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Sendai virus

Sendai virus (SeV)
Virus classification
Group: Group V ((−)ssRNA)
Order: Mononegavirales
Family: Paramyxoviridae
Genus: Respirovirus
Species: Sendai virus

Sendai virus (SeV), previously also known as murine parainfluenza virus type 1 or hemagglutinating virus of Japan (HVJ), is a negative sense, single-stranded RNA virus of the family Paramyxoviridae, a group of viruses featuring, notably, the genera Morbillivirus and Rubulavirus. SeV is a member of genus Respirovirus, members of which primarily infect mammals.

SeV is responsible for a highly transmissible respiratory tract infection in mice, hamsters, guinea pigs, rats, and occasionally pigs, and marmosets with infection passing through both air and direct contact routes. The virus can be detected in mouse colonies worldwide, generally in suckling to young adult mice. Epizootic infections of mice are usually associated with a high mortality rate, while enzootic disease patterns suggest that the virus is latent and can be cleared over the course of a year. Sublethal exposure to SeV can promote long-lasting immunity to further lethal doses of SeV.

A novel and well-recognized use for SeV is the fusion of eukaryotic cells, especially to produce hybridoma cells capable of manufacturing monoclonal antibodies in large quantities.

SeV induces lesions within the respiratory tract, usually associated with bacterial inflammation of the trachea and lung (tracheitis and bronchopneumonia, respectively). However, the lesions are limited, and aren't indicative solely of SeV infection. Detection, therefore, makes use of SeV-specific antigens in several serological methods, including ELISA, immunofluorescence, and hemagglutination assays, with particular emphasis on use of the ELISA for its high sensitivity (unlike the hemagglutination assay) and its fairly early detection (unlike the immunofluorescence assay).

In a natural setting, the respiratory infection of Sendai virus in mice is acute. From the extrapolation of the infection of laboratory mice, the presence of the virus may first be detected in the lungs 48 to 72 hours following exposure. As the virus replicates in the respiratory tract of an infected mouse, the concentration of the virus grows most quickly during the third day of infection. After that, the growth of the virus is slower but consistent. Typically, the peak concentration of the virus is on the sixth or seventh day, and rapid decline follows that by the ninth day. A fairly vigorous immune response mounted against the virus is the cause of this decline. The longest period of detected presence of the virus in a mouse lung is fourteen days after infection.


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