Table 1.
Anti-ssRNA viral mechanisms targeted by RNases
| RNases | Proposed Mechanism (tested in vitro or in vivo)a | ssRNA Viruses |
Refs | ||
|---|---|---|---|---|---|
| Nameb | ENVc | Sense | |||
| RNase A | • Inhibits replication (in PHA-stimulated T cell blasts) | HIV-1 | Y | + | [223] |
| RNase 2 /EDN | • Inhibits replication (in PHA-stimulated T cell blasts) | HIV-1 | Y | + | [204,223] |
| • Degrades viral RNA (in total RNA from infected ACH2 cells) | |||||
| • Ribonuclease-dependent activity (in RhMk cells) | PIV | Y | - | [19] | |
| • Ribonuclease-dependent activity (in HEp-2 cells) | RSV-B | Y | - | [19,212] | |
| • A unique loop helps its interaction with viral capsid and penetration into the virion (in HEp-2 cells) | |||||
| RNase 3 /ECP | • Ribonuclease-dependent activity (in HEp-2 and THP-1 cells) | RSV-B | Y | - | [208,209] |
| RNase 5 /ANG | • Inhibits replication (in PHA-stimulated T cell blasts or PBMCs) | HIV-1 | Y | + | [220,223] |
| BS-RNase | • Inhibits replication (in H9 leukaemia cells) | HIV-1 | Y | + | [224] |
| Onconase | • Inhibits replication (in H9 and U937 leukaemia cells) | HIV-1 | Y | + | [224,230,231] |
| • Inhibits replication by removal of the transcription primer (tRNA synthesized in vitro) | |||||
| RNase L | • OAS/RNase L pathway is necessary for IFN-α but not for IFN- γ to inhibit viral replication (pancreatic islet from mouse) | CV-B4 | N | + | [268] |
| • Inhibits viral RNA synthesis (in LS1 cells) | EMCV | N | + | [20,247,269,270] | |
| • Increases the antiviral activity of IFN when overexpressed (in LS1 cells) | |||||
| • RNase L helps to amplify IFN-β signalling (in mouse) | |||||
| • Autophagy (in MEFs) | |||||
| • Apoptosis | |||||
| • UA and UU dinucleotides in viral RNA is the main cleavage site of RNase L (HCV mRNA synthesized in vitro) | HCV | Y | + | [244,271] | |
| • A small RNA cleaved by RNase L activates RIG-I and thereby promotes IFN-β response (in mouse) | |||||
| • Inhibits HIV-1 replication by 8 times (in Jurkat cells) | HIV-1 | Y | + | [245] | |
| • RNase L cleaves viral RNAs in absence of viral resistance protein NS1 (in A549 cells) | IAV | Y | - | [272] | |
| • IFN-γ-mediated inhibition in human epithelial cells involves the OAS/RNase L pathway (in HEp-2 cells) | RSV | Y | - | [246] | |
| • RNase L helps to amplify IFN-β signalling (in mouse) | SeV | Y | - | [20,242,273] | |
| • SGs formation (in HT1080 cells) | |||||
| • Autophagy (in MEFs) | |||||
| • Contributes to IFN-α/β–mediated protection (in MEFs) | SINV | Y | + | [274,275] | |
| • Interferes with the synthesis of minus strands of heat-resistant strain (in MEFs) | |||||
| • Autophagy (in MEFs) | VSV | Y | - | [247] | |
| • Cleaves viral genomic RNA (in vitro) | WNV | Y | + | [276,277] | |
| • Contributes to IFN-mediated protection (in CD11b+ cells) | |||||
| Regnase/MCPIP1 | • Inhibits replication (in hepatoma cells) | HCV | Y | + | [278] |
| • Degrades viral RNA (in vitro) | |||||
| • Degrades viral RNA (in vitro) | DENV | Y | + | [263] | |
| JEV | Y | + | |||
| RNase P | • Cleaves HCV RNA transcripts (in vitro) | HCV | Y | + | [264] |
| Binase | • Inhibits replication (in MRC5 cells) | MERS-CoV | Y | + | [267] |
| • Direct action on the viral mRNA (in A549 and MDCK-II cells) | IAV | Y | - | [265,266] | |
aA549: human lung adenocarcinoma epithelial cells; HEp-2: human laryngeal carcinoma/human type 2 epithelial cells; MDCK-II: Madin-Darby canine kidney epithelial cells; MEF: mouse embryonic fibroblasts; MRC5: human fetal lung fibroblasts; PBMC: peripheral blood mononuclear cells; PHA: phytohemagglutinin; RhMk: rhesus monkey kidney; THP-1: a human monocytic cell line.
bCV-B4: Coxsackie virus B4; DENV: Dengue virus; EMCV: Encephalomyocarditis virus; HCV: Hepatitis C virus; HIV: Human Immunodeficiency virus; IAV: Influenza A virus; JEV: Japanese Encephalitis virus; MERS-CoV: Middle East Respiratory Syndrome Coronavirus; PIV: Human Parainfluenza virus; RSV: Respiratory Syncytial virus; SeV: Sendai virus; SINV: Sindbis virus; VSV: Vesicular Stomatitis virus; WNV: West Nile virus.
cENV: Enveloped; Y: Yes; N: No.