Parainfluenza virus 5 (PIV5) belongs to the family Paramyxoviridae and the genus Rubulavirus. It is an enveloped, single-stranded, negative-sense RNA virus. The virus was first discovered in canine populations and was historically referred to as simian virus 5 (SV5) or canine parainfluenza virus. It is a pathogen widely found in multiple mammalian species. PIV5 is broadly distributed in nature but typically causes asymptomatic or mild respiratory infections, which is why its epidemiological significance has long been underrecognized. The virus exhibits high genetic stability and favorable safety characteristics, making it an important model system for the development of novel vaccine platforms.

The Parainfluenza virus 5 virion is pleomorphic, typically spherical, with a diameter of approximately 150–250 nm, and exhibits typical paramyxovirus structural features. The outermost layer of the virion is a lipid envelope derived from the host cell membrane. The envelope surface is regularly studded with two key viral glycoprotein spikes: the hemagglutinin-neuraminidase (HN) protein and the fusion (F) protein. The HN protein possesses both receptor-binding and neuraminidase activities, enabling it to recognize sialic acid receptors on the host cell surface and facilitate viral uncoating. The F protein mediates the fusion of the viral envelope with the host cell membrane. Beneath the envelope lies the matrix (M) protein layer, which plays a critical role in maintaining viral morphology and regulating viral assembly. The viral core consists of a helical ribonucleoprotein complex formed by the tightly bound viral genomic RNA and the nucleoprotein (NP), phosphoprotein (P), and large polymerase (L) proteins. The PIV5 genome is a non-segmented, single-stranded, negative-sense RNA approximately 15,246 nucleotides in length. It follows the gene order "3'-NP-P/V/I-M-F-SH-HN-L-5'" and encodes at least seven structural proteins and two non-structural proteins (V and I proteins). Among these, the V protein plays a significant role in modulating the host's innate immune responses. The virus completes its replication and assembly within the host cell cytoplasm and is released via budding.

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