“Sendai virus”的意思、由来-开放百科全书

SeV is responsible for a highly transmissible respiratory tract infection in mice, hamsters, guinea pigs, rats, and occasionally pigs, and marmosets^[3] 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.^[4]

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.

Symptoms

Sendai Fusion

One recognized feature of the Sendai virus, shared with members of its genus, is the ability to induce syncytia formation in vitro in eukaryotic cell cultures. 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^[5] and a conformation change in the bound HN protein,^[6] 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.^[7]

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.^[8]

Diagnosis and Prophylaxis

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).^[9]

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.^[10]

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.^[11]

References

1. ^¹{{cite journal | last = Faísca | first = P |author2=Desmecht D | title = Sendai virus, the mouse parainfluenza type 1: a longstanding pathogen that remains up-to-date. | journal = Res Vet Sci | volume = 82 | pages = 115–25 | date=Mar 8, 2006 | pmid = 16759680 | url= http://linkinghub.elsevier.com/retrieve/pii/S0034-5288(06)00070-1 | doi = 10.1016/j.rvsc.2006.03.009 | issue = 1}}
2. ^{{cite web | url = http://phene.cpmc.columbia.edu/Ictv/fs_param.htm | title = Paramyxoviridae | accessdate = 2007-06-13 | date = July 15, 2005 | publisher = International Union of Microbiological Societies, Virology Division}}
3. ^{{Cite journal|last=Flecknell, P. A. |display-authors=etal |year=1983|title=Respiratory disease associated with parainfluenza type 1 (Sendai) virus in a colony of marmosets (C. jacchus).|url=|journal=Laboratory Animals|volume=17|issue=2|pages=111–113|via=|doi=10.1258/002367783780959448|pmid=6306336}}
4. ^{{cite journal | last = López | first = CB |author2=Yount JS |author3=Hermesh T |author4=Moran TM | title = Sendai Virus Infection Induces Efficient Adaptive Immunity Independently of Type I Interferons. | journal = J Virol | volume = 80 | issue = 9 | pages = 4538–45 |date=May 2006 | pmid = 16611914 | doi = 10.1128/JVI.80.9.4538-4545.2006 | pmc = 1472017}}
5. ^{{cite journal | last = Hoekstra | first = D |author2=Klapper K |author3=Hoff H |author4=Nir S | title = Mechanism of fusion of Sendai virus: role of hydrophobic interactions and mobility constraints of viral membrane protein. | journal = J Biol Chem | volume =264 | issue = 12 | pages = 6786–92 |date=April 1989 | pmid = 2540161 }}
6. ^{{cite journal | last = Takimoto | first = T |author2=Taylor GL |author3=Connaris HC |author4=Crennell SJ |author5=Portner A | title = Role of the hemagglutinin-neuraminidase protein in the mechanism of paramyxovirus-cell membrane fusion. | journal = J Virol | volume =76 | issue = 24 | pages = 13028–33 |date=December 2002 | pmid = 12438628 | doi = 10.1128/JVI.76.24.13028-13033.2002 | pmc = 136693 }}
7. ^{{cite journal | last = Novick | first = SL |author2=Hoekstra D | title = Membrane penetration of Sendai virus glycoproteins during the early stages of fusion with liposomes as determined by hydrophobic photoaffinity labeling. | journal = Proc Natl Acad Sci USA | volume =85 | issue = 20 | pages = 7433–7 |date=October 1988 | pmid = 2845406 | doi = 10.1073/pnas.85.20.7433 | pmc = 282205 }}
8. ^{{cite journal | last = Köhler | first = G |author2=Milstein C | title = Continuous cultures of fused cells secreting antibody of predefined specificity. | journal = Nature | volume =256 | issue = 5 | pages = 495–497 |date=August 1975 | pmid = 1172191 | doi=10.1038/256495a0}}
9. ^{{cite journal | last = Kraft | first = V |author2=Meyer B | title = Diagnosis of murine infections in relation to test methods employed. | journal = Lab Anim Sci | volume =36 | issue = 3 | pages = 271–6 |date=June 1986 | pmid = 3014210 }}
10. ^{{cite book|last=Fox|first=James G.|title=The Mouse in Biomedical Research, 2nd Edition|year=2007|publisher=Academic Press|location=Burlington|pages=281–309|url=http://www.sciencedirect.com/science/article/pii/B978012369454650039X}}
11. ^{{cite journal | last = Eaton | first = GJ |author2=Lerro A |author3=Custer RP |author4=Crane AR | title = Eradication of Sendai pneumonitis from a conventional mouse colony. | journal = Lab Anim Sci | volume =32 | issue = 4 | pages = 384–6 |date=August 1982 | pmid = 6292576 }}

Symptoms

Sendai Fusion

Diagnosis and Prophylaxis

References

External links