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a harmful or corrupting agency; "bigotry is a virus that must not be allowed to spread"; "the virus of jealousy is latent in everyone"
(virology) ultramicroscopic infectious agent that replicates itself only within cells of living hosts; many are pathogenic; a piece of nucleic acid (DNA or RNA) wrapped in a thin coat of protein
a software program capable of reproducing itself and usually capable of causing great harm to files or other programs on the same computer; "a true virus cannot spread to another computer without human assistance" (同)computer virus
pertaining to or characteristic of birds

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/05/20 20:06:36」(JST)

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Avian sarcoma leukosis virus (ASLV) is an endogenous retrovirus that infects and can lead to cancer in chickens; experimentally it can infect other species of birds and mammals.^[1]^[2] ASLV replicates in chicken embryo fibroblasts, the cells that contribute to the formation of connective tissues. Different forms of the disease exist, including lymphoblastic, erythroblastic, and osteopetrotic.

Avian sarcoma leukosis virus is characterized by a wide range of tumors, the most common of which are lymphomas. Lymphoid leukosis is the most common form of this disease and with typical presentation of gradual onset, persistent low mortality, and neoplasia of the bursa.^[3] The disease is also characterized by an enlarged liver due to infiltration of cancerous lymphoid cells. In addition, other abdominal organs and the bursa of Fabricius are often infected.^[4]

Occurrence

Lymphoid leukosis has a worldwide distribution, and is most commonly found in birds 16 weeks or older.

History

Sarcoma in chickens has been studied since the early 1900s when Ellerman and Bang demonstrated that erythroleukemia can be transmitted between chickens by cell-free tissue filtrates, and in 1911 when (Francis) Peyton Rous proved that sarcoma can be transmitted through cell free extracts of solid chicken tumors.^[5] Rous was awarded the Nobel Prize for his discovery in 1966.^[6]

By the 1960s, ASLV became a problem with egg-laying hens and effort was made to isolate the disease. However, the movement was unsuccessful in maintaining leukosis-free flocks. In 1961, Rous sarcoma virus (RSV), which is closely related to ASLV, was shown to contain RNA, and oncogenic viruses, such as RSV and ASLV, were termed RNA tumor viruses. By the late 1960s, Howard Temin hypothesized that RSV made a copy of its own DNA and integrated that into the host cell’s chromosomal DNA. Much debate in the scientific community surrounded this issue until DNA integration was demonstrated by Temin in 1968 and reverse transcriptase was independently discovered by both Temin and David Baltimore in 1970. Temin and Baltimore won the Nobel Prize in Medicine in 1975.^[6]

Lymphoid leukosis was eradicated in primary breeders in the 1980s and 1990s which dramatically reduced the incidence of the disease in commercial laying hens. Commercial broilers are still struggling with ALV-J virus in many countries. Both layers and broilers may still become infected, especially if there are contaminated vaccines.^[7]

Today, research is carried out on ASLV in order to better understand retroviral cell entry. Since ASLV uses distinct cellular receptors to gain entry into cells, it has proven useful for understanding the early events in retroviral infection.^[8] A detailed understanding of retroviral cell entry may lead to the discovery of ways in which to block the viruses from entering cells. Retroviruses also have the potential to serve as gene delivery vectors in gene therapy.

Classification

ASLV is a Group VI virus of the family Retroviridae. It is of the Alpharetrovirus genus, and has a C-type morphology. Hence, it is an enveloped virus with a condensed, central core, and has barely visible envelope spikes, or proteins.^[5]

ASLV is divided into six subgroups, labelled A through E and J, each having a different antigenicity due to variances in viral envelope glycoproteins. Strains A through E are highly related and are believed to have evolved from the same ancestor.^[9] The subgroups evolved to utilize difference cellular receptors to gain entry into avian cells due to the host developing resistance to viral entry.^[10] Some antigenic variation can occur within subgroups, and all strains are oncogenic, but oncogenicity and the ability to replicate varies between subgroups.^[2]

Viral structure and composition

Like many retroviruses, ASLV consists of a lipid envelope containing transmembrane and cell surface glycoproteins. Enclosed within the envelope is a capsid surrounding single stranded RNA, integrase, protease, and reverse transcriptase, an enzyme that allows for the reversal of genetic transcription. As with all retroviruses, the virus is transcribed from RNA to DNA, instead of DNA to RNA as in normal cellular replication.

Viral glycoprotein-receptor interactions are required to initiate membrane fusion of the virus and cell. The surface glycoproteins contain the major domains that interact with the host cell receptor while the transmembrane (TM) glycoproteins anchor the surface glycoproteins to the virus membrane. The TM glycoproteins are directly involved in the fusion of the virus and host membranes for entry. The surface glycoproteins for subgroups A-E are almost identical and include the conservation of all cysteine amino acid residues. Viral specificity is determined by five hyper variable regions, vr1, vr2, hr1, hr2, and vr3, on the surface glycoproteins. Binding specificity is determined primarily by the hr1 and hr2 regions, with the vr3 region contributing to receptor recognition but not to binding specificity of the viral glycoprotein and cellular receptor.^[11]

In chicken chromosomes, three autosomal loci, t-va, t-vb, and t-vc, have been identified which control cell susceptibility of the ASLV virus subgroups A, B, and C respectively. Each of these genes codes for the cellular receptors Tva, Tvb, and Tvc.^[12] Tva contains sequences related to the ligand binding region of low-density lipoprotein receptors (LDLR).^[4] The Tvb receptor is believed to be very closely related to the receptors for both ASLV D and E, so that the ASLV D and E will bind to Tvb. Tvb is a member of the tumor necrosis factor receptor (TNFR) family.^[6] The Tvc receptor is closely related to mammalian butyrophilins, which are members of the immunoglobulin superfamily.^[13]

ASLV is genetically closely related to the Rous sarcoma virus (RSV), but unlike RSV, ASLV does not contain the src gene, which codes for a tyrosine kinase, and does not transform the fibroblasts that it infects.^[2] Both RSV and ASLV contain the gag gene, which is common to most retroviruses and encodes for the capsid proteins, and the pol gene which encodes for the reverse transcriptase enzyme. ASLV and some RSVs also contain the env gene, which encodes a precursor polyprotein that assembles in the endoplasmic reticulum. The polyproteins are then transported to the Golgi apparatus, glycosylated and cleaved to produce two glycoproteins: one surface and one transmembrane.^[8]

Resources

The Avian Diagnostic and Oncology Laboratory, in East Lansing, MI is the primary laboratory for research in ALV and other tumor viruses.

The American Association of Avian Pathologists maintains a fact sheet on viral tumor diseases.

References

^ "Leukosis/Sarcoma Group". The Merck Veterinary Manual. 2006. Retrieved 2007-06-23.
^ ^a ^b ^c Weiss, Robin A. The discovery of endogenous retroviruses. Retrovirology. 3 October 2006. 3:67. www.retrovirology.com/content/3/1/67
^ Swayne, David E., and John R. Glisson. Diseases of Poultry. 13th ed. Ames, IA: Wiley-Blackwell, 2013. Print.
^ ^a ^b cpl May99
^ ^a ^b http://www.microbiologybytes.com/virology/Retroviruses.html, Retroviruses
^ ^a ^b ^c All Nobel Laureates
^ 3
^ ^a ^b Holmen, S.L., and M. J. Federspiel. 2001. Identification of key residues in subgroup A avian leukosis virus envelope determining receptor binding affinity and infectivity of cells expressing chicken or quail Tva receptor. J. Virol. 75:10051–10060.
^ Elleder, D., D.C. Molder, K. Trejbalova, J. Svoboda, and M. J. Federspiel. 2004. Two different molecular defects in the Tva receptor gene explain the resistance of two tva^r lines of chickens to infection by subgroup A avian sarcoma and leukosis viruses. J Virol. 78: in press.
^ Barnard, R.J., D. Elleder, and J.A.T. Young. 2006. Avian sarcoma and leukosis virus-receptor interactions from classical genetics to novel insights into virus-cell membrane fusion. Virology. 344:25–29.
^ Bova, C.A., J.P. Manfredi, and R. Swanstrom. 1988. The avian retrovirus env gene family: molecular analysis of host range and antigenic variants. J. Virol. 62:75–83
^ Dorner, A. J., J. P. Stoye, and J. M. Coffin. 1985. Molecular basis of host range variation in avian retroviruses. J. VIrol. 53: 32–39.
^ Elleder, D., V. Stephanets, D. C. Melder, F. Senigl, and J. Svoboda. 2004. Close linkage of genes encoding receptors for subgroups A and C of avian sarcoma/leucosis virus on chicken chromosome 28. Animal Genetics 35:176–181

UpToDate Contents

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English Journal

Effective signal-on photoelectrochemical immunoassay of subgroup J avian leukosis virus based on Bi2S3 nanorods as photosensitizer and in situ generated ascorbic acid for electron donating.

Sun B1, Qiao F1, Chen L1, Zhao Z1, Yin H1, Ai S2.Author information 1College of Chemistry and Material Science, Shandong Agricultural University, 61 Daizong Street, Taian 271018, Shandong, PR China.2College of Chemistry and Material Science, Shandong Agricultural University, 61 Daizong Street, Taian 271018, Shandong, PR China. Electronic address: ashy@sdau.edu.cn.AbstractA universal and effective photoelectrochemical (PEC) immunosensing device was fabricated on an indium tin oxide (ITO) electrode for sensitive and specific detection of subgroup J of avian leukosis virus (ALVs-J) based on a signal-on strategy. Bismuth sulfide (Bi2S3) nanorods, with good morphology, high crystallinity and differentiated PEC properties, were selected as the photoelectrochemical species and synthesized by a facile hydrothermal method. On the basis of alkaline phosphatase catalytic chemistry to in situ produce ascorbic acid for electron donating, an enhanced photocurrent was obtained. Due to the dependence of the photocurrent signal on the concentration of generated electron donor, an exquisite immunosandwich protocol was successfully constructed for PEC detection of ALVs-J with a linear range from 10(2.14) to 10(3.65)TCID50/mL. The detection limit was 10(2.08)TCID50/mL (S/N=3), and high stability and specificity were obtained. The strategy provides a fast and sensitive method for ALVs-J analysis and opens a general format for future development of PEC immunoanalysis.
Biosensors & bioelectronics.Biosens Bioelectron.2014 Apr 15;54:237-43. doi: 10.1016/j.bios.2013.11.021. Epub 2013 Nov 15.
A universal and effective photoelectrochemical (PEC) immunosensing device was fabricated on an indium tin oxide (ITO) electrode for sensitive and specific detection of subgroup J of avian leukosis virus (ALVs-J) based on a signal-on strategy. Bismuth sulfide (Bi2S3) nanorods, with good morphology, h
PMID 24287410

Development and characterization of monoclonal antibodies to subgroup A avian leukosis virus.

Qiu Y, Li X, Fu L, Cui Z, Li W, Wu Z, Sun S.Author information College of Basic Medicine, Taishan Medical University, Tai'an, China.AbstractAvian leukosis virus subgroup A (ALV-A) is a retrovirus which infects egg-type chickens and is the main pathogen of lymphoid leukosis (LL) and myeloid leukosis (ML). In order to greatly enhance the diagnosis and treatment of clinical avian leukemia, two monoclonal antibodies (MAbs) to ALV-A were developed by fusion between SP2/0 and spleen cells from mice immunized with expressed ALV-A env-gp85 protein. Using immunofluorescence assay (IFA), two MAbs reacted with ALV-A, but not with subgroups B and J of ALV. Western blot tests showed that molecular weight of ALV-A envelope glycoprotein recognized by MAbs was about 53 kD. Isotyping test revealed that two MAbs (A5C1 and A4C8) were IgG1 isotypes. These MAbs can be used for diagnosis and epidemiology of ALV-A.
Veterinary and comparative oncology.Vet Comp Oncol.2014 Mar;12(1):47-51. doi: 10.1111/vco.12036. Epub 2013 Apr 25.
Avian leukosis virus subgroup A (ALV-A) is a retrovirus which infects egg-type chickens and is the main pathogen of lymphoid leukosis (LL) and myeloid leukosis (ML). In order to greatly enhance the diagnosis and treatment of clinical avian leukemia, two monoclonal antibodies (MAbs) to ALV-A were dev
PMID 23615298

Multicentric Histiocytosis Related to Avian Leukosis Virus Subgroup J (ALV-J)-Infection in Meat-Type Local Chickens.

Furukawa S, Tsukamoto K, Maeda M.Author information Fukushima Meat Hygiene Inspection Office, 38-6 Kitasawada, Senouemachi, Fukushima-shi, Fukushima 960-0101, Japan.AbstractGross lesions characterized by swollen livers and spleens accompanied by diffuse white miliary spots, which resembled those of Marek's disease, were detected in two flocks of local meat-type chickens at a Japanese poultry processing plant in June and August 2010. The microscopic examinations revealed proliferative foci consisting of spindle or polymorphic cells in the interstitium of livers, splenic follicles and the interstitium of kidneys. These cells were positive immunohistochemically with Iba1 antibody, indicating they were histiocytic cells. Some of them contained antigens of avian leukosis virus (ALV) by immunohistochemistry,and the env gene of ALV subgroup J was detected from the spleens by polymerase chain reaction (PCR). Phylogenetic analysis of the PCR product indicated that the env gene might be descended from the American ADOL-7501 strain of ALV-J. These results suggest that the swollen livers and spleens of the meat-type chickens may come from histiocytic proliferation caused by ALV-J infection.
The Journal of veterinary medical science / the Japanese Society of Veterinary Science.J Vet Med Sci.2014 Feb 3;76(1):89-92. Epub 2013 Aug 23.
Gross lesions characterized by swollen livers and spleens accompanied by diffuse white miliary spots, which resembled those of Marek's disease, were detected in two flocks of local meat-type chickens at a Japanese poultry processing plant in June and August 2010. The microscopic examinations reveale
PMID 23978900

Japanese Journal

Multicentric Histiocytosis Related to Avian Leukosis Virus Subgroup J (ALV-J)-Infection in Meat-Type Local Chickens

FURUKAWA Seiko,TSUKAMOTO Kenji,MAEDA Minoru
The journal of veterinary medical science 76(1), 89-92, 2014-01
NAID 40019957308

Multicentric Histiocytosis Related to Avian Leukosis Virus Subgroup J (ALV-J)-Infection in Meat-Type Local Chickens

FURUKAWA Seiko,TSUKAMOTO Kenji,MAEDA Minoru
Journal of Veterinary Medical Science 76(1), 89-92, 2014
… Some of them contained antigens of avian leukosis virus (ALV) by immunohistochemistry,and the env gene of ALV subgroup J was detected from the spleens by polymerase chain reaction (PCR). …
NAID 130003362287

Epitope Mapping of a Monoclonal Antibody against the Gp85 of Avian Leukosis Virus Subgroup J

SUN Miao,YU Duo,MO Hongfei [他],CAO Hong,CHEN Chen,CHEN Fuyong
Journal of Veterinary Medical Science 74(6), 693-697, 2012
… Avian leukosis virus subgroup J poses a great threat to the poultry industry in China. … The gp85 gene of avian leukosis virus subgroup J CAUHM01 China isolates was subcloned into the expression vectors pGEX-6p-1 and pET28a and successfully expressed in E. …
NAID 130002090070

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リンク元	「ALV」「avian leukemia virus」「トリ白血病ウイルス」「ニワトリ白血病ウイルス」
関連記事	「avian」「virus」

「ALV」

Avian Sarcoma Leukosis Virus
Virus classification
Group:	Group VI (ssRNA-RT)
Order:	Unassigned
Family:	Retroviridae
Subfamily:	Orthoretrovirinae
Genus:	Alpharetrovirus
Species:	Avian leukosis virus