Chandrasekharan Jayashree A, Sharma-Walia Neelam
Department of Microbiology and Immunology, H.M. Bligh Cancer Research Laboratories, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL, United States.
Front Microbiol. 2019 Mar 12;10:358. doi: 10.3389/fmicb.2019.00358. eCollection 2019.
Kaposi's sarcoma-associated herpesvirus (KSHV) infection, particularly latent infection is often associated with inflammation. The arachidonic acid pathway, the home of several inflammation and resolution associated lipid mediators, is widely altered upon viral infections. Several studies show that these lipid mediators help in the progression of viral pathogenesis. This review summarizes the findings related to human herpesvirus KSHV infection and arachidonic acid pathway metabolites. KSHV infection has been shown to promote inflammation by upregulating cyclooxygenase-2 (COX-2), 5 lipoxygenase (5LO), and their respective metabolites prostaglandin E (PGE) and leukotriene B4 (LTB) to promote latency and an inflammatory microenvironment. Interestingly, the anti-inflammatory lipid mediator lipoxin is downregulated during KSHV infection to facilitate infected cell survival. These studies aid in understanding the role of arachidonic acid pathway metabolites in the progression of viral infection, the host inflammatory response, and pathogenesis. With limited therapeutic options to treat KSHV infection, use of inhibitors to these inflammatory metabolites and their synthetic pathways or supplementing anti-inflammatory lipid mediators could be an effective alternative therapeutic.
卡波西肉瘤相关疱疹病毒（KSHV）感染，尤其是潜伏感染，常与炎症相关。花生四烯酸途径是多种与炎症和炎症消退相关的脂质介质的产生场所，在病毒感染时会发生广泛改变。多项研究表明，这些脂质介质有助于病毒发病机制的进展。本综述总结了与人类疱疹病毒KSHV感染及花生四烯酸途径代谢产物相关的研究结果。已表明KSHV感染通过上调环氧化酶-2（COX-2）、5-脂氧合酶（5LO）及其各自的代谢产物前列腺素E（PGE）和白三烯B4（LTB）来促进炎症，从而促进潜伏和炎症微环境的形成。有趣的是，抗炎脂质介质脂氧素在KSHV感染期间下调，以促进受感染细胞的存活。这些研究有助于理解花生四烯酸途径代谢产物在病毒感染进展、宿主炎症反应和发病机制中的作用。鉴于治疗KSHV感染的治疗选择有限，使用这些炎症代谢产物及其合成途径的抑制剂或补充抗炎脂质介质可能是一种有效的替代治疗方法。
