Publications
111 results found
Kattan T, MacNamara A, Rowan AG, et al., 2009, The Avidity and Lytic Efficiency of the CTL Response to HTLV-1, JOURNAL OF IMMUNOLOGY, Vol: 182, Pages: 5723-5729, ISSN: 0022-1767
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- Citations: 48
Asquith B, Borghans JAM, Ganusov VV, et al., 2009, Lymphocyte kinetics in health and disease, TRENDS IN IMMUNOLOGY, Vol: 30, Pages: 182-189, ISSN: 1471-4906
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- Citations: 22
MacNamara A, Kadolsky U, Bangham CRM, et al., 2009, T-Cell Epitope Prediction: Rescaling Can Mask Biological Variation between MHC Molecules, PLOS COMPUTATIONAL BIOLOGY, Vol: 5
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- Citations: 25
Bangham CRM, Meekings K, Toulza F, et al., 2009, The immune control of HTLV-1 infection: selection forces and dynamics, FRONTIERS IN BIOSCIENCE-LANDMARK, Vol: 14, Pages: 2889-2903, ISSN: 2768-6701
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- Citations: 39
Macallan DC, Asquith B, Zhang Y, et al., 2009, Measurement of proliferation and disappearance of rapid turnover cell populations in human studies using deuterium-labeled glucose, NATURE PROTOCOLS, Vol: 4, Pages: 1313-1327, ISSN: 1754-2189
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- Citations: 33
Asquith B, 2008, The evolutionary selective advantage of HIV-1 escape variants and the contribution of escape to the HLA-associated risk of AIDS progression, PLoS One, Vol: 3, Pages: 1-10, ISSN: 1932-6203
HIV-1 escape from surveillance by cytotoxic T lymphocytes (CTL) is thought to cause at least transient weakening of immune control. However, the CTL response is highly adaptable and the long-term consequences of viral escape are not fully understood. The objective of this study was to address the question “to what extent does HIV-1 escape from CTL contribute to HLA-associated AIDS progression?” We combined an analysis of 21 escape events in longitudinally-studied HIV-1 infected people with a population-level analysis of the functional CTL response in 150 subjects (by IFNg ELISpot) and an analysis of the HIV-1 sequence database to quantify the contribution of escape to the HLA-associated rate of AIDS progression. We found that CTL responses restricted by protective HLA class I alleles, which are associated with slow progression to AIDS, recognised epitopes where escape variants had a weak evolutionary selective advantage (P = 0.008) and occurred infrequently (P = 0.017). Epitopes presented by protective HLA class I alleles were more likely to elicit a CTL response (P = 0.001) and less likely to contain sequence variation (P = 0.006). A third of between-individual variation in HLA-associated disease risk was predicted by the selective advantage of escape variants: a doubling in the evolutionary selective advantage was associated with a decrease in the AIDS-free period of 1.2 yrs. These results contribute to our understanding of what makes a CTL response protective and why some individuals progress to AIDS more rapidly than others.
Defoiche J, Debacq C, Asquith B, et al., 2008, Reduction of B cell turnover in chronic lymphocytic leukaemia, BRITISH JOURNAL OF HAEMATOLOGY, Vol: 143, Pages: 240-247, ISSN: 0007-1048
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- Citations: 37
Asquith B, Bangharn CRM, 2008, How does HTLV-I persist despite a strong cell-mediated immune response?, TRENDS IN IMMUNOLOGY, Vol: 29, Pages: 4-11, ISSN: 1471-4906
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- Citations: 46
Lezin A, Gillet N, Olindo S, et al., 2007, Histone deacetylase-mediated transcriptional activation reduces proviral loads in HTLV-1-associated myelopathy/tropical spastic paraparesis patients, BLOOD, Vol: 110, Pages: 3722-3728, ISSN: 0006-4971
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- Citations: 61
Zhang Y, Wallace DL, de Lara CM, et al., 2007, <i>In vivo</i> kinetics of human natural killer cells:: the effects of ageing and acute and chronic viral infection, IMMUNOLOGY, Vol: 121, Pages: 258-265, ISSN: 0019-2805
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- Citations: 184
Asquith B, Bangham CRM, 2007, Quantifying HTLV-I dynamics, IMMUNOLOGY AND CELL BIOLOGY, Vol: 85, Pages: 280-286, ISSN: 0818-9641
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- Citations: 58
Florins A, Gillet N, Asquith B, et al., 2007, Cell dynamics and immune response to BLV infection: A unifying model, 13th International Conference on Human Retrovirology - HTLV and Related Viruses, Publisher: MARY ANN LIEBERT INC, Pages: 589-589, ISSN: 0889-2229
Lezin A, Gillet N, Olindo S, et al., 2007, Activation of latent provirus: nEw therapy for HTLV-1-associated myelopathy/tropical spastic paraparesis? (a proof-of-concept study), 13th International Conference on Human Retrovirology - HTLV and Related Viruses, Publisher: MARY ANN LIEBERT INC, Pages: 643-644, ISSN: 0889-2229
Gillet N, Lezin A, Mosley A, et al., 2007, HTLV-1 can infect human lung epithelial cells and induce gene expression of cytokines, chemokines, and cell adhesion molecules, 13th International Conference on Human Retrovirology - HTLV and Related Viruses, Publisher: MARY ANN LIEBERT INC, Pages: 618-619, ISSN: 0889-2229
Florins A, Gillet N, Asquith B, et al., 2007, Cell dynamics and immune response to BLV infection: a unifying model, FRONTIERS IN BIOSCIENCE-LANDMARK, Vol: 12, Pages: 1520-1531, ISSN: 1093-9946
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- Citations: 57
Asquith B, Zhang Y, Mosley A, et al., 2007, In vivo T lymphocyte dynamics in humans and the impact of human T-lymphotropic virus 1 infection, PNAS, Vol: 104, Pages: 8035-8040, ISSN: 0027-8424
Asquith B, McLean A, 2007, In vivo CD8+ T cell control of immunodeficiency virus infection in humans and macaques, PNAS, Vol: 104, Pages: 6365-6370, ISSN: 1091-6490
Florins A, Gillet N, Asquith B, et al., 2006, Spleen-dependent turnover of CD11b peripheral blood B lymphocytes in bovine leukemia virus-infected sheep, JOURNAL OF VIROLOGY, Vol: 80, Pages: 11998-12008, ISSN: 0022-538X
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- Citations: 15
Defoiche J, Debacq C, Asquith B, et al., 2006, Reduced rates of B cell proliferation in chronic lymphocytic leukemia., 48th Annual Meeting of the American-Society-of-Hematology, Publisher: AMER SOC HEMATOLOGY, Pages: 798A-798A, ISSN: 0006-4971
Debacq C, Gillet N, Asquith B, et al., 2006, Peripheral blood B-cell death compensates for excessive proliferation in lymphoid tissues and maintains homeostasis in bovine leukemia virus-infected sheep, JOURNAL OF VIROLOGY, Vol: 80, Pages: 9710-9719, ISSN: 0022-538X
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- Citations: 19
Asquith B, Debacq C, Florins A, et al., 2006, Quantifying lymphocyte kinetics <i>in vivo</i> using carboxyfluorescein diacetate succinimidyl ester (CFSE), PROCEEDINGS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES, Vol: 273, Pages: 1165-1171, ISSN: 0962-8452
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- Citations: 55
B Asquith, C Edwards, M Lipsitch, et al., 2006, Inefficient cytotoxic T lymphocyte-mediated killing of HIV-1-infected cells in vivo, PLoS Biology, Vol: 4, Pages: 583-592, ISSN: 1544-9173
Understanding the role of cytotoxic T lymphocytes (CTLs) in controlling HIV-1 infection is vital for vaccine design. However, it is difficult to assess the importance of CTLs in natural infection. Different human leukocyte antigen (HLA) class I alleles are associated with different rates of progression to AIDS, indicating that CTLs play a protective role. Yet virus clearance rates following antiretroviral therapy are not impaired in individuals with advanced HIV disease, suggesting that weakening of the CTL response is not the major underlying cause of disease progression and that CTLs do not have an important protective role. Here we reconcile these apparently conflicting studies. We estimate the selection pressure exerted by CTL responses that drive the emergence of immune escape variants, thereby directly quantifying the efficiency of HIV-1–specific CTLs in vivo. We estimate that only 2% of productively infected CD4+ cell death is attributable to CTLs recognising a single epitope. We suggest that CTLs kill a large number of infected cells (about 107) per day but are not responsible for the majority of infected cell death.
Asquith B, Mosley AJ, Heaps A, et al., 2005, Quantification of the virus-host interaction in human T lymphotropic virus I infection, Retrovirology, Vol: 2, Pages: 1-9, ISSN: 1742-4690
BackgroundHTLV-I causes the disabling inflammatory disease HAM/TSP: there is no vaccine, no satisfactory treatment and no means of assessing the risk of disease or prognosis in infected people. Like many immunopathological diseases with a viral etiology the outcome of infection is thought to depend on the virus-host immunology interaction. However the dynamic virus-host interaction is complex and current models of HAM/TSP pathogenesis are conflicting. The CD8+ cell response is thought to be a determinant of both HTLV-I proviral load and disease status but its effects can obscure other factors.ResultsWe show here that in the absence of CD8+ cells, CD4+ lymphocytes from HAM/TSP patients expressed HTLV-I protein significantly more readily than lymphocytes from asymptomatic carriers of similar proviral load (P = 0.017). A high rate of viral protein expression was significantly associated with a large increase in the prevalence of HAM/TSP (P = 0.031, 89% of cases correctly classified). Additionally, a high rate of Tax expression and a low CD8+ cell efficiency were independently significantly associated with a high proviral load (P = 0.005, P = 0.003 respectively).ConclusionThese results disentangle the complex relationship between immune surveillance, proviral load, inflammatory disease and viral protein expression and indicate that increased protein expression may play an important role in HAM/TSP pathogenesis. This has important implications for therapy since it suggests that interventions should aim to reduce Tax expression rather than proviral load per se.
Debacq C, Héraud JM, Asquith B, et al., 2005, Reduced cell turnover in lymphocytic monkeys infected by human T-lymphotropic virus type 1, ONCOGENE, Vol: 24, Pages: 7514-7523, ISSN: 0950-9232
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- Citations: 9
Mosley AJ, Asquith B, Bangham CRM, 2005, Cell-mediated immune response to human T-lymphotropic virus type I, VIRAL IMMUNOLOGY, Vol: 18, Pages: 293-305, ISSN: 0882-8245
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- Citations: 11
Macallan DC, Wallace DL, Zhang Y, et al., 2005, B-cell kinetics in humans: rapid turnover of peripheral blood memory cells, BLOOD, Vol: 105, Pages: 3633-3640, ISSN: 0006-4971
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- Citations: 117
Heaps AG, Vine AM, Kaftantzi L, et al., 2005, Gene expression analysis of the T lymphocyte response to HTLV-1, 12th International Conference on Human Retrovirology - HTLV and Related Viruses, Publisher: MARY ANN LIEBERT INC, Pages: 483-483, ISSN: 0889-2229
Florins A, Debacq C, Gillet N, et al., 2005, Key role of the spleen in the cell turnover of bovine leukemia virus infected B lymphocytes, 12th International Conference on Human Retrovirology - HTLV and Related Viruses, Publisher: MARY ANN LIEBERT INC, Pages: 512-512, ISSN: 0889-2229
Asquith B, Mosley A, Barfield A, et al., 2005, Determinants of HTLV-I proviral load and HAM/TSP risk, 12th International Conference on Human Retrovirology - HTLV and Related Viruses, Publisher: MARY ANN LIEBERT INC, Pages: 482-482, ISSN: 0889-2229
Asquith B, Mosley AJ, Barfield A, et al., 2005, A functional CD8<SUP>+</SUP> cell assay reveals individual variation in CD8<SUP>+</SUP> cell antiviral efficacy and explains differences in human T-lymphotropic virus type 1 proviral load, JOURNAL OF GENERAL VIROLOGY, Vol: 86, Pages: 1515-1523, ISSN: 0022-1317
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- Citations: 70
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