Mechanisms involved in the Abacavir-mediated hypersensitivity syndrome
The potentially life-threatening adverse reactions to Abavacir (ABC), a nucleoside analog reverse transcriptase inhibitor for the treatment of H1V infection, have been known for several years to be limited to individu- als expressing the HLA-B*57:01 gene. Why the ABC hypersensitivity syn- drome is o...
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Published in | Cell research Vol. 22; no. 12; pp. 1637 - 1639 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
01.12.2012
Nature Publishing Group |
Subjects | |
Online Access | Get full text |
ISSN | 1001-0602 1748-7838 1748-7838 |
DOI | 10.1038/cr.2012.105 |
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Summary: | The potentially life-threatening adverse reactions to Abavacir (ABC), a nucleoside analog reverse transcriptase inhibitor for the treatment of H1V infection, have been known for several years to be limited to individu- als expressing the HLA-B*57:01 gene. Why the ABC hypersensitivity syn- drome is only seen in HLA-B*57:01- expressing subjects and what the precise mechanisms underlying this intolerance are remain however con- troversial. A series of recent studies, particularly a study by Illing et al. recently published in Nature, now answer some of these questions and offer new opportunities to better understand autoimmune disorders and prevent adverse reactions to other drugs. |
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Bibliography: | The potentially life-threatening adverse reactions to Abavacir (ABC), a nucleoside analog reverse transcriptase inhibitor for the treatment of H1V infection, have been known for several years to be limited to individu- als expressing the HLA-B*57:01 gene. Why the ABC hypersensitivity syn- drome is only seen in HLA-B*57:01- expressing subjects and what the precise mechanisms underlying this intolerance are remain however con- troversial. A series of recent studies, particularly a study by Illing et al. recently published in Nature, now answer some of these questions and offer new opportunities to better understand autoimmune disorders and prevent adverse reactions to other drugs. 31-1568/Q ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 ObjectType-Article-2 ObjectType-Feature-1 |
ISSN: | 1001-0602 1748-7838 1748-7838 |
DOI: | 10.1038/cr.2012.105 |