Herpes simplex virus type 2-mediated disease is reduced in mice lacking RNase L
Herpes simplex virus type 2-mediated disease is reduced in mice lacking RNase L
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DOI：
10.1016/j.virol.2006.10.042
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发表时间：
2007-04-10
期刊：
影响因子：
3.7
通讯作者：
Morrison, Lynda A.
中科院分区：
文献类型：
--
作者：
Duerst, Rebecca J.;Morrison, Lynda A.
RNase L有助于介导由I型干扰素（IFN α β）诱导的抗病毒状态。虽然单纯疱疹病毒（HSV）编码IFN α β诱导的抗病毒反应的抑制剂，但IFN α β系统作为抵抗HSV的第一道防线服务于身体。我们研究了RNase L是否限制HSV-2的复制和毒力。RNaseL（-/-）和野生型C57 BL/6小鼠阴道内感染HSV-2菌株333。虽然在生殖器上皮细胞的初始复制是相似的，但缺乏RNase L的小鼠比野生型小鼠发生较轻的生殖器和神经系统疾病，存活时间更长，神经系统中的病毒滴度更低。RNase L-/-小鼠生殖道和脊髓中的CD 4（+）T细胞浸润减少，表明受限的炎症反应可能是疾病减少的原因。因此，RNA酶L在体内控制HSV-2感染中不起重要作用;相反，RNA酶L可以调节导致疾病的炎症反应的各个方面。(c)2006年爱思唯尔公司All rights reserved.
RNase L helps mediate the antiviral state induced by type I interferons (IFN alpha beta). Although herpes simplex virus (HSV) encodes inhibitors of the IFN alpha beta-induced antiviral response, the IFN alpha beta system serves the body as a first line of defense against HSV. We investigated whether RNase L limits HSV-2 replication and virulence. RNaseL(-/-) and wild-type C57BL/6 mice were infected intravaginally with HSV-2 strain 333. Although initial replication in the genital epithelium was similar, mice lacking RNase L developed less severe genital and neurologic disease than wild-type mice, survived longer, and contained lower viral titers in the nervous system. CD4(+) T cell infiltration into the genital tract and spinal cord of RNase L-/- mice was reduced, suggesting that a restricted inflammatory response may account for reduction in disease. Thus, RNase L does not play a significant role in control of HSV-2 infection in vivo; instead, RNase L may regulate aspects of the inflammatory response that contribute to disease. (c) 2006 Elsevier Inc. All rights reserved.