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This Research Topic is part of the Significance of Cellular Lipids for Viral Replication and Pathogenesis community series:

This Research Topic is part of the Significance of Cellular Lipids for Viral Replication and Pathogenesis community series:
Significance of Cellular Lipids for Viral Replication and Pathogenesis, Volume II

Viral replication is increasingly recognized to be dependent on cellular lipids for various aspects of their replication cycles, ranging from viral entry, genome replication, to assembly and egress. These cellular lipids include various structural molecules, such a gangliosides, phospholipids, sterols and sphingolipids, found in cellular membranes and lipid droplets. Alterations of lipid homeostasis promote or block viral replication, often resulting in the increased production of pro-inflammatory cytokines. In addition, lipid metabolites, such as eicosanoids play an important role in viral replication and modulation of the immune responses to viral infection. Therefore, modulation of cellular lipid composition could interfere with these processes and raises interesting prospects for the development of new broad-spectrum antiviral therapies.

The biosynthesis of intracellular fatty acids and sterols as well as their metabolic pathways are well researched. Lipid droplets, which are major storage organelles of neutral lipids, such as triacylglycerols and cholesterol esters and also act as vehicles for intracellular transport, are important for the replication of various RNA viruses such as hepatitis C viruses, Dengue viruses, species A rotaviruses, picornaviruses, noroviruses and some DNA viruses (Marek's disease virus). Certain viruses, including those causing hepatitis C, Dengue and Japanese encephalitis, also alter lipid metabolic processes, such as beta-oxidation, while a role for the pro-inflammatory eicosanoid prostaglandin E2 has been implicated in various steps of viral replication, including viral binding to cellular receptors, viral gene expression and the production and release of nascent virions. However, the specific mechanisms by which some of these viruses interact with the cellular lipidome remain incompletely understood. Lipid components interacting with viruses of the same or different families should be explored for the development of potentially broad-spectrum antivirals. Since most of cogent work to date has been performed in vitro, its relevance for animal virus disease models should be examined and the potential of clinical significance be explored.

The aim of the Research Topic is therefore to contribute to our understanding of the significance of cellular lipids in viral replication and pathogenesis and in this context explore the development of broad-spectrum antiviral therapies. We specifically welcome articles (Reviews, Perspectives and Original Research articles) that:
· Investigate the molecular mechanisms by which disturbance of cellular lipid homeostasis affects viral replication;
· Comparative studies that focus on the identification of cellular lipid targets shared by different viruses in their replication for the development of broad-spectrum antiviral therapies;
· Investigate the clinical relevance of the disruption of the cellular lipid homeostasis during viral infections.

The Guest Editors of this Research Topic encourage interested individuals or groups to submit an abstract to this collection. However, please know that abstract submission is not mandatory before sending a manuscript. Manuscript submission deadline: 30 June 2021.

Keywords: fatty acids, cholesterol, lipid droplets, viral replication, viral pathogenesis, antiviral development

Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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