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Zebrafish C-reactive protein isoforms inhibit SVCV replication by blocking autophagy through interactions with cell
Melissa Bello-Perez1, Patricia Pereiro2, Julio Coll3
1Instituto de Investigación, Desarrollo e Innovación en Biotecnología Sanitaria de Elche (IDiBE), Miguel Hernández University (UMH), Elche, 03202, Spain.
Scientific Reports
|January 19, 2020
Summary
Zebrafish CRP1-7 protein inhibits fish rhabdovirus by disrupting cellular autophagy. This antiviral mechanism involves altering cholesterol, reactive oxygen species, and lysosomal pH, ultimately blocking viral entry.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Zebrafish C-reactive protein-like protein (CRP1-7) exhibits antiviral activity against spring viraemia of carp rhabdovirus (SVCV).
- The precise mechanisms underlying CRP1-7's antiviral effects require elucidation.
Purpose of the Study:
- To investigate the molecular mechanisms of CRP1-7's antiviral activity against SVCV.
- To determine if CRP1-7 interferes with viral attachment, fusion, or host interferon responses.
- To explore the role of autophagy and cholesterol in CRP1-7's antiviral action.
Main Methods:
- Utilized SVCV-infected fish models and cell cultures.
- Assessed viral replication, attachment, and fusion assays.
- Investigated host interferon response and autophagic processes.
- Employed cholesterol-modulating agents like methyl-β-cyclodextrin and 25-hydroxycholesterol.
Main Results:
- CRP1-7 did not block viral attachment or fusion directly, nor did it stimulate the host interferon system.
- Antiviral protection was primarily mediated by the inhibition of host autophagic processes.
- Cholesterol-complexing agents and 25-hydroxycholesterol mimicked CRP1-7's antiviral effects by modulating autophagy.
- CRP1-7 disturbed cellular cholesterol ratios, impacting reactive oxygen species (ROS) and increasing lysosomal pH.
Conclusions:
- CRP1-7 confers antiviral protection against SVCV mainly by inhibiting autophagy.
- The mechanism involves disrupting cellular cholesterol homeostasis, leading to altered ROS levels and increased lysosomal pH.
- Elevated lysosomal pH directly inhibits SVCV replication by affecting the pH-dependent membrane fusion of the viral glycoprotein G.
