Rang Andreas
Institute of Medical Virology, University Hospital, Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, Berlin, D-10098, Germany.
Crit Rev Immunol. 2010;30(6):515-27. doi: 10.1615/critrevimmunol.v30.i6.20.
Hantavirus infection can cause hantavirus cardiopulmonary syndrome or hemorrhagic fever with renal syndrome depending on the virus species involved. The determinants for the virus species specific virulence in humans are unclear. Successful infection is a conditio sine qua non for the virulence of a virus and it is well-known that the innate interferon (IFN) system generally plays a decisive role to prevent establishment of an infection. The importance of the IFN system is underscored by the fact that viruses have developed an amazing number of different escape mechanisms to enable replication in face of the antiviral host response. Interestingly, pathogenic hantaviruses escape induction of innate antiviral responses in the early phase of the infection, which are elicited in a pronounced manner by nonpathogenic hantaviruses in vitro. This differential response might be important for the pathogenicity of hantaviruses in humans. This review aims to summarize the current knowledge about the interaction between hantaviruses and the innate IFN system. Detailed characterization of the cellular sensors and pathways that lead to activation of the IFN system on one side and the viral escape mechanisms on the other might help to develop novel vaccination strategies and therapeutic approaches.
汉坦病毒感染可导致汉坦病毒心肺综合征或肾综合征出血热,具体取决于所涉及的病毒种类。人类中病毒种类特异性毒力的决定因素尚不清楚。成功感染是病毒具有毒力的必要条件,众所周知,先天性干扰素(IFN)系统通常在预防感染的建立中起决定性作用。病毒已经发展出大量不同的逃逸机制以在面对抗病毒宿主反应时实现复制,这一事实凸显了IFN系统的重要性。有趣的是,致病性汉坦病毒在感染早期逃避先天性抗病毒反应的诱导,而非致病性汉坦病毒在体外能显著引发这种反应。这种差异反应可能对汉坦病毒在人类中的致病性很重要。本综述旨在总结关于汉坦病毒与先天性IFN系统相互作用的当前知识。详细表征导致IFN系统激活的细胞传感器和途径以及病毒逃逸机制,可能有助于开发新的疫苗策略和治疗方法。