HAEM5:Systemic chronic active EBV disease: Difference between revisions
| [unchecked revision] | [unchecked revision] |
Karin.Miller (talk | contribs) |
Karin.Miller (talk | contribs) |
||
| Line 190: | Line 190: | ||
==Familial Forms== | ==Familial Forms== | ||
* Germline mutations have only rarely been detected in CAEBV<ref>{{Cite journal|last=Okuno|first=Yusuke|last2=Murata|first2=Takayuki|last3=Sato|first3=Yoshitaka|last4=Muramatsu|first4=Hideki|last5=Ito|first5=Yoshinori|last6=Watanabe|first6=Takahiro|last7=Okuno|first7=Tatsuya|last8=Murakami|first8=Norihiro|last9=Yoshida|first9=Kenichi|date=2019-03|title=Defective Epstein-Barr virus in chronic active infection and haematological malignancy|url=https://pubmed.ncbi.nlm.nih.gov/30664667|journal=Nature Microbiology|volume=4|issue=3|pages=404–413|doi=10.1038/s41564-018-0334-0|issn=2058-5276|pmid=30664667}}</ref> | * Germline mutations have only rarely been detected in CAEBV<ref>{{Cite journal|last=Okuno|first=Yusuke|last2=Murata|first2=Takayuki|last3=Sato|first3=Yoshitaka|last4=Muramatsu|first4=Hideki|last5=Ito|first5=Yoshinori|last6=Watanabe|first6=Takahiro|last7=Okuno|first7=Tatsuya|last8=Murakami|first8=Norihiro|last9=Yoshida|first9=Kenichi|date=2019-03|title=Defective Epstein-Barr virus in chronic active infection and haematological malignancy|url=https://pubmed.ncbi.nlm.nih.gov/30664667|journal=Nature Microbiology|volume=4|issue=3|pages=404–413|doi=10.1038/s41564-018-0334-0|issn=2058-5276|pmid=30664667}}</ref> | ||
==Additional Information== | ==Additional Information== | ||
* CAEBV shows an increased prevalence in populations from Asia and natives from Central and South America, suggesting a potential for genetic polymorphisms in immune-modulating genes to play a role in disease pathogenesis.<ref>{{Cite journal|last=Kimura|first=Hiroshi|last2=Cohen|first2=Jeffrey I.|date=2017|title=Chronic Active Epstein-Barr Virus Disease|url=https://pubmed.ncbi.nlm.nih.gov/29375552|journal=Frontiers in Immunology|volume=8|pages=1867|doi=10.3389/fimmu.2017.01867|issn=1664-3224|pmc=5770746|pmid=29375552}}</ref> <ref>{{Cite journal|last=Kimura|first=Hiroshi|date=2006|title=Pathogenesis of chronic active Epstein-Barr virus infection: is this an infectious disease, lymphoproliferative disorder, or immunodeficiency?|url=https://pubmed.ncbi.nlm.nih.gov/16791843|journal=Reviews in Medical Virology|volume=16|issue=4|pages=251–261|doi=10.1002/rmv.505|issn=1052-9276|pmid=16791843}}</ref> | |||
* EBV clonality testing showed monoclonality (84%), oligoclonality (11%), or polyclonality (5%).<ref>{{Cite journal|last=Kimura|first=Hiroshi|last2=Ito|first2=Yoshinori|last3=Kawabe|first3=Shinji|last4=Gotoh|first4=Kensei|last5=Takahashi|first5=Yoshiyuki|last6=Kojima|first6=Seiji|last7=Naoe|first7=Tomoki|last8=Esaki|first8=Shinichi|last9=Kikuta|first9=Atsushi|date=2012-01-19|title=EBV-associated T/NK-cell lymphoproliferative diseases in nonimmunocompromised hosts: prospective analysis of 108 cases|url=https://pubmed.ncbi.nlm.nih.gov/22096243|journal=Blood|volume=119|issue=3|pages=673–686|doi=10.1182/blood-2011-10-381921|issn=1528-0020|pmid=22096243}}</ref> TCR clonality testing is described above (see gene rearrangements) | * EBV clonality testing showed monoclonality (84%), oligoclonality (11%), or polyclonality (5%).<ref>{{Cite journal|last=Kimura|first=Hiroshi|last2=Ito|first2=Yoshinori|last3=Kawabe|first3=Shinji|last4=Gotoh|first4=Kensei|last5=Takahashi|first5=Yoshiyuki|last6=Kojima|first6=Seiji|last7=Naoe|first7=Tomoki|last8=Esaki|first8=Shinichi|last9=Kikuta|first9=Atsushi|date=2012-01-19|title=EBV-associated T/NK-cell lymphoproliferative diseases in nonimmunocompromised hosts: prospective analysis of 108 cases|url=https://pubmed.ncbi.nlm.nih.gov/22096243|journal=Blood|volume=119|issue=3|pages=673–686|doi=10.1182/blood-2011-10-381921|issn=1528-0020|pmid=22096243}}</ref> TCR clonality testing is described above (see gene rearrangements) | ||