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Mutation Takes No Vacation: Can Structured Treatment Interruptions Increase the Risk of Drug-Resistant HIV-1?
Author(s) -
Karin S. Dorman,
Andrew H. Kaplan,
Kenneth Lange,
Janet S. Sinsheimer
Publication year - 2000
Publication title -
journal of acquired immune deficiency syndromes
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.162
H-Index - 157
eISSN - 1944-7884
pISSN - 1525-4135
DOI - 10.1097/00042560-200012150-00003
Subject(s) - mutation , drug resistance , virology , viral replication , virus , drug , resistance mutation , human immunodeficiency virus (hiv) , biology , replication (statistics) , mutant , viral load , medicine , immunology , genetics , pharmacology , reverse transcriptase , gene , rna
We use a mathematical model to study the dynamics of HIV-1 replication during structured treatment interruptions (STIs) in infected patients. The model predicts rapid viral rebound, restoration of a latently infected cell pool, and critically, partially resistant mutant rebound that may be missed because of high levels of wild type virus. Because partially resistant viruses are capable of mutating to full resistance, a substantial increase in their numbers represents a threat to therapeutic response durability. Compared with continued treatment, STIs may increase the chance of mutation to full resistance by several thousandfold.

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