Abstract
BACKGROUND AND AIM: Canine parvovirus 2 (CPV-2) is a highly contagious virus that infects wild and domestic canines. Despite the use of a routine vaccination protocol, it is endemic in Iraq. The genetic drift of CPV-2 is a major issue worldwide because it abrogates virus control. In Iraq, there is a knowledge gap regarding the genetic sequences of asymptomatic and symptomatic CPV-2 cases. Therefore, this study aimed to perform a genetic analysis of viral capsid protein 1 (VP1) and viral capsid protein 2 (VP2), two major capsid-encoding genes, to demonstrate the possible role of certain mutations in triggering infection. MATERIALS AND METHODS: Symptomatic and asymptomatic cases (n = 100/each) were tested by a polymerase chain reaction targeting VP1 and VP2 genes. RESULTS: The analysis revealed numerous synonymous and nonsynonymous mutations in VP1 and VP2 and in the intergenic sequence. CONCLUSION: The study identified significant genetic mutations in VP1, VP2, and the intergenic regions of CPV-2 in symptomatic and asymptomatic cases in Iraq. These mutations may contribute to the virus's ability to evade control measures such as vaccination. These findings indicate that CPV-2 polymorphisms can influence the clinical state of the disease and/or trigger infection. Understanding these genetic variations provides critical insights into CPV-2 pathogenesis and could inform improved vaccination strategies to mitigate the virus's impact in endemic regions.