Journal
VIRULENCE
Volume 12, Issue 1, Pages 1011-1021Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/21505594.2021.1908742
Keywords
Porcine deltacoronavirus; porcine reproductive and respiratory syndrome virus; coinfection; proinflammatory cytokines; pathogenicity
Categories
Funding
- National Key Research and Development Program of China [2018YFD0500103]
- Earmarked Fund for Modern Agroindustry Technology Research System of China [CARS-35]
- National Natural Science Foundation of China [31772759]
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The study showed that coinfection with PRRSV reduced the severity of PDCoV-induced diarrhea, potentially due to an increase in proinflammatory cytokines TNF-alpha, IL-1, and IL-6 in the intestinal microenvironment.
Porcine deltacoronavirus (PDCoV) is a potentially emerging zoonotic pathogen that causes severe diarrhea in young pigs, with a risk of fatal dehydration. Its pathogenicity on neonatal piglet has been previously reported, however, it is less known if the coinfection with immunosuppressive pathogens can influence PDCoV disease manifestation. Here, a coinfection model of PDCoV and porcine reproductive and respiratory syndrome virus (PRRSV), a global-spread immunosuppressive virus, was set to study their interaction. Weaning pigs in the coinfection group were intranasally inoculated with PRRSV NADC30-like virus and latterly orally inoculated with PDCoV at three day-post-inoculation (DPI). Unexpectedly, compared with pigs in the PDCoV single-infected group, the coinfected pigs did not show any obvious diarrhea, as PDCoV fecal shedding, average daily weight gain (ADWG), gross and microscopic lesions and PDCoV IHC scores consistently indicated that PRRSV coinfection lessened PDCoV caused diarrhea. Additionally, three proinflammatory cytokines TNF-alpha, IL-1 and IL-6, which can be secreted by PRRSV infected macrophages, were detected to be highly expressed at the intestine from both PRRSV infected groups. By adding to PDCoV-infected cells, these three cytokines were further confirmed to be able to inhibit the PDCoV replication post its cellular entry. Meanwhile, the inhibition effect of the supernatant from PRRSV-infected PAMs could be obviously blocked by the antagonist of these three cytokines. In conclusion, PRRSV coinfection increased TNF-alpha, IL-1, and IL-6 in the microenvironment of intestines, which inhibits the PDCoV proliferation, leading to lessened severity of diarrhea. The findings provide some new insight into the pathogenesis and replication regulation of PDCoV.
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