出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2013/05/04 13:35:10」(JST)
JC virus | |
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Immunohistochemical detection of JC virus protein (stained brown) in a brain biopsy (glial cells demonstrating progressive multifocal leukoencephalopathy (PML)) | |
Virus classification | |
Group: | Group I (dsDNA) |
Family: | Polyomaviridae |
Genus: | Polyomavirus |
Species: | JC polyomavirus |
The JC virus or John Cunningham virus (JCV) is a type of human polyomavirus (formerly known as papovavirus) and is genetically similar to BK virus and SV40. It was discovered in 1971 and named using the two initials of a patient with progressive multifocal leukoencephalopathy (PML).[1] The virus causes PML and other diseases only in cases of immunodeficiency, as in AIDS or during treatment with drugs intended to induce a state of immunosuppression (e.g., organ transplant patients).
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The virus is very common in the general population, infecting 70 to 90 percent of humans; most people acquire JCV in childhood or adolescence.[2][3][4] It is found in high concentrations in urban sewage worldwide, leading some researchers to suspect contaminated water as a typical route of infection.[5]
Minor genetic variations are found consistently in different geographic areas; thus, genetic analysis of JC virus samples has been useful in tracing the history of human migration.[6] 14 subtypes or genotypes are recognised each associated with a specific geographical region. Three are found in Europe (a, b and c). A minor African type - Af1 - occurs in Central and West Africa. The major African type - Af2 - is found throughout Africa and also in West and South Asia. Several Asian types are recognised B1-a, B1-b, B1-d, B2, CY, MY and SC.
An alternative numbering scheme numbers the genotypes 1-8 with additional lettering. Types 1 and 4 are found in Europe and in indigenous populations in northern Japan, North-East Siberia and northern Canada. These two types are closely related. Types 3 and 6 are found in sub-Saharan Africa: type 3 was isolated in Ethiopia, Tanzania and South Africa. Type 6 is found in Ghana. Both types are also found in the Biaka Pygmies and Bantus from Central Africa. Type 2 has several variants: subtype 2A is found mainly in the Japanese population and native Americans (excluding Inuit); 2B is found in Eurasians; 2D is found in Indians and 2E is found in Australians and western Pacific populations. Subtype 7A is found in southern China and South-East Asia. Subtype 7B is found in northern China, Mongolia and Japan Subtype 7C is found in northern and southern China. Subtype 8 is found in Papua New Guinea and the Pacific Islands.
The initial site of infection may be the tonsils,[7] or possibly the gastrointestinal tract.[5] The virus then remains latent in the gastrointestinal tract [8] and can also infect the tubular epithelial cells in the kidneys,[9] where it continues to reproduce, shedding virus particles in the urine.
JCV can cross the blood–brain barrier into the central nervous system, where it infects oligodendrocytes and astrocytes, possibly through the 5-HT2A serotonin receptor.[10] JC viral DNA can be detected in both non-PML affected and PML-affected (see below) brain tissue.[11]
Immunodeficiency or immunosuppression allows JCV to reactivate. In the brain it causes the usually fatal progressive multifocal leukoencephalopathy, or PML, by destroying oligodendrocytes. Whether this represents the reactivation of JCV within the CNS or seeding of newly reactivated JCV via blood or lymphatics is unknown.[12] Several studies since 2000 have suggested that the virus is also linked to colorectal cancer, as JCV has been found in malignant colon tumors, but these findings are still controversial.[13]
Since immunodeficiency causes this virus to progress to PML, immunosuppressants are contraindicative to those infected.
The boxed warning for the drug rituximab (Rituxan, co-marketed by Genentech BioOncology and Biogen Idec) includes a statement that JC virus infection resulting in progressive multifocal leukoencephalopathy, and death has been reported in patients treated with the drug.[14]
The boxed warning for the drug natalizumab (Tysabri, marketed by Elan and developed by Biogen Idec) includes a statement that JC virus resulted in progressive multifocal leukoencephalopathy developing in three patients who received natalizumab in clinical trials.
The boxed warning was added on Feb. 19, 2009, for the drug efalizumab (Raptiva, marketed in the U.S. by Genentech, and marketed in Europe by Swiss drugmaker Merck Serono) includes a statement that JC virus, resulting in progressive multifocal leukoencephalopathy, developed in three patients who received efalizumab in clinical trials. The drug was pulled off the U.S. market because of the association with PML on April 10, 2009.
A boxed warning for brentuximab vedotin (Adcetris) was issued by the FDA on January 13, 2011 after two cases of PML were reported, bringing the total number of associated cases to three.[15]
In June 2010, the first case report appeared of a PML patient being successfully treated with mefloquine. Mefloquine is an antimalarial drug that can also act against the JC virus. Administration of mefloquine seemed to eliminate the virus from the patient's body and prevented further neurological deterioration.[16]
On November 30, 2010, Cytheris announced that they had eradicated the JC virus from a PML patient, using their human interleukin-7 investigational drug (CYT107) combined with Chimerix's investigational, orally-available lipid conjugate prodrug of Cidofovir (CMX001).[17]
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リンク元 | 「髄膜炎」「JCウイルス」「human polyomavirus JC」「JC polyomavirus」「JCV」 |
拡張検索 | 「JC virus infection」 |
関連記事 | 「J」「virus」 |
4ヶ月未満 | B群溶連菌(50%) | 大腸菌(25%) | インフルエンザ菌(20%) | リステリア菌(1%) | |
4ヶ月~6歳未満 | インフルエンザ菌(70%) | 肺炎球菌(25%) | |||
6歳~50歳未満 | 肺炎球菌(65%) | インフルエンザ菌(10%) | 髄膜炎菌 | ||
50歳以上 | 肺炎球菌(80%) | 黄色ブドウ球菌 | |||
免疫不全者 | クレブシエラ | 連鎖球菌 | 緑膿菌 | 黄色ブドウ球菌 | 真菌 |
Newborn (0–6 mos) | Children (6 mos–6 yrs) | 6–60 yrs | 60 yrs + |
Streptococcus agalactiae | Streptococcus pneumoniae | Neisseria meningitidis | Streptococcus pneumoniae |
Escherichia coli | Neisseria meningitidis | Enteroviruses | Gram-negative rods |
Listeria | Haemophilus influenzae type B | Streptococcus pneumoniae | Listeria |
Enteroviruses | HSV |
1位 | 2位 | 3位 | |
新生児 | 大腸菌 | B群溶連菌 | リステリア菌 |
小児期(6歳以下) | インフルエンザ菌 | 肺炎球菌 | |
成人 | 肺炎球菌 | 髄膜炎菌 |
年齢 | 病原体 | ||
3ヶ月未満 | B群溶連菌 | 大腸菌 | リステリア菌 |
3ヶ月以上の乳小児 | インフルエンザ菌 | 肺炎球菌 | |
成人 | 肺炎球菌 | 髄膜炎菌 | |
高齢者 | 肺炎球菌 | グラム陰性桿菌 | リステリア菌 |
細菌性髄膜炎 | ウイルス性髄膜炎 | 結核性髄膜炎 | 真菌性髄膜炎 | 癌性髄膜炎 | |
外観 | 混濁 | clear | 水様~ キサントクロミー 日光微塵 |
clear~ 日光微塵 |
clear~ キサントクロミー |
圧 70-180 (mmH2O) |
↑↑ 200~800以上 |
↑ 200~300 |
↑ 200~800 |
↑ 200~800 |
↑ 200~300 |
細胞 0-5 (/mm3) |
500~数百万 | 10~1,000 | 25~1,000 | 25~1,000 | 25~500 |
好中球 | リンパ球 | リンパ球 | リンパ球 | 好中球 | |
タンパク 15-45 mg/dl |
↑↑ 50~1,500 |
↑ 正常~100 |
↑ 50~500 |
↑ 100~500 |
↑ 50~500 |
糖 50-80 mg/dl |
↓↓ 0~40 |
→ 正常 |
↓↓ ~40 |
↓↓ ~40 |
↓ ~40 |
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