{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T07:55:33Z","timestamp":1792569333631,"version":"4.5.0"},"reference-count":42,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2023,10,20]],"date-time":"2023-10-20T00:00:00Z","timestamp":1697760000000},"content-version":"vor","delay-in-days":19,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal of Medical Virology"],"published-print":{"date-parts":[[2023,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    The etiology of viral blips is not yet fully elucidated. One of the hypotheses is that blips reflect variations in residual viremia (RV) near the detectability threshold. In this study, we evaluated whether RV is associated with viral blips and which factors are associated with RV. All treatment regimens in 2010\u20132020 consisting of two nucleos(\u2010t)ide reverse transcriptase inhibitors and one anchor (integrase strand transfer inhibitor [INSTI], non\u2010nucleoside reverse transcriptase inhibitor [NNRTI], or protease inhibitor [PI]) in people with HIV (PWH) were evaluated for RV (detectable viremia &lt;50 cp\/mL) and blips (isolated viral loads [VLs] 50\u2013499 cp\/mL between measurements &lt;50 cp\/mL). All medical records were reviewed and regimens in which a VL\u2009\u2265\u200950 cp\/mL was deemed to result from non\u2010adherence (based on the documented conclusion by the treating physician) were excluded. Factors associated with blips and RV were identified using generalized linear mixed models. In total, 24\u2009518 VLs from 1658 PWH were analyzed. VLs were measured during INSTI\u2010 (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20095119; 20.9%), PI\u2010 (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20098935; 36.4%), and NNRTI\u2010use (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u200910\u2009464; 42.7%). VLs were categorized as blips in 1.4% (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u2009332). The 24,186 non\u2010blip VLs were RNA\n                    <jats:sup>neg<\/jats:sup>\n                    (no RV) (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u200915\u2009326; 63.4%), 1\u201319 cp\/mL (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20096318; 26.1%), 20\u201349 cp\/mL (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20091620; 6.7%), or &lt;50 cp\/mL with an unknown RV level (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u2009922; 3.8%). In 193\/1658 PWH (11.6%), the RV level was RNA\n                    <jats:sup>neg<\/jats:sup>\n                    in all VLs assessed. RV 1\u201319 cp\/mL and 20\u201349 cp\/mL (vs. RNA\n                    <jats:sup>neg<\/jats:sup>\n                    ) were significantly associated with subsequent viral blips (respective odds ratio 2.66 and 4.90 [95% confidence intervals: 1.98\u20133.58 and 3.41\u20137.04]). Zenith VL and use of PIs (vs. INSTIs\/NNRTIs) were associated with higher RV and blip odds. This large cohort study showed that blips were associated with higher preceding RV. Both the anchor type and factors previously linked to the latent viral reservoir were associated with RV, suggesting blips having a multifactorial origin.\n                  <\/jats:p>","DOI":"10.1002\/jmv.29178","type":"journal-article","created":{"date-parts":[[2023,10,20]],"date-time":"2023-10-20T10:18:17Z","timestamp":1697797097000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Integrated analysis of viral blips, residual viremia, and associated factors in people with HIV: Results from a retrospective cohort study"],"prefix":"10.1002","volume":"95","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0455-7394","authenticated-orcid":false,"given":"Patrick G. A.","family":"Oomen","sequence":"first","affiliation":[{"name":"Department of Infectious Diseases University Medical Center Utrecht Utrecht The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Suzan","family":"Dijkstra","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases University Medical Center Utrecht Utrecht The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L. 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J.","family":"Wensing","sequence":"additional","affiliation":[{"name":"Department of Medical Microbiology, Translational Virology University Medical Center Utrecht Utrecht The Netherlands"},{"name":"Ezintsha, Wits Reproductive Health and HIV Institute, Faculty of Health Sciences University of the Witwatersrand Johannesburg South Africa"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andy I. 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