{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,28]],"date-time":"2025-11-28T11:53:10Z","timestamp":1764330790616},"reference-count":77,"publisher":"American Society for Microbiology","issue":"18","license":[{"start":{"date-parts":[[2008,9,15]],"date-time":"2008-09-15T00:00:00Z","timestamp":1221436800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2008,9,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            CD4\n            <jats:sup>+<\/jats:sup>\n            T-cell depletion is the hallmark of AIDS pathogenesis. Multiple mechanisms may contribute to the death of productively infected CD4\n            <jats:sup>+<\/jats:sup>\n            T cells and innocent-bystander cells. In this study, we characterize a novel mechanism in which human immunodeficiency virus type 1 (HIV-1) infection preferentially depletes peripheral memory CD4\n            <jats:sup>+<\/jats:sup>\n            T cells before the completion of reverse transcription. Using a recombinant HIV-1 carrying the green fluorescent protein reporter gene, we demonstrate that memory CD4\n            <jats:sup>+<\/jats:sup>\n            T cells were susceptible to infection-induced cell death at a low multiplicity of infection. Infected memory CD4\n            <jats:sup>+<\/jats:sup>\n            T cells underwent rapid necrotic cell death. Killing of host cells was dependent on X4 envelope-mediated viral fusion, but not on virion-associated Vpr or Nef. In contrast to peripheral resting CD4\n            <jats:sup>+<\/jats:sup>\n            T cells, CD4\n            <jats:sup>+<\/jats:sup>\n            T cells stimulated by mitogen or certain cytokines were resistant to HIV-1-induced early cell death. These results demonstrate that early steps in HIV-1 infection have a detrimental effect on certain subsets of CD4\n            <jats:sup>+<\/jats:sup>\n            T cells. The early cell death may serve as a selective disadvantage for X4-tropic HIV-1 in acute infection but may play a role in accelerated disease progression, which is associated with the emergence of X4-tropic HIV-1 in the late stage of AIDS.\n          <\/jats:p>","DOI":"10.1128\/jvi.00773-08","type":"journal-article","created":{"date-parts":[[2008,7,3]],"date-time":"2008-07-03T00:44:25Z","timestamp":1215045865000},"page":"9154-9163","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":16,"title":["Preferential Cytolysis of Peripheral Memory CD4\n            <sup>+<\/sup>\n            T Cells by In Vitro X4-Tropic Human Immunodeficiency Virus Type 1 Infection before the Completion of Reverse Transcription"],"prefix":"10.1128","volume":"82","author":[{"given":"Yan","family":"Zhou","sequence":"first","affiliation":[{"name":"Department of Medicine, Johns Hopkins University School of Medicine"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lin","family":"Shen","sequence":"additional","affiliation":[{"name":"Department of Medicine, Johns Hopkins University School of Medicine"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hung-Chih","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Medicine, Johns Hopkins University School of Medicine"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robert F.","family":"Siliciano","sequence":"additional","affiliation":[{"name":"Department of Medicine, Johns Hopkins University School of Medicine"},{"name":"Howard Hughes Medical Institute, Baltimore, 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