Evolución del parvovirus canino y la emergencia de la variante 2c en Sudamérica: Perspectivas virológicas y epidemiológicas

Abstract

Since its emergence in the late 1970´s, canine parvovirus type 2 (CPV-2) has undergone significant evolution, giving rise to successive antigenic variants CPV-2a, CPV-2b, and more recently, CPV-2c, which have modified both the pathogenicity and the infection spectrum. This editorial addresses the evolution of CPV from virological and epidemiological perspectives, with a special emphasis on South America, and analyzes aspects of immune responses and vaccination strategies against variant 2c. CPV-2 emerged in 1978 as a highly virulent canine pathogen originating from a feline virus, the feline panleukopenia virus, through a species-jump event. It rapidly disseminated worldwide, causing devastating epidemics in puppies1,2. The genomic evolution of CPV-2 was remarkably swift, partly due to a mutation rate approximating 10-4 per site per year, comparable to some RNA viruses, potentially explaining the generation of new variants with substantial antigenic differences3-5. These variants, designated CPV-2a and CPV-2b, emerged in the early 1980´s, progressively displacing the original virus, increasing infectivity and broadening the host range6-9. With the appearance of the CPV-2c variant in 2000, a key modification occurred at residue 426 of the VP2 protein (from Asp to Glu), affecting neutralizing antibody recognition and presenting new challenges for epidemiological control and vaccine efficacy3,10,11.