Sendai virus

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Sendai virus
Virus classification
Group: Group V ((-)ssRNA)
Order: Mononegavirales
Family: Paramyxoviridae
Subfamily: Paramyxovirinae
Genus: Respirovirus
Type species
Sendai virus

Sendai virus (SeV), 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,[1] a group of viruses featuring, notably, the genera Morbillivirus and Rubulavirus. SeV is a member of the paramyxovirus subfamily Paramyxovirinae, genus Respirovirus, members of which primarily infect mammals.[2]

SeV is responsible for a highly transmissible respiratory tract infection in mice, hamsters, guinea pigs, rats, and occasionally pigs, 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.[1] Sublethal exposure to SeV can promote long-lasting immunity to further lethal doses of SeV.[3]

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.

Diagnosis and Prophylaxis[edit]

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).[4]

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.[5]

Eaton et al. advises that, when controlling an outbreak of SeV, disinfecting the laboratory environment and vaccinating the breeders, as well as eliminating infected animals and screening incoming animals, should clear the problem very quickly. Imported animals should be vaccinated with SeV and placed in quarantine, while, in the laboratory environment, breeding programs should be discontinued, and the non-breeding adults isolated for two months.[6]

Symptoms[edit]

  • Sneezing
  • Hunched posture
  • Respiratory distress
  • Porphyrin discharge from eyes and/or nose
  • Lethargy
  • Failure to thrive in surviving babies and young rats
  • Anorexia

Sendai Fusion[edit]

One recognized feature of the Sendai virus, shared with members of its genus, is the ability to induce syncytia formation in vitro in eukaryotic colonies. The mechanism for this process is fairly well understood and is very similar to the fusion process employed by the virion to facilitate cellular entry. The activities of the receptor binding hemagglutinin-neuraminidase protein is solely responsible for inducing close interaction between the virus envelope and the cellular membrane. However, it is the F protein (one of many membrane fusion proteins) that, when triggered by local dehydration[7] and a conformation change in the bound HN protein,[8] actively inserts into the cellular membrane, which causes the envelope and the membrane to merge, followed shortly by virion entry. When the HN and F protein are manufactured by the cell and expressed on the surface, the same process may occur between adjacent cells, causing extensive membrane fusion and resulting in the formation of a syncytium.[9]

This behavior of SeV was utilized by Köhler and Milstein, who published an article in 1975 outlining a revolutionary method of manufacturing monoclonal antibodies. In need of a reliable method to produce large quantities of a specific antibody, the two merged a monoclonal B cell, exposed to a chosen antigen, and a myeloma tumor cell to produce hybridomas, capable of being grown indefinitely and of producing significant amounts of an antibody specifically targeting the chosen antigen. Though more efficient methods of creating such hybrids have since been found, Köhler and Milstein first used Sendai virus to create their revolutionary cells.[10]

References[edit]

  1. ^ a b Faísca, P; Desmecht D (Mar 8, 2006). "Sendai virus, the mouse parainfluenza type 1: a longstanding pathogen that remains up-to-date.". Res Vet Sci 82 (1): 115–25. doi:10.1016/j.rvsc.2006.03.009. PMID 16759680. 
  2. ^ "Paramyxoviridae". International Union of Microbiological Societies, Virology Division. Reviewed on July 15, 2005. Retrieved 2007-06-13. 
  3. ^ López, CB; Yount JS; Hermesh T; Moran TM (May 2006). "Sendai Virus Infection Induces Efficient Adaptive Immunity Independently of Type I Interferons.". J Virol 80 (9): 4538–45. doi:10.1128/JVI.80.9.4538-4545.2006. PMC 1472017. PMID 16611914. 
  4. ^ Kraft, V; Meyer B (June 1986). "Diagnosis of murine infections in relation to test methods employed.". Lab Anim Sci 36 (3): 271–6. PMID 3014210. 
  5. ^ Fox, James G. (2007). The Mouse in Biomedical Research, 2nd Edition. Burlington: Academic Press. pp. 281–309. 
  6. ^ Eaton, GJ; Lerro A; Custer RP; Crane AR (August 1982). "Eradication of Sendai pneumonitis from a conventional mouse colony.". Lab Anim Sci 32 (4): 384–6. PMID 6292576. 
  7. ^ Hoekstra, D; Klapper K; Hoff H; Nir S (April 1989). "Mechanism of fusion of Sendai virus: role of hydrophobic interactions and mobility constraints of viral membrane protein.". J Biol Chem 264 (12): 6786–92. PMID 2540161. 
  8. ^ Takimoto, T; Taylor GL; Connaris HC; Crennell SJ; Portner A (December 2002). "Role of the hemagglutinin-neuraminidase protein in the mechanism of paramyxovirus-cell membrane fusion.". J Virol 76 (24): 13028–33. doi:10.1128/JVI.76.24.13028-13033.2002. PMC 136693. PMID 12438628. 
  9. ^ Novick, SL; Hoekstra D (October 1988). "Membrane penetration of Sendai virus glycoproteins during the early stages of fusion with liposomes as determined by hydrophobic photoaffinity labeling.". Proc Natl Acad Sci USA 85 (20): 7433–7. doi:10.1073/pnas.85.20.7433. PMC 282205. PMID 2845406. 
  10. ^ Köhler, G; Milstein C (March 2005). "Continuous cultures of fused cells secreting antibody of predefined specificity.". J Immunol 17 (5): 2453–5. PMID 15728446. 
  • Simon AY, Moritoh K, Torigoe D, Asano A, Sasaki N, Agui T. Multigenic control of resistance to Sendai virus infection in mice.Infect Genet Evol. 2009 Dec;9(6):1253–9 PMID:19733691[PubMed - indexed for MEDLINE]

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