Abstract
Frog virus 3 (FV3) is the type species of the genus Ranavirus (family Iridoviridae). FV3 and FV3-like viruses are globally distributed infectious agents with the capacity to replicate in three vertebrate classes (teleosts, amphibians, and reptiles). At the cellular level, FV3 and FV3-like viruses can infect cells from virtually all vertebrate classes. To date, the cellular receptors that are involved in the FV3 entry process are unknown. Class A scavenger receptors (SR-As) are a family of evolutionarily conserved cell-surface receptors that bind a wide range of chemically distinct polyanionic ligands and can function as cellular receptors for other DNA viruses, including vaccinia virus and herpes simplex virus. The present study aimed to determine whether SR-As are involved in FV3 cellular entry. By using well-defined SR-A competitive and non-competitive ligand-blocking assays and absolute qPCR, we demonstrated that the SR-A competitive ligands drastically reduced the quantities of cell-associated viral loads in frog cells. Moreover, inducing the expression of a human SR-AI in an SR-A null cell line significantly increased FV3–cell association. Together, our results indicate that SR-As are utilized by FV3 during the cellular entry process.
Highlights
Ranaviruses (RVs) are members of the family Iridoviridae with large double-stranded DNA genomes and are currently considered to be important emerging pathogens of cold-blooded vertebrates around the globe [1]
Guo et al recently showed that tiger frog virus and infectious spleen and kidney necrosis virus enter cells via mechanisms that share many features with caveolae-mediated endocytosis [19,20]
BHK-21-derived Frog virus 3 (FV3) was used for the X. laevis macrophage experiments, while EPC-derived FV3 was used for infections with the other frog and human cell lines
Summary
Ranaviruses (RVs) are members of the family Iridoviridae with large double-stranded DNA (dsDNA) genomes and are currently considered to be important emerging pathogens of cold-blooded vertebrates around the globe [1]. Guo et al recently showed that tiger frog virus (an amphibian ranavirus that is genetically similar to FV3 and STIV) and infectious spleen and kidney necrosis virus (a fish iridovirus belonging to the genus Megalocytivirus) enter cells via mechanisms that share many features with caveolae-mediated endocytosis [19,20]. SR-As are present in all vertebrates and absent in invertebrates [33], ubiquitously expressed by many distinct cell types [27,29,32,34,35], function at a wide range of temperatures, exhibit evolutionarily conserved ligand binding properties [27,34,35,36,37], and facilitate clathrin/caveola-mediated endocytosis and macropinocytosis [38,39,40]. In light of the above, in the present study we examined the putative roles of SR-As as receptors for FV3 cellular entry into an array of amphibian cell types
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