranded RNA (dsRNA) trigger for RNAi, showed no change in EGFP expression when reared at 18°C. Sequencing small RNAs in sensor mosquitoes reared at low temperature revealed normal processing of dsRNA substrates, suggesting the observed deficiency in RNAi occurs downstream of DCR-2. Rearing at cooler temperatures also predisposed mosquitoes to higher levels of infection with both chikungunya and yellow fever viruses. Conclusions/Significance This data suggest that microclimates, such as those present in mosquito breeding sites, as well as more general climactic variables may influence the dynamics of mosquito-borne viral diseases by affecting the antiviral immunity of disease vectors.
