Yurochko Andrew D
Department of Microbiology and Immunology, Center for Molecular and Tumor Virology, Louisiana State University Health Sciences Center, Shreveport, Louisiana, USA
Center of Excellence in Arthritis and Rheumatology, Louisiana State University Health Sciences Center, Shreveport, Louisiana, USA.
mBio. 2017 Apr 18;8(2):e00505-17. doi: 10.1128/mBio.00505-17.
Viruses have evolved many novel mechanisms to promote infection and to mitigate the host cell response to that infection. In the article by M. H. Hancock et al. (mBio 8:e00109-17, 2017, https://doi.org/10.1128/mBio.00109-17), the authors describe a new mechanism by which human cytomegalovirus (HCMV) microRNAs (miRNAs; miR-US5-1 and miR-UL112-3p) negate the proinflammatory response to infection. The authors document that these two viral miRNAs downregulate the NF-κB response through direct targeting of the IKKα and IKKβ mRNAs, which in turn, through diminished IκB kinases (IKKs), block production of proinflammatory cytokines (interleukin-6 [IL-6], CCL5, and tumor necrosis factor alpha [TNF-α]). Because most signaling pathways that promote NF-κB activation and nuclear translocation ultimately converge on the activation of the IKK complex, this new study documents that HCMV can strongly dictate how infected cells respond to internal and/or external stimuli and thus positively influence the outcome of both lytic and latent infection.
病毒已经进化出许多新颖的机制来促进感染，并减轻宿主细胞对该感染的反应。在M. H. 汉考克等人的文章（《mBio》8：e00109 - 17，2017年，https://doi.org/10.1128/mBio.00109 - 17）中，作者描述了一种新机制，通过该机制人类巨细胞病毒（HCMV）的微小RNA（miRNA；miR - US5 - 1和miR - UL112 - 3p）可消除对感染的促炎反应。作者证明这两种病毒miRNA通过直接靶向IKKα和IKKβ mRNA来下调NF - κB反应，进而通过减少IκB激酶（IKK）来阻断促炎细胞因子（白细胞介素 - 6 [IL - 6]、CCL5和肿瘤坏死因子α [TNF - α]）的产生。由于大多数促进NF - κB激活和核转位的信号通路最终都汇聚于IKK复合物的激活，这项新研究证明HCMV能够强烈决定受感染细胞对内部和/或外部刺激的反应方式，从而对裂解性感染和潜伏性感染的结果产生积极影响。
