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Cytotoxic T-cell antagonism in HIV-1
Institution:1. Département de gériatrie Bichat–Beaujon–Bretonneau, hôpitaux universitaires Paris Nord Val-de-Seine, AP–HP, faculté de médecine Denis-Diderot, 46, rue Henri-Huchard, 75018 Paris, France;2. Unité d’assistance nutritionnelle, unité transversale de nutrition, service de nutrition–endocrinologie–diabétologie, CHU de Nancy, 54500 Vandœuvre-les-Nancy, France;1. Department of Instrumentation and Analytical Chemistry, CAS Key Laboratory of Separation Science for Analytical Chemistry, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, 457 Zhongshan Road, Dalian 116023, PR China;2. University of Chinese Academy of Sciences, Beijing 100049, PR China;1. Protechnik Laboratories, A Division of ARMSCOR SOC Ltd., 103 Combretum Crescent, Centurion, Pretoria 0001, South Africa;2. Department of Internal Medicine, 1 Military Hospital, South African Military Health Services, Voortrekker Street, Pretoria 0001, South Africa;3. Department of Chemistry, University of Pretoria, Lynwood Road, Pretoria 0001, South Africa;1. Yale School of Medicine, New Haven, Connecticut;2. Department of Neurology, Yale School of Medicine, New Haven, Connecticut;3. Department of Dermatology, Yale School of Medicine, New Haven, Connecticut;1. The Royal Melbourne Hospital, Grattan Street, Parkville, VIC 3050, Australia;2. The University of Melbourne, Parkville, VIC, Australia;1. Laboratoire de Mathématiques Nicolas Oresme, Université de Caen, France;2. Indian Statistical Institute, New Delhi, India;3. Mashhad University of Medical Sciences, Mashhad, Iran
Abstract:The cytotoxic T-cell (CTL) response to human immunodeficiency virus Type 1 (HIV-1) is vigorous and sustained, but despite this, the virus persists. Natural variation arising within CTL epitopes may affect CTL recognition of infected targets and allow viral escape. Some of these variant epitopes appear to engage T-cell receptors but fail to activate the CTL normally. This can interfere with recognition of the unmutated epitope — a phenomenon known as T-cell antagonism. We discuss the evidence for this in HIV-1 using CTL and epitope variants derived from infected donors, and discuss its possible relevancein vivo.
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