Plos Pathogens：疱疹病毒和疟原虫或形成致命组合
http://www-bioon.qiniudn.com/tm/UploadFiles/201506/2015061811314624.png2015年6月18日/生物谷BIOON/-- 疟疾一直是困扰人类的高致死性疾病之一。患上严重疟疾的儿童大约有20%会死亡。实际上，让患上疟疾的情况更加糟糕的是，同时感染了疟原虫和其他致病菌（或寄生虫）。在非洲泛撒哈拉地区，很多婴儿在出生六个月的时候就感染了人类四型疱疹病毒（EBV）。而这个时间正好是婴儿体内来自母亲的抗体开始减弱的时候，这个阶段也很容易感染上疟原虫而患上疟疾。近期发表在《Plos Pathogens》的研究文章称，他们发现了感染疟人类疱疹病毒（EBV）可能导致人体对疟疾的免疫能力严重下降。通常在第一二次局部区域接触恶性疟原虫并患上疟疾的时候，人体即获得免疫。再次感染疟原虫时，免疫系统会调动身体消灭这些病原体。而该课题组在实验发现，如果小鼠急性感染了非致死性人类疱疹病毒MHV68（一种非致死性的人类疱疹病毒），针对约氏疟原虫（一种非致死性疟原虫）的二次感染的免疫力严重降低，并导致这种非致死性的疟原虫成为了小鼠新的致死性威胁。他们还发现，非致死性人类疱疹病毒MHV68的一种膜蛋白M2起了很大作用。首先，在MHV68急性感染时，这种蛋白质能够抑制宿主对该病毒的抗病毒反应。其次，在这种病毒和疟原虫共感染的情况下，宿主针对疟原虫的免疫反应的抑制与M2相关联，让非致死性的约氏疟原虫变成致命的感染源。作者们总结道，在小鼠实验中，发现急性感染人类疱疹病毒导致针对疟原虫的免疫力下降，对人类也有重要启示。对新生儿而言，同时感染人类疱疹病毒和疟原虫会带来很高的风险。同时，在新生儿中，针对疱疹病毒的疫苗，可能也为抵抗疟疾提供新的解决方案。（生物谷Bioon.com）Gammaherpesvirus Co-infection with Malaria Suppresses Anti-parasitic Humoral Immunity
Caline G. Matar, Neil R. Anthony, Brigid M. O’Flaherty, Nathan T. Jacobs, Lalita Priyamvada, Christian R. Engwerda, Samuel H. Speck , Tracey J. Lamb
AbstractImmunity to non-cerebral severe malaria is estimated to occur within 1-2 infections in areas of endemic transmission for Plasmodium falciparum. Yet, nearly 20% of infected children die annually as a result of severe malaria. Multiple risk factors are postulated to exacerbate malarial disease, one being co-infections with other pathogens. Children living in Sub-Saharan Africa are seropositive for Epstein Barr Virus (EBV) by the age of 6 months. This timing overlaps with the waning of protective maternal antibodies and susceptibility to primaryPlasmodium infection. However, the impact of acute EBV infection on the generation of anti-malarial immunity is unknown. Using well established mouse models of infection, we show here that acute, but not latent murine gammaherpesvirus 68 (MHV68) infection suppresses the anti-malarial humoral response to a secondary malaria infection. Importantly, this resulted in the transformation of a non-lethal P. yoelii XNL infection into a lethal one; an outcome that is correlated with a defect in the maintenance of germinal center B cells and T follicular helper (Tfh) cells in the spleen. Furthermore, we have identified the MHV68 M2 protein as an important virus encoded protein that can: (i) suppress anti-MHV68 humoral responses during acute MHV68 infection; and (ii) plays a critical role in the observed suppression of anti-malarial humoral responses in the setting of co-infection. Notably, co-infection with an M2-null mutant MHV68 eliminates lethality of P. yoelii XNL. Collectively, our data demonstrates that an acute gammaherpesvirus infection can negatively impact the development of an anti-malarial immune response. This suggests that acute infection with EBV should be investigated as a risk factor for non-cerebral severe malaria in young children living in areas endemic for Plasmodiumtransmission.
Author SummaryNearly 1 million deaths occur annually as a result of complications associated with P.falciparum infection, with children younger than 5 being the most susceptible age group. Earlier studies have demonstrated that children co-infected with P. falciparum and Epstein-Barr virus (EBV) have impaired immune responses to control EBV, and this can result in the development of a jaw tumor called endemic Burkitt’s lymphoma (eBL). It is not known if there is any impact of acute EBV infection on the generation of anti-malarial immunity. We have used mouse models of EBV and malaria (P. yoelii XNL) to demonstrate that acute gammaherpesvirus infection can impair the generation of antibodies that control Plasmodium parasitemia, in turn causing a non-lethal P. yoelii XNL infection to become lethal. We identify a critical role for the MHV68 M2 protein in mediating the suppressive effect of acute MHV68 infection on the generation of humoral immunity to a secondary malaria infection. This work demonstrates that gammaherpesvirus infections can suppress the generation of an effective anti-malaria immune response and suggests that acute EBV infection should be investigated as a risk factor for the development of severe malaria in young children.http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1004858
共感染的情况太复杂了。有些细菌与病毒共感染时也是致命的
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