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Published on: December 3, 2013
Canine Coronavirus Activates Aryl Hydrocarbon Receptor during In Vitro Infection
Claudia Cerracchio1, Francesco Serra2, Maria Grazia Amoroso2
1Department of Veterinary Medicine and Animal Production, University of Naples Federico II, 80137 Naples, Italy.
Abstract:
The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that interacts with substrates, including microbial metabolites. Recent advances reveal that AhR is involved in the host response to coronaviruses (CoVs) infection. Particularly, AhR antagonists decrease the expression of angiotensin-converting enzyme 2 (ACE2) via AhR up-regulation, resulting in suppression of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection in mammalian cells. Herein, we report that AhR is expressed in canine fibrosarcoma (A72) cells, where it is considerably activated by infection with genotype II of canine coronavirus (CCoV-II). The pharmacological inhibition of AhR, by CH223191, suppressed cell death signs and increased cell viability. Furthermore, the AhR antagonist induced a meaningful decline in virus yield, accompanied by the inhibition of the expression of viral nuclear protein (NP). Fascinatingly, during CCoV infection, a novel co-expression of NP and AhR expression was found. Taken together, our preliminary findings show that infection with CCoV activates AhR, and pharmacologic AhR inhibition reduces CCoV replication, identifying AhR as a possible candidate target for CCoV antiviral therapy.
Insights
Canine coronavirus (CCoV) infection activates the aryl hydrocarbon receptor (AhR). Inhibiting AhR with CH223191 reduced CCoV replication and cell death, suggesting AhR as a potential antiviral target.
Area of Science:
- Virology
- Immunology
- Molecular Biology
Background:
- The aryl hydrocarbon receptor (AhR) is a transcription factor involved in host responses to viral infections.
- AhR antagonists have shown potential in suppressing SARS-CoV-2 infection by downregulating ACE2 expression.
- Canine coronavirus (CCoV) is a significant pathogen affecting canine health.
Purpose of the Study:
- To investigate the role of AhR in CCoV-II infection in canine fibrosarcoma (A72) cells.
- To evaluate the therapeutic potential of AhR inhibition against CCoV-II.
Main Methods:
- Expression of AhR in A72 cells was confirmed.
- Cells were infected with CCoV-II and treated with the AhR antagonist CH223191.
- Cell viability, cell death, viral nuclear protein (NP) expression, and virus yield were assessed.
Main Results:
- CCoV-II infection significantly activated AhR in A72 cells.
- Pharmacological inhibition of AhR by CH223191 suppressed CCoV-II-induced cell death and enhanced cell viability.
- AhR inhibition led to a significant reduction in viral yield and inhibited the expression of viral NP.
- A novel co-expression of NP and AhR was observed during CCoV infection.
Conclusions:
- CCoV infection activates AhR in canine cells.
- Pharmacological inhibition of AhR effectively reduces CCoV replication and viral load.
- AhR represents a promising therapeutic target for developing antiviral strategies against CCoV infections.
