1. Involvement of canine parvovirus in mRNA expression levels of key lectins and caspases in blood leukocytes.
- Author
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Neyestani N, Madani K, Shirani D, and Mehrzad J
- Subjects
- Animals, Dogs, RNA, Messenger genetics, RNA, Messenger metabolism, Lectins genetics, Male, Female, Parvovirus, Canine genetics, Parvoviridae Infections veterinary, Parvoviridae Infections virology, Parvoviridae Infections immunology, Dog Diseases virology, Dog Diseases blood, Leukocytes metabolism, Caspases genetics, Caspases metabolism
- Abstract
Canine parvovirus disease (CPVD) is one of the most common causes of viral diarrhea in dogs. The disease has a mortality rate of up to 90% if left untreated, and can cause gastroenteritis, vomiting, mucoid/hemorrhagic diarrhea, lymphopenia and even immunosuppression. Based on the effects of canine parvovirus type 2 (CPV-2) on the immune system, we investigated the effects of the CPV-2 on hematological indices and the expression of certain immune molecules in blood leukocytes of CPV-positive and non-CPV dogs. The dogs were (para)clinically evaluated, and their disease status was confirmed by antigen rapid detection kits and polymerase chain reaction (PCR). To elucidate the nature of the immunosuppression seen in CPVD, we investigated the expression of caspases 3/7 and 9, and some lectin family molecules such as galectin-1 (important in viral adhesion) and Mincle (macrophage‑inducible C‑type lectin receptor), in blood leukocytes using reverse transcription quantitative PCR (RT-qPCR). We observed remarkable lymphopenia, lower Hb concentration and higher red blood cell distribution width (RDW) value in CPV-positive dogs. No significant changes in expression of caspases 3/7 and 9 were detected, but galectin-1 and Mincle showed remarkable down and up-regulation, respectively. This proves that the immunosuppression seen in most CPVD is not caused by lymphocyte apoptosis in blood, and that Mincle is partially involved in the immune response to CPV-2. The observed changes in galectin-1 and Mincle may be a defense mechanism against parvovirus by potentially preventing the parvovirus from adhering to the cells. Further research is, nonetheless, needed to elucidate the possible roles of these molecules in CPV-2 pathogenesis and the immune system's response to parvovirus., Competing Interests: Declarations Competing interests The authors declare no competing interests., (© 2024. The Author(s), under exclusive licence to Springer Nature B.V.)
- Published
- 2024
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