CPV2

Canine parvovirus type 2 (CPV2, colloquially parvo) is a contagious virus mainly affecting dogs, and thought to originate in cats. The current consensus is that the feline panleukopenia virus mutated into CPV2. Parvo is highly contagious and is spread from dog to dog by direct or indirect contact with their feces. Vaccines can prevent this infection, but mortality can reach 91% in untreated cases. Treatment often involves veterinary hospitalization. Canine parvovirus may infect other mammals including foxes, wolves, cats, and skunks; however, it will not infect humans.

Full Name

Canine parvovirus type 2

Function

Capsid protein self-assembles to form an icosahedral capsid with a T=1 symmetry, about 22 nm in diameter, and consisting of 60 copies of two size variants of the capsid proteins, VP1 and VP2, which differ by the presence of an N-terminal extension in the minor protein VP1. The capsid encapsulates the genomic ssDNA. Capsid proteins are responsible for the attachment to host cell receptor TFRC. This attachment induces virion internalization predominantly through clathrin-endocytosis. Binding to the host receptors also induces capsid rearrangements leading to surface exposure of VP1 N-terminus, specifically its phospholipase A2-like region and nuclear localization signal(s). VP1 N-terminus might serve as a lipolytic enzyme to breach the endosomal membrane during entry into host cell. Intracytoplasmic transport involves microtubules and interaction between capsid proteins and host dynein. Exposure of nuclear localization signal probably allows nuclear import of capsids (By similarity).

Biological Process

Adhesion receptor-mediated virion attachment to host cell Source: UniProtKB-KW
Clathrin-dependent endocytosis of virus by host cell Source: UniProtKB-KW
Entry receptor-mediated virion attachment to host cell Source: UniProtKB-KW
Microtubule-dependent intracellular transport of viral material towards nucleus Source: UniProtKB-KW
Permeabilization of host organelle membrane involved in viral entry into host cell Source: UniProtKB-KW
Viral entry via permeabilization of inner membrane Source: UniProtKB-KW
Viral penetration into host nucleus Source: UniProtKB-KW