Abstract
Herpesviruses utilize various host factors to establish latent infection, survival, and spread disease in the host. These factors include host cellular machinery, host proteins, gene expression, multiple transcription factors, cellular signal pathways, immune cell activation, transcription factors, cytokines, angiogenesis, invasion, and factors promoting metastasis. The knowledge and understanding of host genes, protein products, and biochemical pathways lead to discovering safe and effective antivirals to prevent viral reactivation and spread infection. Here, we focus on the contribution of pro-inflammatory, anti-inflammatory, and resolution lipid metabolites of the arachidonic acid (AA) pathway in the lifecycle of herpesvirus infections. We discuss how various herpesviruses utilize these lipid pathways to their advantage and how we target them to combat herpesvirus infection. We also summarize recent development in anti-herpesvirus therapeutics and new strategies proposed or under clinical trials. These anti-herpesvirus therapeutics include inhibitors blocking viral life cycle events, engineered anticancer agents, epigenome influencing factors, immunomodulators, and therapeutic compounds from natural extracts.
Highlights
Epstein-Barr virus (EBV) is primarily found in the tumor cells of Burkitt’s lymphoma (BL), lymphomas associated with immunosuppression, other non-Hodgkin’s lymphomas (NHL), Hodgkin’s disease, nasopharyngeal carcinoma (NPC), gastric adenocarcinoma, lymphoepithelioma-like carcinomas, posttransplant lymphoproliferative disorder (PTLD), nasal angiocentric T/NK-cell lymphoma, natural killer (NK)/T-cell lymphoma, and immunodeficiency-related leiomyosarcoma (Hsu and Glaser, 2000; Ambinder, 2003). g-herpesvirus Kaposi’s sarcoma herpesvirus (KSHV) is etiologically associated with Kaposi’s sarcoma (KS), B cell lymphoproliferative primary effusion lymphoma (PEL), multicentric Castleman’s disease (MCD), and KICS (KSHV inflammatory cytokines syndrome) (Cesarman et al, 1995; Soulier et al, 1995; Karass et al, 2017)
Co-infections with multiple viruses, parasites, malarial vector mosquitoes, and periodontal pathogens and antiviral resistance and the emergence of resistant viruses add to the complexity and severity of disease pathogenesis in immunocompromised patients, children, and neonates
Monotherapy fails in the immunocompromised patients as prolonged therapies are associated with the risk of antiviral resistance and combination antiviral therapy is preferred and more efficacious choice
Summary
Herpesviruses utilize various host factors to establish latent infection, survival, and spread disease in the host. These factors include host cellular machinery, host proteins, gene expression, multiple transcription factors, cellular signal pathways, immune cell activation, transcription factors, cytokines, angiogenesis, invasion, and factors promoting metastasis. We discuss how various herpesviruses utilize these lipid pathways to their advantage and how we target them to combat herpesvirus infection. We summarize recent development in anti-herpesvirus therapeutics and new strategies proposed or under clinical trials. These anti-herpesvirus therapeutics include inhibitors blocking viral life cycle events, engineered anticancer agents, epigenome influencing factors, immunomodulators, and therapeutic compounds from natural extracts
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
