This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Carbone, K. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Carbone, K. M.

 Previous Article  |  Next Article 

Clinical Microbiology Reviews, July 2001, p. 513-527, Vol. 14, No. 3
0893-8512/01/$04.00+0   DOI: 10.1128/CMR.14.3.513-527.2001

Borna Disease Virus and Human Disease

Kathryn M. Carbone*

FDA/CBER, HFM 460, Bethesda, Maryland 20892

The biology of Borna disease virus (BDV) strongly supports the likelihood of human infection with BDV or a variant of BDV. Thus far, the evidence supporting BDV infection in humans has initiated much controversy among basic and clinical scientists; only time and additional research will support or refute the hypothesis of human BDV infection. Until an assay of acceptable specificity and sensitivity has been developed, validated, and used to document human BDV infection, scientists cannot reasonably begin to associate BDV infection with specific disease syndromes. Clinical studies seeking causal associations between BDV infection and specific diseases must ensure the proper identification of the BDV infection status of patients and control subjects by using a validated, highly sensitive, and highly specific assay (or series of assays). For clinical studies, a highly sensitive "screening" test followed by a highly specific confirmatory test will be of significant benefit. Although it is possible to formulate hypotheses about the clinical outcomes of human BDV infection based on animal model work, to date no human disease has been causally linked to human BDV infection. Scientists all over the world are actively pursuing these issues, and with continuing advances in clinical and basic BDV research, the answers cannot be far away.


* Mailing address: FDA/CBER, HFM 460, 8800 Rockville Pike, Bethesda, MD 20892. Phone: (301) 827-1973. Fax: (301) 480-5679. E-mail: Carbonek{at}cber.fda.gov.


Clinical Microbiology Reviews, July 2001, p. 513-527, Vol. 14, No. 3
0893-8512/01/$04.00+0   DOI: 10.1128/CMR.14.3.513-527.2001



This article has been cited by other articles:

  • Perez, M., de la Torre, J. C. (2005). Identification of the Borna disease virus (BDV) proteins required for the formation of BDV-like particles. J. Gen. Virol. 86: 1891-1895 [Abstract] [Full Text]  
  • Rosario, D., Perez, M., de la Torre, J. C. (2005). Functional Characterization of the Genomic Promoter of Borna Disease Virus (BDV): Implications of 3'-Terminal Sequence Heterogeneity for BDV Persistence. J. Virol. 79: 6544-6550 [Abstract] [Full Text]  
  • Bajramovic, J. J., Volmer, R., Syan, S., Pochet, S., Gonzalez-Dunia, D. (2004). 2'-Fluoro-2'-Deoxycytidine Inhibits Borna Disease Virus Replication and Spread. Antimicrob. Agents Chemother. 48: 1422-1425 [Abstract] [Full Text]  
  • Cotto, E., Neau, D., Cransac-Neau, M., Auriacombe, M., Pellegrin, J.-L., Ragnaud, J.-M., Fillet, A.-M., Belnard, M., Fleury, H., Lafon, M.-E. (2003). Borna Disease Virus RNA in Immunocompromised Patients in Southwestern France. J. Clin. Microbiol. 41: 5577-5581 [Abstract] [Full Text]  
  • Bajramovic, J. J., Munter, S., Syan, S., Nehrbass, U., Brahic, M., Gonzalez-Dunia, D. (2003). Borna Disease Virus Glycoprotein Is Required for Viral Dissemination in Neurons. J. Virol. 77: 12222-12231 [Abstract] [Full Text]  
  • Zhang, G., Kobayashi, T., Kamitani, W., Komoto, S., Yamashita, M., Baba, S., Yanai, H., Ikuta, K., Tomonaga, K. (2003). Borna Disease Virus Phosphoprotein Represses p53-Mediated Transcriptional Activity by Interference with HMGB1. J. Virol. 77: 12243-12251 [Abstract] [Full Text]  
  • Perez, M., Sanchez, A., Cubitt, B., Rosario, D., de la Torre, J. C. (2003). A reverse genetics system for Borna disease virus. J. Gen. Virol. 84: 3099-3104 [Abstract] [Full Text]  
  • Kamitani, W., Ono, E., Yoshino, S., Kobayashi, T., Taharaguchi, S., Lee, B.-J., Yamashita, M., Kobayashi, T., Okamoto, M., Taniyama, H., Tomonaga, K., Ikuta, K. (2003). Glial expression of Borna disease virus phosphoprotein induces behavioral and neurological abnormalities in transgenic mice. Proc. Natl. Acad. Sci. USA 100: 8969-8974 [Abstract] [Full Text]  
  • Bode, L., Ludwig, H. (2003). Borna Disease Virus Infection, a Human Mental-Health Risk. Clin. Microbiol. Rev. 16: 534-545 [Abstract] [Full Text]  
  • Geib, T., Sauder, C., Venturelli, S., Hassler, C., Staeheli, P., Schwemmle, M. (2003). Selective Virus Resistance Conferred by Expression of Borna Disease Virus Nucleocapsid Components. J. Virol. 77: 4283-4290 [Abstract] [Full Text]  
  • Bajramovic, J. J., Syan, S., Brahic, M., de la Torre, J. C., Gonzalez-Dunia, D. (2002). 1-{beta}-D-Arabinofuranosylcytosine Inhibits Borna Disease Virus Replication and Spread. J. Virol. 76: 6268-6276 [Abstract] [Full Text]