Publications
198 results found
Stebbing J, Gazzard B, Patterson S, et al., 2004, Simplified one-step antibody-HLA directed expansion of HIV-specific cytotoxic T lymphocytes:: a system suited for use <i>in vivo</i> (vol 18, pg 2099, 2004), AIDS, Vol: 18, Pages: 2099-2101, ISSN: 0269-9370
- Author Web Link
- Cite
- Citations: 1
Greenspan G, Geiger D, Gotch F, et al., 2004, Model-based inference of recombination hotspots in a highly variable oncogene (vol 58, pg 239, 2004), JOURNAL OF MOLECULAR EVOLUTION, Vol: 59, Pages: 283-283, ISSN: 0022-2844
Prakash M, Kapembwa MS, Gotch F, et al., 2004, Chemokine receptor expression on mucosal dendritic cells from the endocervix of healthy women, JOURNAL OF INFECTIOUS DISEASES, Vol: 190, Pages: 246-250, ISSN: 0022-1899
- Author Web Link
- Cite
- Citations: 29
Belshe R, Franchini G, Girard MP, et al., 2004, Support for the RV144 HIV vaccine trial, SCIENCE, Vol: 305, Pages: 177-177, ISSN: 0036-8075
- Author Web Link
- Cite
- Citations: 16
Pires A, Hardy G, Gazzard B, et al., 2004, Initiation of antiretroviral therapy during recent HIV-1 infection results in lower residual viral reservoirs, JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES, Vol: 36, Pages: 783-790, ISSN: 1525-4135
- Author Web Link
- Cite
- Citations: 23
Stebbing J, Patterson S, Portsmouth S, et al., 2004, Studies on the allostimulatory function of dendritic cells from HCV-HIV-1 co-infected patients, CELL RESEARCH, Vol: 14, Pages: 251-256, ISSN: 1001-0602
- Author Web Link
- Cite
- Citations: 12
Kebba A, Kaleebu P, Rowland S, et al., 2004, Distinct patterns of peripheral HIV-1-specific interferon-γ responses in exposed HIV-1-seronegative individuals, JOURNAL OF INFECTIOUS DISEASES, Vol: 189, Pages: 1705-1713, ISSN: 0022-1899
- Author Web Link
- Cite
- Citations: 28
Stebbing J, Gazzard B, Patterson S, et al., 2004, Antibody-targeted MHC complex-directed expansion of HIV-1- and KSHV-specific CD8<SUP>+</SUP> lymphocytes:: a new approach to therapeutic vaccination, BLOOD, Vol: 103, Pages: 1791-1795, ISSN: 0006-4971
- Author Web Link
- Cite
- Citations: 13
Hardy G, Worrell S, Hayes P, et al., 2004, Evidence of thymic reconstitution after highly active antiretroviral therapy in HIV-1 infection, HIV MEDICINE, Vol: 5, Pages: 67-73, ISSN: 1464-2662
- Author Web Link
- Cite
- Citations: 26
Greenspan G, Geiger D, Gotch F, et al., 2004, Model-based inference of recombination hotspots in a highly, variable oncogene, JOURNAL OF MOLECULAR EVOLUTION, Vol: 58, Pages: 239-251, ISSN: 0022-2844
- Author Web Link
- Cite
- Citations: 4
Greenspan G, Geiger D, Gotch F, et al., 2004, Recombination does not occur in newly identified diverged oceanic picornaviruses, JOURNAL OF MOLECULAR EVOLUTION, Vol: 58, Pages: 359-360, ISSN: 0022-2844
- Author Web Link
- Cite
- Citations: 1
Goodier MR, Imami N, Moyle G, et al., 2004, Loss of the CD56(hi) CD16(-) NK cell subset and NK cell interferon-gamma production during antiretroviral therapy for HIV-1: partial recovery by human growth hormone (vol 134, pg 470, 2003), Clinical and Experimental Immunology, Vol: 135, Pages: 344-344, ISSN: 0009-9104
Pires A, Pido-Lopez J, Moyle G, et al., 2004, Enhanced T-cell maturation, differentiation and function in HIV-1-infected individuals after growth hormone and highly active antiretroviral therapy, ANTIVIRAL THERAPY, Vol: 9, Pages: 67-75, ISSN: 1359-6535
- Author Web Link
- Cite
- Citations: 19
Stebbing J, Gazzard B, Newsom-Davis T, et al., 2004, Nadir B cell counts are significantly correlated with the risk of Kaposi's sarcoma, INTERNATIONAL JOURNAL OF CANCER, Vol: 108, Pages: 473-474, ISSN: 0020-7136
- Author Web Link
- Cite
- Citations: 19
Portsmouth S, Imami N, Pires A, et al., 2004, Treatment of primary HIV-1 infection with nonnucleoside reverse transcriptase inhibitor-based therapy is effective and well tolerated, HIV MEDICINE, Vol: 5, Pages: 26-29, ISSN: 1464-2662
- Author Web Link
- Cite
- Citations: 9
Kebba A, Kaleebu P, Serwanga J, et al., 2004, HIV type 1 antigen-responsive CD4+ T-lymphocytes in exposed yet HIV Type 1 seronegative Ugandans, AIDS Res Hum Retroviruses, Vol: 20, Pages: 67-75, ISSN: 0889-2229
Rutebemberwa A, Auma B, Gilmour J, et al., 2004, HIV type 1-specific inter- and intrasubtype cellular immune responses in HIV type 1-infected Ugandans, AIDS Res Hum Retroviruses, Vol: 20, Pages: 763-771, ISSN: 0889-2229
Chadwick D, Pido-Lopez J, Pires A, et al., 2003, A pilot study of the safety and efficacy of thymosin α<sub>1</sub> in augmenting immune reconstitution in HIV-infected patients with low CD4 counts taking highly active antiretroviral therapy, CLINICAL AND EXPERIMENTAL IMMUNOLOGY, Vol: 134, Pages: 477-481, ISSN: 0009-9104
- Author Web Link
- Cite
- Citations: 28
Goodier MR, Imami N, Moyle G, et al., 2003, Loss of the CD56<SUP>hi</SUP>CD16<SUP>-</SUP> NK cell subset and NK cell interferon-γ production during antiretroviral therapy for HIV-1:: partial recovery by human growth hormone, CLINICAL AND EXPERIMENTAL IMMUNOLOGY, Vol: 134, Pages: 470-476, ISSN: 0009-9104
- Author Web Link
- Cite
- Citations: 38
Stebbing J, Wildfire A, Portsmouth S, et al., 2003, Paclitaxel for anthracycline-resistant AIDS-related Kaposi's sarcoma: clinical and angiogenic correlations, ANNALS OF ONCOLOGY, Vol: 14, Pages: 1660-1666, ISSN: 0923-7534
- Author Web Link
- Cite
- Citations: 42
Hardy GAD, Imami N, Sullivan AK, et al., 2003, Reconstitution of CD4<SUP>+</SUP> T cell responses in HIV-1 infected individuals initiating highly active antiretroviral therapy (HAART) is associated with renewed interleukin-2 production and responsiveness, CLINICAL AND EXPERIMENTAL IMMUNOLOGY, Vol: 134, Pages: 98-106, ISSN: 0009-9104
- Author Web Link
- Cite
- Citations: 27
Stebbing J, Gazzard B, Flore O, et al., 2003, Natural killer cells are not infected by Kaposi's sarcoma-associated herpesvirus <i>in vivo</i>, and natural killer cell counts do not correlate with the risk of developing Kaposi's sarcoma, AIDS, Vol: 17, Pages: 1998-2000, ISSN: 0269-9370
- Author Web Link
- Cite
- Citations: 12
Stebbing J, Gazzard B, Portsmouth S, et al., 2003, Disease-associated dendritic cells respond to disease-specific antigens through the common heat shock protein receptor, BLOOD, Vol: 102, Pages: 1806-1814, ISSN: 0006-4971
- Author Web Link
- Cite
- Citations: 32
Stebbing J, Gotch F, Gazzard B, 2003, Bella and the blood sample, BMJ, Vol: 327, ISSN: 0959-8138
Donaghy H, Gazzard B, Gotch F, et al., 2003, Dysfunction and infection of freshly isolated blood myeloid and plasmacytoid dendritic cells in patients infected with HIV-1, BLOOD, Vol: 101, Pages: 4505-4511, ISSN: 0006-4971
- Author Web Link
- Cite
- Citations: 218
Sullivan AK, Burton CT, Nelson MR, et al., 2003, Restoration of human immunodeficiency virus-1-specific responses in patients changing from protease to non-nucleoside reverse transcriptase inhibitor-based antiretroviral therapy, Scandinavian Journal of Immunology, Vol: 57, Pages: 600-607, ISSN: 0300-9475
The effect of altering antiretroviral therapy (ART) on responses to viral, recall and human immunodeficiency virus (HIV)-1-specific recombinant antigens and interleukin-2 (IL-2) in HIV-1-infected patients was assessed. A longitudinal cohort study in eight HIV-1 infected individuals following a clinically indicated therapy change (seven for drug intolerance and one for virological failure) from protease inhibitor (PI) to non-nucleoside reverse transcriptase inhibitor (NNRTI)-based antiretroviral regimens was performed. CD4 T-cell counts, viral loads, lymphoproliferative responses, cytokine production and latent proviral deoxyribonucleic acid (DNA) were measured at baseline and at weeks 12 and 24 after therapy substitution. Following therapy-switch there was a 33% proportional increase in mitogen response (95% confidence interval (CI), 3–33%) and a 31% increase (95% CI, 15–48%) in viral and recall-antigen responses. Six patients developed proliferative responses to low concentration IL-2 stimulation. All patients demonstrated an increase in median HIV-1-specific responses, as three had detectable virus at baseline (two being viral rebound); this may reflect an autovaccination effect. Proviral DNA changes largely reflected plasma HIV-1 ribonucleic acid (RNA). In conclusion, NNRTI substitution for a PI may favour immune reconstitution with an improvement in HIV-1-specific responses, which may reflect differential effects on antigen processing and presentation, an autovaccination effect or alternatively a potential suppressive effect of the PI.
Imami N, Gotch F, 2003, Twenty years of HIV-1 research: what the future holds, NATURE IMMUNOLOGY, Vol: 4, Pages: 501-501, ISSN: 1529-2908
- Author Web Link
- Cite
- Citations: 1
Stebbing J, Gazzard B, Kim L, et al., 2003, The heat-shock protein receptor CD91 is up-regulated in monocytes of HIV-1-infected "true" long-term nonprogressors, BLOOD, Vol: 101, Pages: 4000-4004, ISSN: 0006-4971
- Author Web Link
- Cite
- Citations: 41
Stebbing J, Portsmouth S, Gotch F, et al., 2003, Kaposi's sarcoma - an update, INTERNATIONAL JOURNAL OF STD & AIDS, Vol: 14, Pages: 225-227, ISSN: 0956-4624
- Author Web Link
- Cite
- Citations: 8
Stebbing J, Bourboulia D, Johnson M, et al., 2003, Kaposi's sarcoma-associated herpesvirus cytotoxic T lymphocytes recognize and target Darwinian positively selected autologous K1 epitopes, Journal of Virology, Vol: 77, Pages: 4306-4314, ISSN: 0022-538X
Kaposi's sarcoma-associated herpesvirus (KSHV) is the infectious cause of Kaposi's sarcoma (KS) and certain lymphoproliferations particularly in the context of human immunodeficiency virus (HIV) type 1-induced immunosuppression. The introduction of effective therapies to treat HIV has led to a decline in the incidence of KS, suggesting that immune responses may play a role in controlling KSHV infection and pathogenesis. Cytotoxic-T-lymphocyte (CTL) activity against KSHV proteins has been demonstrated; however, the identification of KSHV CTL epitopes remains elusive and problematic. Although the herpesvirus genomic layout is generally conserved, KSHV encodes a unique hypervariable protein, K1, with intense biological selection pressure at specific amino acid sites. To investigate whether this variability is partly driven by cellular immunity, we designed K1 peptides that match only the unique viral sequence for every individual studied here (autologous peptides). We identified functional CTL epitopes within K1's most variable areas, and we show that a given individual responds only to autologous peptides and not to peptides from other individuals. Furthermore, these epitopes are highly conserved sequences within KSHV isolates from a specific strain but are not conserved between different strains. We conclude that CTL recognition contributes to K1, and therefore to KSHV, evolution.
This data is extracted from the Web of Science and reproduced under a licence from Thomson Reuters. You may not copy or re-distribute this data in whole or in part without the written consent of the Science business of Thomson Reuters.