Canine coronavirus infection is intensified by 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Abstract

In humans as well as in animals, the toxic contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) stimulates immunosuppression and increases responsiveness to infectious diseases. The relationship between environmental contaminants and different infectious diseases, including COVID-19, has been described. Nevertheless, reports about the potential impact of TCDD on coronaviruses (CoVs) are limited. In this study, the impact of TCDD (0-100 pg/mL) was assessed during infection in vitro with canine coronavirus (CCoV-II), the alphaCoV causing moderate enteric disease in dogs, although genetic alterations may surprisingly generate new dangerous strains. For instance, outbreaks of lethal infections in dogs were related to highly virulent CCoV strains, and cases of pneumonia and malaise in humans were associated with new canine-feline recombinant strains of CCoV, underlining the cross-species spread capability of CoVs. Herein, during CCoV infection, TCDD induced a substantial growth in virus yield and in the expression of viral nucleocapsid protein in infected groups. Infected cells exhibited alterations in cell morphology, extensively enhanced by TCDD. Moreover, in infection, TCDD modulated the protein levels of aryl hydrocarbon receptor (AHR), a signaling responsive to both environmental contaminant and CoVs infections. Overall, our findings showed that TCDD, playing a role in AHR signaling, may worsen CCoV infection.