{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T11:35:44Z","timestamp":1791286544951,"version":"4.1.0"},"reference-count":36,"publisher":"National Academy of Sciences","issue":"18","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2001,8,28]]},"abstract":"<jats:p>\n                    A number of perturbations of B cells has been described in the setting of HIV infection; however, most remain poorly understood. To directly address the effect of HIV replication on B cell function, we investigated the capacity of B cells isolated from HIV-infected patients to respond to a variety of stimuli before and after reduction of viremia by effective antiretroviral therapy. B cells taken from patients with high levels of plasma viremia were defective in their proliferative responses to various stimuli. Viremia was also associated with the appearance of a subpopulation of B cells that expressed reduced levels of CD21. After fractionation into CD21\n                    <jats:sup>high<\/jats:sup>\n                    - and CD21\n                    <jats:sup>low<\/jats:sup>\n                    -expressing B cells, the CD21\n                    <jats:sup>low<\/jats:sup>\n                    fraction showed dramatically reduced proliferation in response to B cell stimuli and enhanced secretion of immunoglobulins when compared with the CD21\n                    <jats:sup>high<\/jats:sup>\n                    fraction. Electron microscopic analysis of each fraction revealed cells with plasmacytoid features in the CD21\n                    <jats:sup>low<\/jats:sup>\n                    B cell population but not in the CD21\n                    <jats:sup>high<\/jats:sup>\n                    fraction. These results indicate that HIV viremia induces the appearance of a subset of B cells whose function is impaired and which may be responsible for the hypergammaglobulinemia associated with HIV disease.\n                  <\/jats:p>","DOI":"10.1073\/pnas.181347898","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T10:37:36Z","timestamp":1027679856000},"page":"10362-10367","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":270,"title":["HIV-1 induces phenotypic and functional perturbations of B cells in chronically infected individuals"],"prefix":"10.1073","volume":"98","author":[{"given":"Susan","family":"Moir","sequence":"first","affiliation":[{"name":"Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, and Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892; Science Applications International Corporation\/National Cancer Institute\u2013Frederick Cancer and Development Center, Frederick, MD 21702; and Department of Pathology, George Washington University, Washington, DC 20037"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Angela","family":"Malaspina","sequence":"additional","affiliation":[{"name":"Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, and Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892; Science Applications International Corporation\/National Cancer Institute\u2013Frederick Cancer and Development Center, Frederick, MD 21702; and Department of Pathology, George Washington University, Washington, DC 20037"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kisani M.","family":"Ogwaro","sequence":"additional","affiliation":[{"name":"Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, and Surgery Branch, National Cancer Institute, National Institutes 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