{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,20]],"date-time":"2026-08-20T15:22:55Z","timestamp":1787239375367,"version":"build-2736575974"},"reference-count":83,"publisher":"MDPI AG","issue":"10","license":[{"start":{"date-parts":[[2019,10,1]],"date-time":"2019-10-01T00:00:00Z","timestamp":1569888000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Viruses"],"abstract":"<jats:p>Several notable human diseases are caused by enveloped RNA viruses: Influenza, AIDS, hepatitis C, dengue hemorrhagic fever, microcephaly, and Guillain\u2013Barr\u00e9 Syndrome. Being enveloped, the life cycle of this group of viruses is critically dependent on host lipid biosynthesis. Viral binding and entry involve interactions between viral envelope glycoproteins and cellular receptors localized to lipid-rich regions of the plasma membrane. Subsequent infection by these viruses leads to reorganization of cellular membranes and lipid metabolism to support the production of new viral particles. Recent work has focused on defining the involvement of specific lipid classes in the entry, genome replication assembly, and viral particle formation of these viruses in hopes of identifying potential therapeutic targets for the treatment or prevention of disease. In this review, we will highlight the role of host sphingolipids in the lifecycle of several medically important enveloped RNA viruses.<\/jats:p>","DOI":"10.3390\/v11100912","type":"journal-article","created":{"date-parts":[[2019,10,1]],"date-time":"2019-10-01T11:11:16Z","timestamp":1569928276000},"page":"912","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":30,"title":["Sphingolipids as Potential Therapeutic Targets against Enveloped Human RNA Viruses"],"prefix":"10.3390","volume":"11","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6118-7487","authenticated-orcid":false,"given":"Eric J.","family":"Yager","sequence":"first","affiliation":[{"name":"Department of Basic and Clinical Sciences, Albany College of Pharmacy and Health Sciences, Albany, NY 12208, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3713-8751","authenticated-orcid":false,"given":"Kouacou V.","family":"Konan","sequence":"additional","affiliation":[{"name":"Department of Immunology and Microbial Disease, Albany Medical College, Albany, NY 12208-3479, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2019,10,1]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"591","DOI":"10.1016\/j.stem.2016.03.012","article-title":"Expression Analysis Highlights AXL as a Candidate Zika Virus Entry Receptor in Neural Stem Cells","volume":"18","author":"Nowakowski","year":"2016","journal-title":"Cell Stem Cell"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"2024","DOI":"10.1073\/pnas.1620558114","article-title":"AXL-dependent infection of human fetal endothelial cells distinguishes Zika virus from other pathogenic flaviviruses","volume":"114","author":"Richard","year":"2017","journal-title":"Proc. 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