دورية أكاديمية
High-level HIV-1 viremia suppresses viral antigen-specific CD4(+) T cell proliferation.
| العنوان: | High-level HIV-1 viremia suppresses viral antigen-specific CD4(+) T cell proliferation. |
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| المؤلفون: | McNeil AC; Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA., Shupert WL, Iyasere CA, Hallahan CW, Mican JA, Davey RT Jr, Connors M |
| المصدر: | Proceedings of the National Academy of Sciences of the United States of America [Proc Natl Acad Sci U S A] 2001 Nov 20; Vol. 98 (24), pp. 13878-83. |
| نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
| اللغة: | English |
| بيانات الدورية: | Publisher: National Academy of Sciences Country of Publication: United States NLM ID: 7505876 Publication Model: Print Cited Medium: Print ISSN: 0027-8424 (Print) Linking ISSN: 00278424 NLM ISO Abbreviation: Proc Natl Acad Sci U S A Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: Washington, DC : National Academy of Sciences |
| مواضيع طبية MeSH: | CD4-Positive T-Lymphocytes/*cytology , HIV Antigens/*immunology , HIV Infections/*immunology , HIV-1/*growth & development , Viremia/*immunology , Virus Replication/*immunology, CD4-Positive T-Lymphocytes/immunology ; Cell Division ; HIV Infections/virology ; HIV-1/physiology ; Humans ; T-Lymphocyte Subsets/cytology ; T-Lymphocyte Subsets/immunology ; Viremia/virology |
| مستخلص: | In chronic viral infections of humans and experimental animals, virus-specific CD4(+) T cell function is believed to be critical for induction and maintenance of host immunity that mediates effective restriction of viral replication. Because in vitro proliferation of HIV-specific memory CD4(+) T cells is only rarely demonstrable in HIV-infected individuals, it is presumed that HIV-specific CD4(+) T cells are killed upon encountering the virus, and maintenance of CD4(+) T cell responses in some patients causes the restriction of virus replication. In this study, proliferative responses were absent in patients with poorly restricted virus replication although HIV-specific CD4(+) T cells capable of producing IFN-gamma were detected. In a separate cohort, interruption of antiretroviral therapy resulted in the rapid and complete abrogation of virus-specific proliferation although HIV-1-specific CD4(+) T cells were present. HIV-specific proliferation returned when therapy was resumed and virus replication was controlled. Further, HIV-specific CD4(+) T cells of viremic patients could be induced to proliferate in response to HIV antigens when costimulation was provided by anti-CD28 antibody in vitro. Thus, HIV-1-specific CD4(+) T cells persist but remain poorly responsive (produce IFN-gamma but do not proliferate) in viremic patients. Unrestricted virus replication causes diminished proliferation of virus-specific CD4(+) T cells. Suppression of proliferation of HIV-specific CD4(+) T cells in the context of high levels of antigen may be a mechanism by which HIV or other persistently replicating viruses limit the precursor frequency of virus-specific CD4(+) T cells and disrupt the development of effective virus-specific immune responses. |
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| المشرفين على المادة: | 0 (HIV Antigens) |
| تواريخ الأحداث: | Date Created: 20011122 Date Completed: 20020108 Latest Revision: 20181113 |
| رمز التحديث: | 20221213 |
| مُعرف محوري في PubMed: | PMC61135 |
| DOI: | 10.1073/pnas.251539598 |
| PMID: | 11717444 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 0027-8424 |
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| DOI: | 10.1073/pnas.251539598 |