Arachidonic Acid derived lipid mediators influence Kaposi’s Sarcoma Associated Herpes Virus (KSHV) infection and pathogenesis
- 1Rosalind Franklin University of Medicine and Science, United States
Kaposi’s sarcoma associated herpes virus (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 in vitro 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 E2 (PGE2) and leukotriene B4 (LTB4) to promote latency and a pro-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 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.
Keywords: KSHV, latency, Cyclooxegenase-2, Lipoxygenase, Lipoxin A 4
Received: 09 Aug 2018;
Accepted: 11 Feb 2019.
Edited by:Benoit Muylkens, University of Namur, Belgium
Reviewed by:Masahiro Fujimuro, Kyoto Pharmaceutical University, Japan
Carlos A. Sorgi, Universidade de São Paulo Ribeirão Preto, Brazil
Copyright: © 2019 Sharma-walia and Chandrasekharan. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: PhD. Neelam Sharma-walia, Rosalind Franklin University of Medicine and Science, North Chicago, 60064, Illinois, United States, email@example.com