García-Sastre Adolfo, Biron Christine A
Department of Microbiology, Mount Sinai School of Medicine, New York, NY 10029, USA.
Science. 2006 May 12;312(5775):879-82. doi: 10.1126/science.1125676.
The interface between an infectious agent and its host represents the ultimate battleground for survival: The microbe must secure a niche for replication, whereas the host must limit the pathogen's advance. Among the host's arsenal of antimicrobial factors, the type 1 interferons (IFNs) induce potent defense mechanisms against viruses and are key in the host-virus standoff. Viruses have evolved multiple tricks to avoid the immediate antiviral effects of IFNs and, in turn, hosts have adapted use of this innate cytokine system to galvanize multiple additional layers of immune defense. The plasticity that exists in these interactions provides us with a lesson in détente.
微生物必须确保有一个复制的生态位,而宿主则必须限制病原体的进展。在宿主的抗菌因子库中,1型干扰素(IFN)可诱导针对病毒的有效防御机制,是宿主与病毒对峙中的关键因素。病毒已经进化出多种策略来避免IFN的直接抗病毒作用,反过来,宿主也已适应利用这种先天性细胞因子系统来激发多层额外的免疫防御。这些相互作用中存在的可塑性为我们提供了有关缓和的经验教训。