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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.<ref name=Eaton>{{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 }}</ref>
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.<ref name=Eaton>{{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 }}</ref>


== Sendai virus as an oncolytic agent ==
⚫
==References==
Sendai virus-based anticancer therapy for model<ref>{{Cite journal|last=Saga|first=Kotaro|last2=Kaneda|first2=Yasufumi|date=2015|title=Oncolytic Sendai virus-based virotherapy for cancer: recent advances|url=https://www.ncbi.nlm.nih.gov/pubmed/27512677|journal=Oncolytic Virotherapy|volume=4|pages=141–147|doi=10.2147/OV.S66419|issn=2253-1572|pmc=4918391|pmid=27512677}}</ref>,<ref>{{Cite journal|last=Matveeva|first=O. V.|last2=Kochneva|first2=G. V.|last3=Netesov|first3=S. V.|last4=Onikienko|first4=S. B.|last5=Chumakov|first5=P. M.|date=2015-4|title=Mechanisms of Oncolysis by Paramyxovirus Sendai|url=https://www.ncbi.nlm.nih.gov/pubmed/26085940|journal=Acta Naturae|volume=7|issue=2|pages=6–16|issn=2075-8251|pmc=4463408|pmid=26085940}}</ref> and companion animals<ref name=":0">{{Cite journal|last=Chumakov|first=Peter M.|last2=Matveeva|first2=Olga V.|last3=Soboleva|first3=Alesya V.|last4=Mukhina|first4=Elena V.|last5=Ilyinskaya|first5=Galina V.|date=2018|title=Oncolytic Sendai Virus Therapy of Canine Mast Cell Tumors (A Pilot Study)|url=https://www.frontiersin.org/articles/10.3389/fvets.2018.00116/full|journal=Frontiers in Veterinary Science|language=English|volume=5|doi=10.3389/fvets.2018.00116|issn=2297-1769}}</ref> has been described in several scientific papers. After the virus was first isolated in the early 1950s in Japan<ref>{{Cite journal|last=Ishida|first=N.|last2=Homma|first2=M.|date=1978|title=Sendai virus|url=https://www.ncbi.nlm.nih.gov/pubmed/219669|journal=Advances in Virus Research|volume=23|pages=349–383|issn=0065-3527|pmid=219669}}</ref> there was some concern that the virus causes human respiratory infection, but it was later recognized that Sendai virus infection is host restrictive and the virus is not infectious for humans. Therefore, one of the great advantages of the Sendai virus as a potential oncolytic agent is its safety. Even though the virus is widespread in rodent colonies<ref>{{Cite journal|last=Faísca|first=P.|last2=Desmecht|first2=D.|date=2007-2|title=Sendai virus, the mouse parainfluenza type 1: a longstanding pathogen that remains up-to-date|url=https://www.ncbi.nlm.nih.gov/pubmed/16759680|journal=Research in Veterinary Science|volume=82|issue=1|pages=115–125|doi=10.1016/j.rvsc.2006.03.009|issn=0034-5288|pmid=16759680}}</ref> and has been used in laboratory research for decades<ref>{{Cite journal|last=Nakanishi|first=Mahito|last2=Otsu|first2=Makoto|date=2012-10|title=Development of Sendai Virus Vectors and their Potential Applications in Gene Therapy and Regenerative Medicine|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3504922/|journal=Current Gene Therapy|volume=12|issue=5|pages=410–416|doi=10.2174/156652312802762518|issn=1566-5232|pmc=3504922|pmid=22920683}}</ref>, it has never been observed that it can cause human disease. Moreover, Sendai virus has been used in clinical trials involving both adults<ref>{{Cite journal|last=Slobod|first=Karen S.|last2=Shenep|first2=Jerry L.|last3=Luján-Zilbermann|first3=Jorge|last4=Allison|first4=Kim|last5=Brown|first5=Brita|last6=Scroggs|first6=Ruth Ann|last7=Portner|first7=Allen|last8=Coleclough|first8=Chris|last9=Hurwitz|first9=Julia L.|date=2004-08-13|title=Safety and immunogenicity of intranasal murine parainfluenza virus type 1 (Sendai virus) in healthy human adults|url=https://www.ncbi.nlm.nih.gov/pubmed/15297072|journal=Vaccine|volume=22|issue=23-24|pages=3182–3186|doi=10.1016/j.vaccine.2004.01.053|issn=0264-410X|pmid=15297072}}</ref> and children<ref>{{Cite journal|last=Adderson|first=Elisabeth|last2=Branum|first2=Kristen|last3=Sealy|first3=Robert E.|last4=Jones|first4=Bart G.|last5=Surman|first5=Sherri L.|last6=Penkert|first6=Rhiannon|last7=Freiden|first7=Pamela|last8=Slobod|first8=Karen S.|last9=Gaur|first9=Aditya H.|date=2015-3|title=Safety and Immunogenicity of an Intranasal Sendai Virus-Based Human Parainfluenza Virus Type 1 Vaccine in 3- to 6-Year-Old Children|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4340902/|journal=Clinical and Vaccine Immunology : CVI|volume=22|issue=3|pages=298–303|doi=10.1128/CVI.00618-14|issn=1556-6811|pmc=4340902|pmid=25552633}}</ref> to immunize against human parainfluenza virus type 1, since the two viruses share common antigenic determinants and trigger the generation of cross-reactive neutralizing antibodies. The Sendai virus administration in the form of nasal drops induced the production of neutralizing antibodies to the human virus without any measurable side effects. The results of these trials represent additional evidence of Sendai virus safety for humans.

For cancer studies, it is desirable that the oncolytic virus be non-pathogenic for experimental animals, but the Sendai virus can cause rodent disease, which is a problem for research strategies. Two approaches have been used to overcome this problem and make Sendai virus non-pathogenic for mice and rats. One of these approaches included the creation of a set of genetically modified attenuated viral strains. Representatives of this set were tested on model animals carrying a wide range of transplantable human tumors. It has been shown that they can cause suppression or even eradication of fibrosarcoma<ref>{{Cite journal|last=Hasegawa|first=M.|last2=Nagai|first2=Y.|last3=Iida|first3=A.|last4=Tokusumi|first4=Y.|last5=Fujikawa|first5=S.|last6=Yamamoto|first6=T.|last7=Washizawa|first7=K.|last8=Inoue|first8=M.|last9=Kinoh|first9=H.|date=2004-07|title=Generation of a recombinant Sendai virus that is selectively activated and lyses human tumor cells expressing matrix metalloproteinases|url=https://www.nature.com/articles/3302272|journal=Gene Therapy|language=en|volume=11|issue=14|pages=1137–1145|doi=10.1038/sj.gt.3302272|issn=1476-5462}}</ref>,<ref>{{Cite journal|last=Kinoh|first=Hiroaki|last2=Inoue|first2=Makoto|date=2008-01-01|title=New cancer therapy using genetically-engineered oncolytic Sendai virus vector|url=https://www.ncbi.nlm.nih.gov/pubmed/17981715|journal=Frontiers in Bioscience: A Journal and Virtual Library|volume=13|pages=2327–2334|issn=1093-9946|pmid=17981715}}</ref> neuroblastoma<ref>{{Cite journal|last=Tatsuta|first=K.|last2=Tanaka|first2=S.|last3=Tajiri|first3=T.|last4=Shibata|first4=S.|last5=Komaru|first5=A.|last6=Ueda|first6=Y.|last7=Inoue|first7=M.|last8=Hasegawa|first8=M.|last9=Suita|first9=S.|date=2009-2|title=Complete elimination of established neuroblastoma by synergistic action of gamma-irradiation and DCs treated with rSeV expressing interferon-beta gene|url=https://www.ncbi.nlm.nih.gov/pubmed/18987675|journal=Gene Therapy|volume=16|issue=2|pages=240–251|doi=10.1038/gt.2008.161|issn=1476-5462|pmid=18987675}}</ref>, hepatocellular carcinoma<ref>{{Cite journal|last=Zimmermann|first=Martina|last2=Armeanu-Ebinger|first2=Sorin|last3=Bossow|first3=Sascha|last4=Lampe|first4=Johanna|last5=Smirnow|first5=Irina|last6=Schenk|first6=Andrea|last7=Lange|first7=Sebastian|last8=Weiss|first8=Thomas S.|last9=Neubert|first9=Wolfgang|date=2014|title=Attenuated and protease-profile modified sendai virus vectors as a new tool for virotherapy of solid tumors|url=https://www.ncbi.nlm.nih.gov/pubmed/24598703|journal=PloS One|volume=9|issue=3|pages=e90508|doi=10.1371/journal.pone.0090508|issn=1932-6203|pmc=3944018|pmid=24598703}}</ref>, melanoma, squamous cell and prostate carcinomas<ref>{{Cite journal|last=Yonemitsu|first=Yoshikazu|last2=Ueda|first2=Yasuji|last3=Kinoh|first3=Hiroaki|last4=Hasegawa|first4=Mamoru|date=2008-01-01|title=Immunostimulatory virotherapy using recombinant Sendai virus as a new cancer therapeutic regimen|url=https://www.ncbi.nlm.nih.gov/pubmed/17981677|journal=Frontiers in Bioscience: A Journal and Virtual Library|volume=13|pages=1892–1898|issn=1093-9946|pmid=17981677}}</ref>. Complete eradication of established gliosarcomas in immunocompetent rats has also been observed<ref>{{Cite journal|last=Iwadate|first=Yasuo|last2=Inoue|first2=Makoto|last3=Saegusa|first3=Takashi|last4=Tokusumi|first4=Yumiko|last5=Kinoh|first5=Hiroaki|last6=Hasegawa|first6=Mamoru|last7=Tagawa|first7=Masatoshi|last8=Yamaura|first8=Akira|last9=Shimada|first9=Hideaki|date=2005-05-15|title=Recombinant Sendai virus vector induces complete remission of established brain tumors through efficient interleukin-2 gene transfer in vaccinated rats|url=https://www.ncbi.nlm.nih.gov/pubmed/15897582|journal=Clinical Cancer Research: An Official Journal of the American Association for Cancer Research|volume=11|issue=10|pages=3821–3827|doi=10.1158/1078-0432.CCR-04-1485|issn=1078-0432|pmid=15897582}}</ref>.

Another approach of making Sendai virus non-pathogenic included the short-term treatment of the virions with ultraviolet light. Such treatment causes a loss of the virus replication ability. However, even this replication-deficient virus can induce the cancer cells death and stimulate anti-tumor immunity. It can trigger extensive apoptosis of human glioblastoma cells in culture, and it can efficiently suppress the growth of these cells in model animals<ref>{{Cite journal|last=Tanaka|first=Masahiko|last2=Shimbo|first2=Takashi|last3=Kikuchi|first3=Yasushi|last4=Matsuda|first4=Masahide|last5=Kaneda|first5=Yasufumi|date=2010-04-15|title=Sterile alpha motif containing domain 9 is involved in death signaling of malignant glioma treated with inactivated Sendai virus particle (HVJ-E) or type I interferon|url=https://www.ncbi.nlm.nih.gov/pubmed/19830690|journal=International Journal of Cancer|volume=126|issue=8|pages=1982–1991|doi=10.1002/ijc.24965|issn=1097-0215|pmid=19830690}}</ref>. The ultraviolet light treated virus can also kill human prostate cancer cells in culture<ref>{{Cite journal|last=Qian|first=Miao|last2=Tan|first2=Hai Ming|last3=Yu|first3=Ning|last4=Wang|first4=Tao|last5=Zhang|first5=Quan|date=2018-4|title=Inactivated Sendai Virus Induces ROS-dependent Apoptosis and Autophagy in Human Prostate Cancer Cells|url=https://www.ncbi.nlm.nih.gov/pubmed/29773091|journal=Biomedical and environmental sciences: BES|volume=31|issue=4|pages=280–289|doi=10.3967/bes2018.036|issn=0895-3988|pmid=29773091}}</ref>, <ref>{{Cite journal|last=Kawaguchi|first=Yoshifumi|last2=Miyamoto|first2=Yasuhide|last3=Inoue|first3=Takehiro|last4=Kaneda|first4=Yasufumi|date=2009-05-15|title=Efficient eradication of hormone-resistant human prostate cancers by inactivated Sendai virus particle|url=https://www.ncbi.nlm.nih.gov/pubmed/19173282|journal=International Journal of Cancer|volume=124|issue=10|pages=2478–2487|doi=10.1002/ijc.24234|issn=1097-0215|pmid=19173282}}</ref> and eradicate tumors that originated from these cells in immuno-deficient model animals<ref>{{Cite journal|last=Kawaguchi|first=Yoshifumi|last2=Miyamoto|first2=Yasuhide|last3=Inoue|first3=Takehiro|last4=Kaneda|first4=Yasufumi|date=2009-05-15|title=Efficient eradication of hormone-resistant human prostate cancers by inactivated Sendai virus particle|url=https://www.ncbi.nlm.nih.gov/pubmed/19173282|journal=International Journal of Cancer|volume=124|issue=10|pages=2478–2487|doi=10.1002/ijc.24234|issn=1097-0215|pmid=19173282}}</ref>. Moreover, it can stimulate immunomodulated tumor regression of colon<ref>{{Cite journal|last=Kurooka|first=Masayuki|last2=Kaneda|first2=Yasufumi|date=2007-01-01|title=Inactivated Sendai virus particles eradicate tumors by inducing immune responses through blocking regulatory T cells|url=https://www.ncbi.nlm.nih.gov/pubmed/17210703|journal=Cancer Research|volume=67|issue=1|pages=227–236|doi=10.1158/0008-5472.CAN-06-1615|issn=0008-5472|pmid=17210703}}</ref> and kidney cancers<ref>{{Cite journal|last=Fujihara|first=Atsuko|last2=Kurooka|first2=Masayuki|last3=Miki|first3=Tsuneharu|last4=Kaneda|first4=Yasufumi|date=2008-1|title=Intratumoral injection of inactivated Sendai virus particles elicits strong antitumor activity by enhancing local CXCL10 expression and systemic NK cell activation|url=https://www.ncbi.nlm.nih.gov/pubmed/17602226|journal=Cancer immunology, immunotherapy: CII|volume=57|issue=1|pages=73–84|doi=10.1007/s00262-007-0351-y|issn=0340-7004|pmid=17602226}}</ref>, <ref>{{Cite journal|last=Nishikawa|first=Tomoyuki|last2=Tung|first2=Li Yu|last3=Kaneda|first3=Yasufumi|date=2014-12|title=Systemic administration of platelets incorporating inactivated Sendai virus eradicates melanoma in mice|url=https://www.ncbi.nlm.nih.gov/pubmed/25023327|journal=Molecular Therapy: The Journal of the American Society of Gene Therapy|volume=22|issue=12|pages=2046–2055|doi=10.1038/mt.2014.128|issn=1525-0024|pmc=4429689|pmid=25023327}}</ref> in immunocompetent mice. Similar regressions caused by the replication-deficient Sendai virus have been observed in animals with transplanted melanoma tumors<ref>{{Cite journal|last=Zhang|first=Quan|last2=Yuan|first2=Wei Feng|last3=Zhai|first3=Guo Qin|last4=Zhu|first4=Shan Yuan|last5=Xue|first5=Zheng Feng|last6=Zhu|first6=Hong Fei|last7=Xu|first7=Xiang Ming|date=2012-10|title=Inactivated Sendai virus suppresses murine melanoma growth by inducing host immune responses and down-regulating β-catenin expression|url=https://www.ncbi.nlm.nih.gov/pubmed/23122307|journal=Biomedical and environmental sciences: BES|volume=25|issue=5|pages=509–516|doi=10.3967/0895-3988.2012.05.003|issn=0895-3988|pmid=23122307}}</ref>,<ref>{{Cite journal|last=Saga|first=Kotaro|last2=Tamai|first2=Katsuto|last3=Yamazaki|first3=Takehiko|last4=Kaneda|first4=Yasufumi|date=2013-02-01|title=Systemic administration of a novel immune-stimulatory pseudovirion suppresses lung metastatic melanoma by regionally enhancing IFN-γ production|url=https://www.ncbi.nlm.nih.gov/pubmed/23251005/|journal=Clinical Cancer Research: An Official Journal of the American Association for Cancer Research|volume=19|issue=3|pages=668–679|doi=10.1158/1078-0432.CCR-12-1947|issn=1078-0432|pmid=23251005}}</ref>.

Some cancer studies with non-rodent animals have been performed with the unmodified Sendai virus. Thus, after intratumoral injections of the virus, complete or partial remission of mast cell tumors (mastocytomas) was observed in dogs affected by this disease<ref name=":0" />.

The described studies demonstrate that Sendai virus has a potential of becoming a safe and effective therapeutic agent against a wide range of human cancers.

⚫
== References ==
{{Reflist}}
{{Reflist}}
* {{cite journal | last1 = Simon | first1 = AY | last2 = Moritoh | first2 = K | last3 = Torigoe | first3 = D | last4 = Asano | first4 = A | last5 = Sasaki | first5 = N | last6 = Agui | first6 = T | date = Dec 2009 | title = Multigenic control of resistance to Sendai virus infection in mice | url = | journal = Infect Genet Evol | volume = 9 | issue = 6| pages = 1253–9 | doi = 10.1016/j.meegid.2009.08.011 | pmid = 19733691 | hdl = 2115/42554 }}
* {{cite journal | last1 = Simon | first1 = AY | last2 = Moritoh | first2 = K | last3 = Torigoe | first3 = D | last4 = Asano | first4 = A | last5 = Sasaki | first5 = N | last6 = Agui | first6 = T | date = Dec 2009 | title = Multigenic control of resistance to Sendai virus infection in mice | url = | journal = Infect Genet Evol | volume = 9 | issue = 6| pages = 1253–9 | doi = 10.1016/j.meegid.2009.08.011 | pmid = 19733691 | hdl = 2115/42554 }}

Revision as of 23:06, 7 August 2019

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

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,[1] a group of viruses featuring, notably, the genera Morbillivirus and Rubulavirus. SeV is a member of 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 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

  • 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

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]

Sendai virus as an oncolytic agent

Sendai virus-based anticancer therapy for model[12],[13] and companion animals[14] has been described in several scientific papers. After the virus was first isolated in the early 1950s in Japan[15] there was some concern that the virus causes human respiratory infection, but it was later recognized that Sendai virus infection is host restrictive and the virus is not infectious for humans. Therefore, one of the great advantages of the Sendai virus as a potential oncolytic agent is its safety. Even though the virus is widespread in rodent colonies[16] and has been used in laboratory research for decades[17], it has never been observed that it can cause human disease. Moreover, Sendai virus has been used in clinical trials involving both adults[18] and children[19] to immunize against human parainfluenza virus type 1, since the two viruses share common antigenic determinants and trigger the generation of cross-reactive neutralizing antibodies. The Sendai virus administration in the form of nasal drops induced the production of neutralizing antibodies to the human virus without any measurable side effects. The results of these trials represent additional evidence of Sendai virus safety for humans.

For cancer studies, it is desirable that the oncolytic virus be non-pathogenic for experimental animals, but the Sendai virus can cause rodent disease, which is a problem for research strategies. Two approaches have been used to overcome this problem and make Sendai virus non-pathogenic for mice and rats. One of these approaches included the creation of a set of genetically modified attenuated viral strains. Representatives of this set were tested on model animals carrying a wide range of transplantable human tumors. It has been shown that they can cause suppression or even eradication of fibrosarcoma[20],[21] neuroblastoma[22], hepatocellular carcinoma[23], melanoma, squamous cell and prostate carcinomas[24]. Complete eradication of established gliosarcomas in immunocompetent rats has also been observed[25].

Another approach of making Sendai virus non-pathogenic included the short-term treatment of the virions with ultraviolet light. Such treatment causes a loss of the virus replication ability. However, even this replication-deficient virus can induce the cancer cells death and stimulate anti-tumor immunity. It can trigger extensive apoptosis of human glioblastoma cells in culture, and it can efficiently suppress the growth of these cells in model animals[26]. The ultraviolet light treated virus can also kill human prostate cancer cells in culture[27], [28] and eradicate tumors that originated from these cells in immuno-deficient model animals[29]. Moreover, it can stimulate immunomodulated tumor regression of colon[30] and kidney cancers[31], [32] in immunocompetent mice. Similar regressions caused by the replication-deficient Sendai virus have been observed in animals with transplanted melanoma tumors[33],[34].

Some cancer studies with non-rodent animals have been performed with the unmodified Sendai virus. Thus, after intratumoral injections of the virus, complete or partial remission of mast cell tumors (mastocytomas) was observed in dogs affected by this disease[14].

The described studies demonstrate that Sendai virus has a potential of becoming a safe and effective therapeutic agent against a wide range of human cancers.

References

  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. July 15, 2005. Retrieved 2007-06-13.
  3. ^ Flecknell, P. A.; et al. (1983). "Respiratory disease associated with parainfluenza type 1 (Sendai) virus in a colony of marmosets (C. jacchus)". Laboratory Animals. 17 (2): 111–113. doi:10.1258/002367783780959448. PMID 6306336.
  4. ^ 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.
  5. ^ 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.
  6. ^ 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.
  7. ^ 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.
  8. ^ Köhler, G; Milstein C (August 1975). "Continuous cultures of fused cells secreting antibody of predefined specificity". Nature. 256 (5): 495–497. doi:10.1038/256495a0. PMID 1172191.
  9. ^ 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.
  10. ^ Fox, James G. (2007). The Mouse in Biomedical Research, 2nd Edition. Burlington: Academic Press. pp. 281–309. doi:10.1016/B978-012369454-6/50039-X.
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