柳叶刀:Zika病毒不仅致“小头症”,或将引发神经性疾病
2016/03/04
此前的科学研究证明,这种病毒会造成严重的先天性缺陷,比如小头症。最近研究者在对2013-2014年法属波里尼西亚爆发的格林巴利综合症(GBS)进行研究时,发现了其与“寨卡”病毒的关联性。在20万受“寨卡”病毒影响的人中,有42例之后会出现格林巴利综合征。


寨卡病毒是一种急性传染病病毒,最初是在猴子身上发现的,有时可以通过蚊虫叮咬传播给人类。由于该病可导致胎儿小头症并可能严重损伤大脑,因此对怀孕妇女更加危险。巴西被认为是世界上感染寨卡病毒最多的国家之一。巴西卫生部消息称,新生儿因感染寨卡病毒而患小头畸形症病例在一周内增加了10%,从583例增加到641例。

Zika病毒或导致严重的神经紊乱

巴斯德研究院流行病教授Arnaud Fontanet医学博士等人发表的一篇文章指出,研究者在对2013-2014年法属波里尼西亚爆发的格林巴利综合症(GBS)进行研究时,发现了其与“寨卡”病毒的关联性。在20万受“寨卡”病毒影响的人中,有42例之后会出现格林巴利综合征。

据悉,格林巴利综合征是一种一种神经系统自身免疫性疾病,可由多种病毒引起,主要症状为四肢软瘫,严重时可因呼吸麻痹而死亡;会造成四肢肌肉无力,死亡率约为5%,另有5%的病人还可能出现永久性残疾。

Arnaud Fontanet表示,这种关系就像烟草会引起肺癌,他们在每个格林巴利综合症患者的身上都发现了‘寨卡’病毒的踪迹,包括相应的抗体。不过Zika病毒引起这种综合征的生物机理还有待进一步确认。

附:Zika病毒常识(由中国科技网制作)


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  • Guillain-Barré Syndrome outbreak associated with Zika virus infection in French Polynesia: a case-control study

    Summary Background Between October, 2013, and April, 2014, French Polynesia experienced the largest Zika virus outbreak ever described at that time. During the same period, an increase in Guillain-Barré syndrome was reported, suggesting a possible association between Zika virus and Guillain-Barré syndrome. We aimed to assess the role of Zika virus and dengue virus infection in developing Guillain-Barré syndrome. Methods In this case-control study, cases were patients with Guillain-Barré syndrome diagnosed at the Centre Hospitalier de Polynésie Française (Papeete, Tahiti, French Polynesia) during the outbreak period. Controls were age-matched, sex-matched, and residence-matched patients who presented at the hospital with a non-febrile illness (control group 1; n=98) and age-matched patients with acute Zika virus disease and no neurological symptoms (control group 2; n=70). Virological investigations included RT-PCR for Zika virus, and both microsphere immunofluorescent and seroneutralisation assays for Zika virus and dengue virus. Anti-glycolipid reactivity was studied in patients with Guillain-Barré syndrome using both ELISA and combinatorial microarrays. Findings 42 patients were diagnosed with Guillain-Barré syndrome during the study period. 41 (98%) patients with Guillain-Barré syndrome had anti-Zika virus IgM or IgG, and all (100%) had neutralising antibodies against Zika virus compared with 54 (56%) of 98 in control group 1 (p<0·0001). 39 (93%) patients with Guillain-Barré syndrome had Zika virus IgM and 37 (88%) had experienced a transient illness in a median of 6 days (IQR 4–10) before the onset of neurological symptoms, suggesting recent Zika virus infection. Patients with Guillain-Barré syndrome had electrophysiological findings compatible with acute motor axonal neuropathy (AMAN) type, and had rapid evolution of disease (median duration of the installation and plateau phases was 6 [IQR 4–9] and 4 days [3–10], respectively). 12 (29%) patients required respiratory assistance. No patients died. Anti-glycolipid antibody activity was found in 13 (31%) patients, and notably against GA1 in eight (19%) patients, by ELISA and 19 (46%) of 41 by glycoarray at admission. The typical AMAN-associated anti-ganglioside antibodies were rarely present. Past dengue virus history did not differ significantly between patients with Guillain-Barré syndrome and those in the two control groups (95%, 89%, and 83%, respectively).

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