Plos Pathogens：疱疹病毒和疟原虫或形成致命组合
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 ImmunityImmunity 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 primary Plasmodium 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 Plasmodium transmission.
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