Even though gammaherpesvirus and parasitic infections are endemic in parts of the world, there is a lack of understanding about the outcome of coinfection. In humans, coinfections usually occur sequentially, with fluctuating order and timing in different hosts. However, experimental studies in mice generally do not address the variables of order and timing of coinfections. We sought to examine the variable of coinfection order in a system of gammaherpesvirus-helminth coinfection. Our previous work demonstrated that infection with the intestinal parasite, Heligmosomoides polygyrus, induced transient reactivation from latency of murine gammaherpesvirus-68 (MHV68). In this report, we reverse the order of coinfection, infecting with H. polygyrus first, followed by MHV68, and examined the effects of preexisting parasite infection on MHV68 acute and latent infection. We found that preexisting parasite infection increased the propensity of MHV68 to reactivate from latency. However, when we examined the mechanism for reactivation, we found that preexisting parasite infection increased the ability of MHV68 to reactivate in a vitamin A dependent manner, a distinct mechanism to what we found previously with parasite-induced reactivation after latency establishment. We determined that H. polygyrus infection increased both acute and latent MHV68 infection in a population of tissue resident macrophages, called large peritoneal macrophages. We demonstrate that this population of macrophages and vitamin A are required for increased acute and latent infection during parasite coinfection.

中文翻译：

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先前存在的蠕虫攻击加剧了组织驻留巨噬细胞中伽马疱疹病毒的感染和重新激活。

尽管伽玛疱疹病毒和寄生虫感染在世界部分地区流行，但人们对同时感染的后果缺乏了解。在人类中，双重感染通常是连续发生的，不同宿主的顺序和时间会有所不同。然而，小鼠实验研究通常没有解决合并感染的顺序和时间变量。我们试图检查伽马疱疹病毒-蠕虫双重感染系统中双重感染顺序的变量。我们之前的工作表明，肠道寄生虫 Heligmosomoides polygyrus 的感染会诱导鼠伽马疱疹病毒 68 (MHV68) 潜伏期短暂重新激活。在本报告中，我们颠倒了混合感染的顺序，首先感染H. polygyrus，然后感染MHV68，并检查了先前存在的寄生虫感染对MHV68急性和潜伏感染的影响。我们发现，先前存在的寄生虫感染增加了 MHV68 从潜伏期重新激活的倾向。然而，当我们检查重新激活机制时，我们发现先前存在的寄生虫感染增加了 MHV68 以维生素 A 依赖性方式重新激活的能力，这与我们之前发现的潜伏期建立后寄生虫诱导重新激活的机制截然不同。我们确定，H. polygyrus 感染增加了组织驻留巨噬细胞（称​​为大腹膜巨噬细胞）群体中的急性和潜伏 MHV68 感染。我们证明，在寄生虫共感染期间，巨噬细胞群和维生素 A 是增加急性和潜伏感染所必需的。