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dc.contributor.authorBedimo, Roger
dc.contributor.authorChen, Ray Y.
dc.contributor.authorWestfall, Andrew O.
dc.contributor.authorRaper, James L
dc.contributor.authorAllison, Jeroan J.
dc.contributor.authorSaag, Michael S.
dc.date2022-08-11T08:10:43.000
dc.date.accessioned2022-08-23T17:17:39Z
dc.date.available2022-08-23T17:17:39Z
dc.date.issued2006-01-28
dc.date.submitted2010-08-05
dc.identifier.citationAIDS Res Hum Retroviruses. 2006 Jan;22(1):40-4. <a href="http://dx.doi.org/10.1089/aid.2006.22.40">Link to article on publisher's site</a>
dc.identifier.issn0889-2229 (Linking)
dc.identifier.doi10.1089/aid.2006.22.40
dc.identifier.pmid16438644
dc.identifier.urihttp://hdl.handle.net/20.500.14038/47675
dc.description.abstractTreatment of HIV-infected patients with HAART can result in long-term suppression of viral loads to undetectable levels. Rapid virologic rebound typically follows treatment interruption (TI), with a potential for significant loss of CD4+ cells. Patients who maintain virologic suppression despite interrupting treatment have not been well described. All patients with a pretreatment viral load (VL) > or = 5000 copies/ml, who had been on therapy for > or = 2 weeks, and who underwent a TI lasting > or = 180 days were analyzed. Patients whose maximum VL did not exceed 5000 copies/ml > or = 6 months after starting TI ("nonrebounders") were compared with those whose VL exceeded 5000 copies/ml (rebounders). Seventy-one patients were included in the analysis. Nineteen (27%) were nonrebounders. Ninety-four percent of patients in each group interrupted treatment for reasons unrelated to virologic response. Median change in CD4 count during TI was not significantly different between the nonrebounder and rebounder groups (-20.5/microl vs. -64.0/microl; p < 0.086). In a multivariate logistic regression analysis, the following factors predicted nonrebounder status: peak VL before TI (log10 copies/ml) (OR = 0.14, 95% CI = 0.04-0.48, p = 0.0016); having received HAART (vs. mono/dual therapy) as initial regimen (OR: 11.0, 95% CI: 2.04-59.8, p = 0.0054); and female gender (OR = 4.8, 95% CI = 1.09-21.5, p = 0.0384). The large majority of chronically infected HIV patients with a TI > or = 180 days interrupted treatment for reasons unrelated to virologic response. Almost 30% did not have a significant virologic rebound. Those patients were more likely to be female, had a lower peak VL prior to treatment, and their initial regimen was more likely to be HAART. Examining the immune responses of nonrebounders may contribute to the understanding of protective immunity to HIV.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=16438644&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1089/aid.2006.22.40
dc.subjectAdult
dc.subject*Antiretroviral Therapy, Highly Active
dc.subjectDrug Administration Schedule
dc.subjectFemale
dc.subjectHIV Infections
dc.subjectHIV-1
dc.subjectHumans
dc.subjectMale
dc.subjectProspective Studies
dc.subjectTreatment Outcome
dc.subjectViral Load
dc.subjectBioinformatics
dc.subjectBiostatistics
dc.subjectEpidemiology
dc.subjectHealth Services Research
dc.titleSustained HIV viral suppression following treatment interruption: an observational study
dc.typeJournal Article
dc.source.journaltitleAIDS research and human retroviruses
dc.source.volume22
dc.source.issue1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/qhs_pp/801
dc.identifier.contextkey1426275
html.description.abstract<p>Treatment of HIV-infected patients with HAART can result in long-term suppression of viral loads to undetectable levels. Rapid virologic rebound typically follows treatment interruption (TI), with a potential for significant loss of CD4+ cells. Patients who maintain virologic suppression despite interrupting treatment have not been well described. All patients with a pretreatment viral load (VL) > or = 5000 copies/ml, who had been on therapy for > or = 2 weeks, and who underwent a TI lasting > or = 180 days were analyzed. Patients whose maximum VL did not exceed 5000 copies/ml > or = 6 months after starting TI ("nonrebounders") were compared with those whose VL exceeded 5000 copies/ml (rebounders). Seventy-one patients were included in the analysis. Nineteen (27%) were nonrebounders. Ninety-four percent of patients in each group interrupted treatment for reasons unrelated to virologic response. Median change in CD4 count during TI was not significantly different between the nonrebounder and rebounder groups (-20.5/microl vs. -64.0/microl; p < 0.086). In a multivariate logistic regression analysis, the following factors predicted nonrebounder status: peak VL before TI (log10 copies/ml) (OR = 0.14, 95% CI = 0.04-0.48, p = 0.0016); having received HAART (vs. mono/dual therapy) as initial regimen (OR: 11.0, 95% CI: 2.04-59.8, p = 0.0054); and female gender (OR = 4.8, 95% CI = 1.09-21.5, p = 0.0384). The large majority of chronically infected HIV patients with a TI > or = 180 days interrupted treatment for reasons unrelated to virologic response. Almost 30% did not have a significant virologic rebound. Those patients were more likely to be female, had a lower peak VL prior to treatment, and their initial regimen was more likely to be HAART. Examining the immune responses of nonrebounders may contribute to the understanding of protective immunity to HIV.</p>
dc.identifier.submissionpathqhs_pp/801
dc.contributor.departmentDepartment of Quantitative Health Sciences
dc.source.pages40-4


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