{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Watkins JM"],"funding":["National Institute of General Medical Sciences","NIGMS NIH HHS"],"pagination":["114694"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11957735"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["43(9)"],"pubmed_abstract":["Subgenomic flavivirus RNAs (sfRNAs) are structured RNAs encoded by flaviviruses that promote viral infection by inhibiting cellular RNA decay machinery. Herein, we analyze sfRNA production and localization using single-molecule RNA fluorescence in situ hybridization (smRNA-FISH) throughout West Nile virus, Zika virus, or dengue virus serotype 2 infection. We observe that sfRNAs are generated during the RNA replication phase of viral infection in the cytosol and accumulate in processing bodies (P-bodies), which contain RNA decay machinery such as XRN1 and Dcp1b. However, upon activation of the host antiviral endoribonuclease, ribonuclease L (RNase L), sfRNAs re-localize to ribonucleoprotein complexes known as RNase L-induced bodies (RLBs). RLB-mediated sequestration of sfRNAs reduces sfRNA association with RNA decay machinery in P-bodies, which coincides with increased viral RNA decay. These findings establish a functional role for RLBs in enhancing the cell-mediated decay of viral RNA by sequestering functional viral RNA decay products."],"journal":["Cell reports"],"pubmed_title":["RNase L-induced bodies sequester subgenomic flavivirus RNAs to promote viral RNA decay."],"pmcid":["PMC11957735"],"funding_grant_id":["R35 GM151249"],"pubmed_authors":["Watkins JM","Burke JM"],"additional_accession":[]},"is_claimable":false,"name":"RNase L-induced bodies sequester subgenomic flavivirus RNAs to promote viral RNA decay.","description":"Subgenomic flavivirus RNAs (sfRNAs) are structured RNAs encoded by flaviviruses that promote viral infection by inhibiting cellular RNA decay machinery. Herein, we analyze sfRNA production and localization using single-molecule RNA fluorescence in situ hybridization (smRNA-FISH) throughout West Nile virus, Zika virus, or dengue virus serotype 2 infection. We observe that sfRNAs are generated during the RNA replication phase of viral infection in the cytosol and accumulate in processing bodies (P-bodies), which contain RNA decay machinery such as XRN1 and Dcp1b. However, upon activation of the host antiviral endoribonuclease, ribonuclease L (RNase L), sfRNAs re-localize to ribonucleoprotein complexes known as RNase L-induced bodies (RLBs). RLB-mediated sequestration of sfRNAs reduces sfRNA association with RNA decay machinery in P-bodies, which coincides with increased viral RNA decay. These findings establish a functional role for RLBs in enhancing the cell-mediated decay of viral RNA by sequestering functional viral RNA decay products.","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Sep","modification":"2026-05-29T16:40:15.997Z","creation":"2026-05-17T03:07:26.939Z"},"accession":"S-EPMC11957735","cross_references":{"pubmed":["39196777"],"doi":["10.1016/j.celrep.2024.114694"]}}