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JC virus

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Title: JC virus  
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Subject: Polyomaviridae, Progressive multifocal leukoencephalopathy, BK virus, Viral disease, SV40
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JC virus

JC virus
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

  • NCBI—JC Virus Complete Genome
  • JC Brain infection MRI Diagnosis of PML

External links

  • Zu Rhein, G.M.; Chou, S.M. (1965). Science 148: 1477–1479.  
  • Silverman, L.; Rubinstein, L.J. (1965). Acta Neuropathologica 5: 215–224.  
  1. ^ Zurhein, G; Chou, S. M. (1965). "Particles Resembling Papova Viruses in Human Cerebral Demyelinating Disease". Science (New York, N.Y.) 148 (3676): 1477–9.  
  2. ^ BL, Walker DL; et al. (1971). "Cultivation of papova-like virus from human brain with progressive multifocal leucoencephalopathy". Lancet 1 (7712): 1257–60.  
  3. ^ a b Ferenczy, MW; Marshall, LJ; Nelson, CD; Atwood, WJ; Nath, A; Khalili, K; Major, EO (July 2012). "Molecular biology, epidemiology, and pathogenesis of progressive multifocal leukoencephalopathy, the JC virus-induced demyelinating disease of the human brain.". Clin. Microbiol. Rev. 25 (3): 471–506.  
  4. ^ Hansjügen T. Agostini, Caroline F. Ryschkewitsch, Rachel Mory, Elyse J. Singer and Gerald L. Stoner (1997). "JC Virus (JCV) genotypes in brain tissue from patients with progressive multifocal leukoencephalopathy (PML) and in urine from controls without PML: increased frequency of JCV Type 2 in PML". The Journal of Infectious Diseases (Oxford University Press) 176 (1): 1–8.  
  5. ^ Laura A. Shackelton, Andrew Rambaut, Oliver G. Pybus, and Edward C. Holmes (2006). "JC Virus evolution and its association with human populations". Journal of Virology (American Society for Microbiology) 80 (20): 9928–9933.  
  6. ^ Padgett, B.L. and Walker, D.L. (1973). "Prevalence of antibodies in human sera against JC virus, an isolate from a case of progressive multifocal leukoencephalopathy". J. Infect. Dis. 127 (4): 467–470.  
  7. ^ a b Bofill-Mas, S., Formiga-Cruz, M., Clemente-Casares, P., Calafell, F. and Girones, R. (2001). "Potential transmission of human polyomaviruses through the gastrointestinal tract after exposure to virions or viral DNA". J. Virol. 75 (21): 10290–10299.  
  8. ^ Pavesi, A. (2005). "Utility of JC polyomavirus in tracing the pattern of human migrations dating to prehistoric times". J. Gen. Virol. 86 (Pt 5): 1315–1326.  
  9. ^ Monaco, M.C., Jensen, P.N., Hou, J., Durham, L.C. and Major, E.O. (1998). "Detection of JC virus DNA in human tonsil tissue: evidence for site of initial viral infection". J. Virol. 72 (12): 9918–9923.  
  10. ^ Ricciardiello, L., Laghi, L., Ramamirtham, P., Chang, C.L., Chang, D.K., Randolph, A.E. and Boland, C.R. (2000). "JC virus DNA sequences are frequently present in the human upper and lower gastrointestinal tract". Gastroenterology 119 (5): 1228–1235.  
  11. ^ Harvey, R. (2007) Microbiology Philadelphia, Lippincott Williams & Wilkins.
  12. ^ Elphick, G.F., Querbes, W., Jordan, J.A., Gee, G.V., Eash, S., Manley, K., Dugan, A., Stanifer, M., Bhatnagar, A., Kroeze, W.K., Roth, B.L. and Atwood, W.J. (2004). "The human polyomavirus, JCV, uses serotonin receptors to infect cells". Science 306 (5700): 1380–1383.  
  13. ^ White, F.A., 3rd., Ishaq, M., Stoner, G.L. and Frisque, R.J. (1992). "JC virus DNA is present in many human brain samples from patients without progressive multifocal leukoencephalopathy". J. Virol. 66 (10): 5726–5734.  
  14. ^ http://www.emedicine.com/neuro/topic450.htm
  15. ^ Theodoropoulos, G., Panoussopoulos, D., Papaconstantinou, I., Gazouli, M., Perdiki, M., Bramis, J. and Lazaris, ACh. (2005). "Assessment of JC polyoma virus in colon neoplasms". Dis. Colon. Rectum. 48 (1): 86–91.  
  16. ^ gene.com/gene/products/information/pdf/rituxan-prescribing.pdf
  17. ^ "Adcetris (brentuximab vedotin): Drug Safety Communication—Progressive Multifocal Leukoencephalopathy and Pulmonary Toxicity". U.S. FDA. Retrieved 14 January 2012. 

References

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.[17]

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.

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 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.[16]

Since immunodeficiency causes this virus to progress to PML, immunosuppressants are contraindicated in those who are infected.

Drugs associated with reactivation

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.[14] 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.[15]

JCV found in the central nervous system of PML patients almost invariably have differences in promoter sequence to the JCV found in healthy individuals. It is thought that these differences in promoter sequence contribute to the fitness of the virus in the CNS and thus to the development of PML.[3]

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.[12] JC viral DNA can be detected in both non-PML affected and PML-affected (see below) brain tissue.[13]

The initial site of infection may be the tonsils,[9] or possibly the gastrointestinal tract.[7] The virus then remains latent in the gastrointestinal tract [10] and can also infect the tubular epithelial cells in the kidneys,[11] where it continues to reproduce, shedding virus particles in the urine.

Infection and pathogenesis

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.

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.[8] 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.

The virus is very common in the general population, infecting 70 to 90 percent of humans; most people acquire JCV in childhood or adolescence.[4][5][6] It is found in high concentrations in urban sewage worldwide, leading some researchers to suspect contaminated water as a typical route of infection.[7]

Epidemiology

Contents

  • Epidemiology 1
  • Infection and pathogenesis 2
  • Drugs associated with reactivation 3
  • References 4
  • External links 5

[3]

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