Tat-specific cytotoxic T lymphocytes select for SIV escape variants during resolution of primary viraemia
| Autor: | Kevin J. Kunstman, David H. O’Connor, Steven M. Wolinsky, Alessandro Sette, John L. Dzuris, Max E. Liebl, Ronald C. Desrosiers, Peicheng Jing, Bianca R. Mothé, Xiaochi Wang, David I. Watkins, Todd M. Allen, Ed Dunphy, Carol Emerson, Austin L. Hughes, David B. Allison, Thorsten U. Vogel, John D. Altman, Nancy A. Wilson |
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| Rok vydání: | 2000 |
| Předmět: |
Cellular immunity
viruses Molecular Sequence Data Simian Acquired Immunodeficiency Syndrome Epitopes T-Lymphocyte medicine.disease_cause Virus Viral life cycle medicine Cytotoxic T cell Animals Amino Acid Sequence Viremia HIV vaccine AIDS Vaccines Multidisciplinary biology Histocompatibility Antigens Class I virus diseases Simian immunodeficiency virus biology.organism_classification Virology Macaca mulatta Viral replication Amino Acid Substitution Lentivirus Immunology Gene Products tat Mutation Simian Immunodeficiency Virus T-Lymphocytes Cytotoxic |
| Zdroj: | Nature. 407(6802) |
| ISSN: | 0028-0836 |
| Popis: | Human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) infections are characterized by early peaks of viraemia that decline as strong cellular immune responses develop. Although it has been shown that virus-specific CD8-positive cytotoxic T lymphocytes (CTLs) exert selective pressure during HIV and SIV infection, the data have been controversial. Here we show that Tat-specific CD8-positive T-lymphocyte responses select for new viral escape variants during the acute phase of infection. We sequenced the entire virus immediately after the acute phase, and found that amino-acid replacements accumulated primarily in Tat CTL epitopes. This implies that Tat-specific CTLs may be significantly involved in controlling wild-type virus replication, and suggests that responses against viral proteins that are expressed early during the viral life cycle might be attractive targets for HIV vaccine development. |
| Databáze: | OpenAIRE |
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