Joseph Sarah B, Hanley Kathryn A, Chao Lin, Burch Christina L
Department of Biology, University of North Carolina Chapel Hill, NC, USA.
Department of Biology, New Mexico State University Las Cruces, NM, USA.
Evol Appl. 2009 Feb;2(1):24-31. doi: 10.1111/j.1752-4571.2008.00055.x. Epub 2008 Dec 23.
Two or more viruses infecting the same host cell can interact in ways that profoundly affect disease dynamics and control, yet the factors determining coinfection rates are incompletely understood. Previous studies have focused on the mechanisms that viruses use to suppress coinfection, but recently the phenomenon of enhanced coinfection has also been documented. In the experiments described here, we explore the hypothesis that enhanced coinfection rates in the bacteriophage Φ6 are achieved by virus-induced upregulation of the Φ6 receptor, which is the bacterial pilus. First, we confirmed that coinfection enhancement in Φ6 is virus-mediated by showing that Φ6 attaches significantly faster to infected cells than to uninfected cells. Second, we explored the hypothesis that coinfection enhancement in Φ6 depends upon changes in the expression of an inducible receptor. Consistent with this hypothesis, the closely related phage, Φ12, that uses constitutively expressed lipopolysaccharide as its receptor, attaches to infected and uninfected cells at the same rate. Our results, along with the previous finding that coinfection in Φ6 is limited to two virions, suggest that viruses may closely regulate rates of coinfection through mechanisms for both coinfection enhancement and exclusion.
两种或更多种感染同一宿主细胞的病毒能够以深刻影响疾病动态和控制的方式相互作用,然而,决定共感染率的因素尚未完全明确。以往的研究主要聚焦于病毒用于抑制共感染的机制,但最近也有文献记载了共感染增强的现象。在此处描述的实验中,我们探讨了这样一种假说:噬菌体Φ6中增强的共感染率是通过病毒诱导的Φ6受体(即细菌菌毛)上调来实现的。首先,我们通过证明Φ6附着于受感染细胞的速度明显快于未受感染细胞,证实了Φ6中的共感染增强是由病毒介导的。其次,我们探讨了Φ6中共感染增强取决于可诱导受体表达变化的假说。与该假说一致的是,密切相关的噬菌体Φ12以组成型表达的脂多糖作为其受体,它以相同的速率附着于受感染和未受感染的细胞。我们的结果,连同之前发现的Φ6中的共感染仅限于两个病毒粒子,表明病毒可能通过共感染增强和排斥机制密切调节共感染率。