title: Mutation takes no vacation: can structured treatment interruptions increase the risk of drug-resistant HIV-1?
abstract: 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.
authors.affiliation: Department of Biomathematics, University of California, Los Angeles, California, USA.
authors.forename: K S
authors.initials: KS
authors.lastname: Dorman
authors.forename: A H
authors.initials: AH
authors.lastname: Kaplan
authors.forename: K
authors.initials: K
authors.lastname: Lange
authors.forename: J S
authors.initials: JS
authors.lastname: Sinsheimer
mesh_terms: D019380:Anti-HIV Agents / Q000008:administration & dosage* / Q000627:therapeutic use; D004334:Drug Administration Schedule; D004352:Drug Resistance, Microbial / Q000235:genetics; D004359:Drug Therapy, Combination; D015658:HIV Infections / Q000188:drug therapy* / Q000821:virology; D015497:HIV-1 / Q000187:drug effects* / Q000235:genetics*; D006801:Humans; D008954:Models, Biological; D009154:Mutation; D012307:Risk Factors; D019562:Viral Load; D017735:Virus Latency
chemical_list: D019380:Anti-HIV Agents