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2. Effect of incident hepatitis C infection on CD4(+) cell count and HIV RNA trajectories based on a multinational HIV seroconversion cohort

Author

van Santen, DK, van der Helm, JJ, Touloumi, G, Pantazis, N, Muga, R, Gunsenheimer-Bartmeyer, B, Gill, MJ, Sanders, E, Kelleher, A, Zangerle, R, Porter, K, Prins, M, Geskus, RB, Del Amo, J, Meyer, L, Bucher, HC, Chene, G, Hamouda, O, Pillay, D, Rosinska, M, Sabin, C, Olson, A, Cartier, A, Fradette, L, Walker, S, Babiker, A, De Luca, A, Fisher, M, Kelleher, T, Cooper, D, Grey, P, Finlayson, R, Bloch, M, Ramacciotti, T, Gelgor, L, Smith, D, Lutsar, I, Dabis, F, Thiebaut, R, Costagliola, D, Guiguet, M, Vanhems, P, Chaix, ML, Ghosn, J, Boufassa, F, Meixenberger, K, Bannert, N, Antoniadou, A, Chrysos, G, Daikos, GL, Katsarou, O, Rezza, G, Dorrucci, M, Monforte, AD, Schuitemaker, H, Sannes, M, Kran, AMB, Tor, J, de Olalla, PG, Cayla, J, Moreno, S, Monge, S, del Romero, J, Perez-Hoyos, S, Sonnerborg, A, Gunthard, H, Scherrer, A, Malyuta, R, Murphy, G, Johnson, A, Phillips, A, Morrison, C, Salata, R, Mugerwa, R, Chipato, T, Price, MA, Gilmour, J, Kamali, A, Karita, E, Burns, F, Giaquinto, C, Grarup, J, Kirk, O, Bailey, H, Anne, AV, Panteleev, A, Thorne, C, Aboulker, JP, Albert, J, Asandi, S, De Wit, S, Reiss, P, Gatell, J, Karpov, I, Ledergerber, B, Lundgren, J, Moller, C, Rakhmanova, A, Rockstroh, J, Sandhu, M, Dedes, N, Fenton, K, Pizzuti, D, Vitoria, M, Faggion, S, Frost, R, Raben, D, Schwimmer, C, and Scott, M

Subjects
hepatitis C virus, HIV RNA, CD4(+) cell count, HIV, MSM
Abstract

Background: Most studies on hepatitis C virus (HCV)/HIV-coinfection do not account for the order and duration of these two infections. We aimed to assess the effect of incident HCVinfection, and its timing relative to HIVseroconversion (HIVsc) in HIV-positiveMSM on their subsequent CD4(+) T-cell count and HIV RNA viral load trajectories. Methods: WeincludedMSMwithwell estimated dates ofHIVsc from 17 cohortswithin the CASCADE Collaboration. HCV-coinfected MSM were matched to as many HIV monoinfected MSM as possible by HIV-infection duration and combination antiretroviral therapy (cART) use. We used multilevel random-effects models stratified by cART use to assess differences inCD4(+) cell count andHIVRNAviral loadtrajectoriesbyHCV-coinfection status. Findings: Wematched 214 (ART-naive) and 147 (on cART) HCV-coinfectedMSMto 5384 and 3954, respectively, matched controls. The timing of HCV seroconversion (HCVsc) relative to HIVsc had no demonstrable effect on HIV RNA viral load or CD4(+) cell count trajectories. In the first 2-3 years following HCVsc CD4(+) cell counts were lower among HCV-coinfected MSM, but became comparable with HIV monoinfected MSM thereafter. In ART-naive MSM, during the first 2 years after HCVsc, HIV RNA viral load levels were lower or comparable with HIV monoinfected, tending to be higher thereafter. In MSM on cART, HCV had no significant effect on having a detectable HIV RNA viral load. Interpretation: Irrespective of the duration of HIV infection when HCV is acquired, CD4(+) cell counts were temporarily lower following HCVsc, even when on cART. The clinical implications of our findings remain to be further elucidated. Copyright (C) 2018 Wolters Kluwer Health, Inc. All rights reserved.

Published
2019

4. Predictors of CD4 cell recovery following initiation of antiretroviral therapy among HIV-1 positive patients with well-estimated dates of seroconversion

Author

Stirrup, O.T. Copas, A.J. Phillips, A.N. Gill, M.J. Geskus, R.B. Touloumi, G. Young, J. Bucher, H.C. Babiker, A.G. Kelleher, T. Cooper, D. Grey, P. Finlayson, R. Bloch, M. Ramacciotti, T. Gelgor, L. Smith, D. Zangerle, R. Gill, J. Lutsar, I. Chêne, G. Dabis, F. Thiebaut, R. Costagliola, D. Guiguet, M. Vanhems, P. Chaix, M.-L. Ghosn, J. Meyer, L. Boufassa, F. Hamouda, O. Meixenberger, K. Bannert, N. Bartmeyer, B. Antoniadou, A. Chrysos, G. Daikos, G.L. Pantazis, N. Katsarou, O. Rezza, G. Dorrucci, M. Monforte, A. Luca, A. Prins, M. Geskus, R. Helm, J. Schuitemaker, H. Sannes, M. Brubakk, O. Kran, A.-M. Rosinska, M. Muga, R. Tor, J. Olalla, P. Cayla, J. Moreno, S. Monge, S. Amo, J. Romero, J. Pérez-Hoyos, S. Sönnerborg, A. Bucher, C. Günthard, H. Scherrer, A. Malyuta, R. Murphy, G. Porter, K. Johnson, A. Babiker, A. Pillay, D. Morrison, C. Salata, R. Mugerwa, R. Chipato, T. Price, M.A. Gilmour, J. Kamali, A. Karita, E. CASCADE Collaboration in EuroCoord

Abstract

Objectives: To investigate factors that predict speed of recovery and long-term CD4 cell count in HIV-1 seroconverters initiating combination antiretroviral therapy (cART), and to quantify the influence of very early treatment initiation. We make use of all pre-treatment CD4 counts, because analyses using only a single observation at initiation may be subject to biases. Methods: We used data from the CASCADE (Concerted Action on SeroConversion to AIDS and Death in Europe) multinational cohort collaboration of HIV-1 seroconverters. We analysed pre- and post-treatment data of patients with seroconversion dates estimated January 2003–March 2014 (n = 7600 for primary analysis) using a statistical model in which the characteristics of recovery in CD4 counts are determined by multiple predictive factors. Secondary analyses were performed incorporating uncertainty in the exact timing of seroconversion to allow more precise estimation of the benefit of very early treatment initiation. Results: ‘True’ CD4 count at cART initiation was the strongest predictor of CD4 count beyond 3 years on cART. Allowing for lack of complete certainty in the date of seroconversion, CD4 recovery was more rapid for patients in whom treatment was initiated within 4 months. For a given CD4 count, higher viral load (VL) at initiation was strongly associated with higher post-treatment CD4 recovery. For other patient and drug characteristics, associations with recovery were statistically significant but small in magnitude. Conclusions: CD4 count at cART initiation is the most important factor in predicting post-treatment recovery, but VL provides substantial additional information. If cART is initiated in the first 4 months following seroconversion, recovery of CD4 counts appears to be more rapid. © 2017 The Authors. HIV Medicine published by John Wiley & Sons Ltd on behalf of British HIV Association

Published
2018

5. Effect of ignoring the time of HIV seroconversion in estimating changes in survival over calendar time in observational studies: results from CASCADE

Author

Porter, K, Babiker, A, Walker, S, Darbyshire, J, Gill, N, Beral, V, Coutinho, R, Lee, C, Meyer, L, Rezza, G, Tyrer, F, Dabis, F, Marimoutou, C, Boufassa, F, Hamouda, O, Brunn, M, Pezzotti, P, Lorenzo, JI, Touloumi, G, Hatzakis, A, Karafoulidou, A, Katsarou, O, Brettle, R, Del Amo, J, del Romero, J, Prins, M, Coutinho, RA, van Benthem, B, Kirk, O, Pedersen, C, AGuado, IH, Perez-Hoyos, S, Eskild, A, Bruun, JN, Sannes, M, Sabin, C, Johnson, AM, Phillips, AN, Darbyshire, JH, Egger, M, Francioli, P, Rickenbach, M, Cooper, D, Kaldor, J, Vizzard, J, Tusell, JM, Ruiz, I, Cayla, JA, de Olalla, PG, Day, NE, De Angelis, D, Collaboration, CASCADE, Infectious diseases, APH - Global Health, AII - Inflammatory diseases, AII - Infectious diseases, and Medical Microbiology and Infection Prevention

Subjects
Adult, Male, Pediatrics, medicine.medical_specialty, HIV seroconversion, Time Factors, Survival, Adolescent, Immunology, Human immunodeficiency virus (HIV), HIV Infections, Cubic Millimeter, HIV Antibodies, medicine.disease_cause, Risk Assessment, Cohort Studies, Prevalent, Acquired immunodeficiency syndrome (AIDS), Bias, HIV Seropositivity, medicine, Prevalence, Immunology and Allergy, Humans, business.industry, Disease progression, Cohort, HIV, Middle Aged, medicine.disease, CD4 Lymphocyte Count, Seroconverters, Infectious Diseases, Observational study, Female, business, Calendar time
Abstract

Objective: To compare estimates of changes in HIV survival over time derived from seroconverter and prevalent cohorts. Design and methods: Using pooled data from 19 seroconverter cohorts (CASCADE), the relative risk of death from HIV seroconversion by calendar time at risk from 1 January 1991 was examined. The analyses were repeated, ignoring knowledge of the time of seroconversion, but adjusting for the CD4 cell count at the time the participant came under observation, thus mimicking a prevalent cohort. Estimates from the 'prevalent' cohort approach were compared with those obtained from the sero-converter cohort. Results: Of 5428 subjects at risk on 1 January 1991 or later, 1312 (24.2%) had died. In the analysis based on time from seroconversion, estimates of the effect of calendar year showed marked reductions in mortality in 1997-1999 only, with no evidence of a linear trend over the period 1991-1996 (P-trend = 0.85). Using the prevalent cohort approach a decrease in the relative risk of death was observed from 1991 to 1998-1999, with a statistically significant trend of a decrease in risk from 1991 to 1996 (P-trend = 0.002). Similar findings were observed when the analyses was repeated taking the start date of the cohort as 1 January 1988. Conclusion: Lack of knowledge of HIV infection duration may lead to biased and exaggerated estimates of survival improvements over time. The adjustment for duration of infection in prevalent HIV cohorts through laboratory markers may compensate inadequately for this. (C) 2000 Lippincott Williams and Wilkins.

Published
2016
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6. Does rapid HIV disease progression prior to combination antiretroviral therapy hinder optimal CD4 + T-cell recovery once HIV-1 suppression is achieved?

Author

Jarrin, I. Pantazis, N. Dalmau, J. Phillips, A.N. Olson, A. Mussini, C. Boufassa, F. Costagliola, D. Porter, K. Blanco, J. Del Amo, J. Martinez-Picado, J. Chene, G. Sabin, C. Walker, S. Fisher, M. Kelleher, T. Cooper, D. Finlayson, R. Bloch, M. Ramacciotti, T. Gelgor, L. Smith, D. Zangerle, R. Gill, J. Lutsar, I. Dabis, F. Thiebaut, R. Guiguet, M. Vanhems, P. Chaix, M.-L. Ghosn, J. Meyer, L. Hamouda, O. Kucherer, C. Bartmeyer, B. Antoniadou, A. Chrysos, G. Daikos, G.L. Touloumi, G. Katsarou, O. Rezza, G. Dorrucci, M. Monforte, A.D. De Luca, A. Prins, M. Geskus, R. Van Der Helm, J. Schuitemaker, H. Sannes, M. Brubakk, O. Kran, A.-M.B. Rosinska, M. Muga, R. Tor, J. De Olalla, P.G. Cayla, J. Moreno, S. Monge, S. Del Romero, J. Perez-Hoyos, S. Sonnerborg, A. Bucher, H.C. Gunthard, H. Rickenbach, M. Malyuta, R. Murphy, G. Johnson, A. Babiker, A. Pillay, D. Morrison, C. Salata, R. Mugerwa, R. Chipato, T. Amornkul, P.N. Gilmour, J. Kamali, A. Karita, E. Burns, F. Giaquinto, C. Grarup, J. Kirk, O. Bailey, H. Anne, A.V. Panteleev, A. Thorne, C. Aboulker, J.-P. Albert, J. Asandi, S. De Wit, S. Reiss, P. Gatell, J. Karpov, I. Ledergerber, B. Lundgren, J. Møller, C. Rakhmanova, A. Rockstroh, J. Sandhu, M. Dedes, N. Fenton, K. Pizzuti, D. Vitoria, M. Faggion, S. Fradette, L. Frost, R. Cartier, A. Raben, D. Schwimmer, C. Scott, M.

Abstract

Objective: This article compares trends in CD4 + T-cell recovery and proportions achieving optimal restoration (≥500cells/μl) after viral suppression following combination antiretroviral therapy (cART) initiation between rapid and nonrapid progressors. Methods: We included HIV-1 seroconverters achieving viral suppression within 6 months of cART. Rapid progressors were individuals experiencing at least one CD4 + less than 200cells/μl within 12 months of seroconverters before cART. We used piecewise linear mixed models and logistic regression for optimal restoration. Results: Of 4024 individuals, 294 (7.3%) were classified as rapid progressors. At the same CD4 + T-cell count at cART start (baseline), rapid progressors experienced faster CD4 + T-cell increases than nonrapid progressors in first month [difference (95% confidence interval) in mean increase/month (square root scale): 1.82 (1.61; 2.04)], which reversed to slightly slower increases in months 1-18 [-0.05 (-0.06; -0.03)] and no significant differences in 18-60 months [-0.003 (-0.01; 0.01)]. Percentage achieving optimal restoration was significantly lower for rapid progressors than nonrapid progressors at months 12 (29.2 vs. 62.5%) and 36 (47.1 vs. 72.4%) but not at month 60 (70.4 vs. 71.8%). These differences disappeared after adjusting for baseline CD4 + T-cell count: odds ratio (95% confidence interval) 0.86 (0.61; 1.20), 0.90 (0.38; 2.17) and 1.56 (0.55; 4.46) at months 12, 36 and 60, respectively. Conclusion: Among people on suppressive antiretroviral therapy, rapid progressors experience faster initial increases of CD4 + T-cell counts than nonrapid progressors, but are less likely to achieve optimal restoration during the first 36 months after cART, mainly because of lower CD4 + T-cell counts at cART initiation. Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.

Published
2015

7. Does rapid HIV disease progression prior to combination antiretroviral therapy hinder optimal CD4 + T-cell recovery once HIV-1 suppression is achieved?

Author

Jarrin, I., Pantazis, N., Dalmau, J., Phillips, A. N., Olson, A., Mussini, C., Boufassa, F., Costagliola, D., Porter, K., Blanco, J., Del Amo, J., Martinez-Picado, J., Chene, G., Sabin, C., Walker, S., Fisher, M., Kelleher, T., Cooper, D., Finlayson, R., Bloch, M., Ramacciotti, T., Gelgor, L., Smith, D., Zangerle, R., Gill, J., Lutsar, I., Dabis, F., Thiebaut, R., Guiguet, M., Vanhems, P., Chaix, M. -L., Ghosn, J., Meyer, L., Hamouda, O., Kucherer, C., Bartmeyer, B., Antoniadou, A., Chrysos, G., Daikos, G. L., Touloumi, G., Katsarou, O., Rezza, G., Dorrucci, M., Monforte, A. D., De Luca, A., Prins, M., Geskus, R., Van Der Helm, J., Schuitemaker, H., Sannes, M., Brubakk, O., Kran, A. -M. B., Rosinska, M., Muga, R., Tor, J., De Olalla, P. G., Cayla, J., Moreno, S., Monge, S., Del Romero, J., Perez-Hoyos, S., Sonnerborg, A., Bucher, H. C., Gunthard, H., Rickenbach, M., Malyuta, R., Murphy, G., Johnson, A., Babiker, A., Pillay, D., Morrison, C., Salata, R., Mugerwa, R., Chipato, T., Amornkul, P. N., Gilmour, J., Kamali, A., Karita, E., Burns, F., Giaquinto, C., Grarup, J., Kirk, O., Bailey, H., Anne, A. V., Panteleev, A., Thorne, C., Aboulker, J. -P., Albert, J., Asandi, S., De Wit, S., Reiss, P., Gatell, J., Karpov, I., Ledergerber, B., Lundgren, J., Moller, C., Rakhmanova, A., Rockstroh, J., Sandhu, M., Dedes, N., Fenton, K., Pizzuti, D., Vitoria, M., Faggion, S., Fradette, L., Frost, R., Cartier, A., Raben, D., Schwimmer, C., Scott, M., and Unión Europea. Comisión Europea. 7 Programa Marco

Subjects
Cart, Adult, CD4-Positive T-Lymphocytes, Male, CD4 responses, HIV-viral suppression, rapid progression, Anti-Retroviral Agents, CD4 Lymphocyte Count, Cohort Studies, Disease Progression, Female, HIV Infections, HIV-1, Humans, Middle Aged, Time Factors, Young Adult, Antiretroviral Therapy, Highly Active, Viral Load, Epidemiology and Social, Immunology, Human immunodeficiency virus (HIV), Antiretroviral Therapy, medicine.disease_cause, 17 Psychology And Cognitive Sciences, Acquired immunodeficiency syndrome (AIDS), Virology, medicine, Immunology and Allergy, Highly Active, Young adult, Cd4 t cell, business.industry, 11 Medical And Health Sciences, 06 Biological Sciences, medicine.disease, Antiretroviral therapy, 3. Good health, Infectious Diseases, business, Viral load, Hiv disease
Abstract

Objective: This article compares trends in CD4þ T-cell recovery and proportions achieving optimal restoration ( 500 cells/ml) after viral suppression following combination antiretroviral therapy (cART) initiation between rapid and nonrapid progressors. Methods: We included HIV-1 seroconverters achieving viral suppression within 6 months of cART. Rapid progressors were individuals experiencing at least one CD4þ less than 200 cells/ml within 12 months of seroconverters before cART. We used piecewise linear mixed models and logistic regression for optimal restoration. Results: Of 4024 individuals, 294 (7.3%) were classified as rapid progressors. At the same CD4þ T-cell count at cART start (baseline), rapid progressors experienced faster CD4þ T-cell increases than nonrapid progressors in first month [difference (95% confidence interval) in mean increase/month (square root scale): 1.82 (1.61; 2.04)], which reversed to slightly slower increases in months 1–18 [0.05 (0.06; 0.03)] and no significant differences in 18–60 months [0.003 (0.01; 0.01)]. Percentage achieving optimal restoration was significantly lower for rapid progressors than nonrapid progressors at months 12 (29.2 vs. 62.5%) and 36 (47.1 vs. 72.4%) but not at month 60 (70.4 vs. 71.8%). These differences disappeared after adjusting for baseline CD4þ T-cell count: odds ratio (95% confidence interval) 0.86 (0.61; 1.20), 0.90 (0.38; 2.17) and 1.56 (0.55; 4.46) at months 12, 36 and 60, respectively. Conclusion: Among people on suppressive antiretroviral therapy, rapid progressors experience faster initial increases of CD4þ T-cell counts than nonrapid progressors, but are less likely to achieve optimal restoration during the first 36 months after cART, mainly because of lower CD4þ T-cell counts at cART initiation. This work was supported by the European Union Seventh Framework Programme (FP7/2007–2013) under EuroCoord grant agreement n° 260694. Sí

Published
2015

8. Impact of HIV-1 subtype on CD4 count at HIV seroconversion, rate of decline, and viral load set point in European seroconverter cohorts

Author

Touloumi, G., Pantazis, N., Pillay, D., Paraskevis, D., Chaix, M.-L., Bucher, H. C., Kucherer, C., Zangerle, R., Kran, A.-M. B., Porter, K., Kelleher, A. D., Cooper, D. A., Grey, P., Finlayson, R., Bloch, M., Kelleher, T., Ramacciotti, T., Gelgor, L., Cooper, D., Smith, D., Gill, J., Jorgensen, L. B., Lutsar, I., Chene, G., Dabis, F., Thiebaut, R., Masquelier, B., Costagliola, D., Guiguet, M., Vanhems, P., Ghosn, J., Goujard, C., Meyer, L., Boufassa, F., Hamouda, O., Bartmeyer, B., Katsarou, O., Paparizos, V., Gargalianos-Kakolyris, P., Lazanas, M., Rezza, G., Dorrucci, M., Monforte, A. d., De Luca, A., Prins, M., Geskus, R., van der Helm, J., Schuitemaker, H., Sannes, M., Brubakk, O., Bakken Kran, A.-M., Rosinska, M., Muga, R., Tor, J., Garcia de Olalla, P., Cayla, J., del Amo, J., Moreno, S., Monge, S., Del Amo, J., del Romero, J., Perez-Hoyos, S., Rickenbach, M., Francioli, P., Malyuta, R., Brettle, R., Murphy, G., Sabin, C., Johnson, A., Phillips, A., Babiker, A., and Delpech, V.

Subjects
Microbiology (medical), Adult, Male, Genotype, Anti-HIV Agents, Human immunodeficiency virus (HIV), HIV Infections, Drug resistance, medicine.disease_cause, 03 medical and health sciences, 0302 clinical medicine, Acquired immunodeficiency syndrome (AIDS), HIV Seropositivity, medicine, Humans, 030212 general & internal medicine, Seroconversion, 030304 developmental biology, HIV-1 subtype, 0303 health sciences, Molecular Epidemiology, Molecular epidemiology, business.industry, Middle Aged, Viral Load, medicine.disease, CD4 decline, Set point, 3. Good health, CD4 Lymphocyte Count, Europe, Infectious Diseases, Treatment Outcome, natural history, Immunology, HIV-1, Female, business, set point, Viral load
Abstract

Background. Human immunodeficiency virus type 1 (HIV-1) subtype may influence disease progression. We compared CD4 lymphocyte cell count levels at seroconversion, decline rates and viral load set point in individuals infected with different HIV-1 subtypes. Methods. We used data from the Concerted Action on SeroConversion to AIDS and Death in Europe (CASCADE) collaboration, restricted to those infected since 1996, aged >= 15 years, and applied mixed effects models for CD4 cell count decline and median regression for viral load set point (mean level 6-24 months from seroconversion). Results. The analysis included 3364 seroconverters with known HIV-1 subtypes. Compared with subtype B, CD4 at seroconversion was significantly higher for subtype CRF01 and lower for subtype C. Subsequent CD4 decline was significantly slower for subtypes A and CRF02 and marginally slower for subtype C compared with B. Mean CD4 loss at 2 years of seroconversion for white men exposed through sex between men, aged 30-39 years, having seroconverted since 2006, enrolled within 6 months of seroconversion, and without acute infection was 88, 142, 100, 130, 103, and 167 cells/mu L for subtypes A, B, C, CRF01_AE, CRF02_AG, and G, respectively. In adjusted analysis, median viral load set point and time to clinical AIDS/death did not differ significantly by subtype, although all subtypes, except C, tended to have lower levels compared with B. Conclusions. HIV-1 subtype significantly influences seroconversion CD4 cell levels and decline rates but not viral load set point. These findings may be helpful to HIV-positive individuals and their attending physicians in understanding disease progression.

Published
2013

9. Natural history of HIV-control since seroconversion

Author

Madec, Y, Boufassa, F, Porter, K, Prins, M, Sabin, C, Monforte, AD, Amornkul, P, Bartmeyer, B, Sannes, M, Venet, A, Lambotte, O, Meyer, L, Garcia-de-Olalla, P, CASCADE Collaboration Eurocoord, AII - Amsterdam institute for Infection and Immunity, APH - Amsterdam Public Health, Infectious diseases, Epidemiology and Data Science, Other departments, Experimental Immunology, Epidémiologie des Maladies Emergentes - Emerging Diseases Epidemiology, Pasteur-Cnam Risques infectieux et émergents (PACRI), Institut Pasteur [Paris]-Conservatoire National des Arts et Métiers [CNAM] (CNAM)-Institut Pasteur [Paris]-Conservatoire National des Arts et Métiers [CNAM] (CNAM), Centre de recherche en épidémiologie et santé des populations (CESP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris-Sud - Paris 11 (UP11)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Versailles Saint-Quentin-en-Yvelines (UVSQ), Medical Research Council Clinical Trials Unit (MRC CTU), University College of London [London] (UCL), Academic Medical Center - Academisch Medisch Centrum [Amsterdam] (AMC), University of Amsterdam [Amsterdam] (UvA), Research Department of Infection and Population Health [London], Ospedale San Paolo, Partenaires INRAE, International AIDS Vaccine Initiative [San Francisco] (AVI), Robert Koch Institute [Berlin] (RKI), Ullevål University Hospital, Régulation de la réponse immune, infection VIH-1 et autoimmunité, Université Paris-Sud - Paris 11 (UP11)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de Médecine Interne - Immunologie Clinique [AP-HP Bicêtre], and AP-HP Hôpital Bicêtre (Le Kremlin-Bicêtre)

Subjects
Adult, Male, medicine.medical_specialty, Canada, Time Factors, Immunology, Viremia, HIV Infections, Kaplan-Meier Estimate, Biology, 03 medical and health sciences, 0302 clinical medicine, Interquartile range, Risk Factors, Internal medicine, HIV Seropositivity, medicine, Immunology and Allergy, Humans, 030212 general & internal medicine, Seroconversion, ComputingMilieux_MISCELLANEOUS, 030304 developmental biology, Proportional Hazards Models, HIV-control, seroconverters, 0303 health sciences, Proportional hazards model, Hazard ratio, Australia, Viral Load, duration of control, medicine.disease, loss of control, Confidence interval, 3. Good health, CD4 Lymphocyte Count, Natural history, Europe, Infectious Diseases, natural history, HIV-1, RNA, Viral, Female, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, Viral load
Abstract

OBJECTIVES HIV-controllers spontaneously maintain HIV viremia at an undetectable level. We aimed to describe the delay to control from seroconversion, the duration of control, and risk factors for losing control. METHODS HIV-controllers were identified from a pooled dataset of 24 seroconverter cohorts from Europe, Australia, and Canada (CASCADE). HIV-controllers had at least five consecutive viral loads less than 400/500 copies/ml, while antiretroviral therapy naive, for at least 5 years after seroconversion. End of control was defined as two consecutive viral loads above 2000 copies/ml. Duration of control was described using Kaplan-Meier estimates; factors associated with duration of control were identified using a Cox model. CD4⁺ cell count evolution during control was described using a mixed model. RESULTS Of 9896 eligible seroconverters, we identified 140 (1.4%) HIV-controllers, the largest database of HIV-controllers followed from seroconversion. For 64 with viral load measured within 24 months from seroconversion, median delay to control was 16.7 (interquartile range: 7.8-37.9) months. Probability of maintaining control 20 years after seroconversion was 0.74 [95% confidence interval (CI): 0.64-0.85]. Occurrence of blips followed by return to undetectability did not increase the risk of loss of control [hazard ratio: 0.81 (95% CI: 0.10-6.70)]. However, CD4⁺ cell loss during control was significantly accelerated in individuals with blips. CONCLUSION In most individuals, control occurred rapidly after seroconversion; however, more than 3 years were required to achieve control in 25% of HIV-controllers. Control may be sustained even when CD4⁺ cell levels are below 500 cells/μl, opening important new perspectives to understand the physiopathology underlying control.

Published
2013
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10. Short-term risk of AIDS according to current CD4 cell count and viral load in antiretroviral drug-naive individuals and those treated in the monotherapy era

Author

Beral, V, Coutinho, R, Darbyshire, J, Del Amo, J, Gill, N, Lee, C, Meyer, L, Rezza, G, Porter, K, Babiker, A, Walker, AS, Tyrer, F, Dabis, F, Thiebaut, R, Chene, G, Lawson-Ayayi, S, Boufassa, F, Vanhems, P, Hamouda, O, Fischer, K, Pezzotti, P, Touloumi, G, Hatzakis, A, Karafoulidou, A, Katsarou, O, Brettle, R, Sabin, C, Johnson, AM, Phillips, AN, Darbyshire, JH, Day, NE, De Angelis, D, del Romero, J, Aguado, IH, Perez-Hoyos, S, Muga, R, van Asten, L, van Benthem, B, Prins, M, Kirk, O, Pedersen, C, Eskild, A, Briuun, JN, Sannes, M, Francioli, P, Egger, M, Rickenbach, M, Cooper, D, Kaldor, J, Ashton, L, Vizzard, J, and Collaboration, CASCADE

Published
2004

12. IR Reikwijdtevoorspeller - Versie 1.0 (IR Range Predictor - Version 1.0)

Author

FYSISCH EN ELEKTRONISCH LAB TNO THE HAGUE (NETHERLANDS), Sannes, M. P., Vuijst, J. C., Eijk, A. M. van, FYSISCH EN ELEKTRONISCH LAB TNO THE HAGUE (NETHERLANDS), Sannes, M. P., Vuijst, J. C., and Eijk, A. M. van

Abstract

No abstract in English possible., Text in Dutch. Abstract in Dutch and English. Original contains color plates: All DTIC/NTIS reproductions will be in black and white.

Published
1996

16. HIV-1 infection in persons homozygous for CCR5-Δ32 allele: The next case and the review

Author

Smoleń-Dzirba, J., Rosińska, M., Janiec, J., Beniowski, M., Cycoń, M., Tomasz J. Wąsik, Wasik, T. J., Kelleher, T., Cooper, D., Grey, P., Finlayson, R., Bloch, M., Ramacciotti, T., Gelgor, L., Smith, D., Zangerle, R., Gill, J., Lutsar, I., Chêne, G., Dabis, F., Thiebaut, R., Masquelier, B., Costagliola, D., Guiguet, M., Vanhems, P., Chaix, M. -L, Ghosn, J., Meyer, L., Boufassa, F., Hamouda, O., Kücherer, C., Bartmeyer, B., Antoniadou, A., Chrysos, G., Daikos, G. L., Touloumi, G., Pantazis, N., Katsarou, O., Rezza, G., Dorrucci, M., Monforte, A. D., Luca, A., Prins, M., Geskus, R., Helm, J., Schuitemaker, H., Sannes, M., Brubakk, O., Kran, A. -M B., Rosinska, M., Muga, R., Tor, J., Olalla, P. G., Cayla, J., Del Amo, J., Moreno, S., Monge, S., Del Romero, J., Pérez-Hoyos, S., Bucher, H. C., Rickenbach, M., Francioli, P., Malyuta, R., Murphy, G., Sabin, C., Porter, K., Johnson, A., Phillips, A., Babiker, A., Pillay, D., Morrison, C., Salata, R., Mugerwa, R., Chipato, T., Amornkul, P. N., Gilmour, J., Kamali, A., Karita, E., Burns, F., Giaquinto, C., Gibb, D., Grarup, J., Kirk, O., Kjaer, J., Panteleev, A., Reiss, P., Thorne, C., Aboulker, J. -P, Albert, J., Asandi, S., Wit, S., Wolf, F., Gatell, J., Karpov, I., Ledergerber, B., Lundgren, J., Møller, C., Rakhmanova, A., Rockstroh, J., Anne, A. V., Dedes, N., Fenton, K., Pizzuti, D., Vitoria, M., Coughlin, K., Faggion, S., Fradette, L., Frost, R., Sabin, M., Schwimmer, C., and Scott, M.

17. Predictors of trend in CD4-positive T-cell count and mortality among HIV-1 infected individuals with virological failure to all three antiretroviral-drug classes

Author

Ledergerber, B, Lundgren, Jd, Walker, As, Sabin, C, Justice, A, Reiss, P, Mussini, C, Wit, F, d'Arminio Monforte, A, Weber, R, Fusco, G, Staszewski, S, Law, M, Hogg, R, Lampe, F, Gill, Mj, Castelli, Francesco, Phillips, An, Rooney, P. q, Taylor, S. q, Couldwell, D. r, Austin, D. s, Block, M. s, Clemons, J. s, Finlayson, R. s, Petoumenos, K. s, Quan, D. s, Smith, D. s, O'Connor, C. t, Gorton, C. t, Allen, D. u, Mulhall, B. u, Mutimer, K. v, Keeffe, N. v, Cooper, D. w, Carr, A. w, Miller, J. w, Pell, C. w, Ellis, D. x, Baker, D. y, Kidd, J. y, Mcfarlane, R. y, Liang, M. T. z, Brown, Aa, K., Huffam, Ab, S., Savage, Ab, J., Morgan, Knibbs, Ab, P., Sowden, Ac, D., Walker, Ac, A., Orth, Ad, D., Lister, Ad, G., Chuah, Ae, J., Fankhauser, Ae, W., Dickson, Ae, B., Bradford, Af, D., Wilson, Af, C., Ree, Ag, H., Magon, Anderson, Ah, J., Moore, Ah, R., Russell, Ah, D., Mcgovern, Ah, G., Mcnair, Bal, Fairley, Ah, K., Roth, Ai, N., Ai, B., Strecker, Ai, S., Ai, D., Wood, Ai, H., Mijch, Aj, A., Hoy, Aj, J., Pierce, Mccormack, Aj, C., Watson, Aj, K., Medland, Ak, N., Daye, Al, J., Mallal, Am, S., French, Am, M., Skett, Am, J., Maxwel, Am, D., Cain, Am, A., Montroni, An, M., Scalise, An, G., Costantini, An, A., Giacometti, Tirelli, Ao, U., Nasti, Ao, G., Pastore, Ap, G., Ladisa, Ap, N., Perulli, M. L., Ap, Suter, Aq, F., Arici, Aq, C., Maggiolo, Chiodo, Ar, F., Gritti, F. M., Ar, Colangeli, Ar, V., Fiorini, Ar, C., Guerra, Ar, L., Carosi, As, G., Cadeo, G. P., As, Minardi, As, C., Vangi, As, D., Paraninfo, Casari, As, S., Pan, As, A., Patroni, Torti, Quiros, Roldan, As, E., Tomasoni, As, L., Moretti, As, F., Nasta, As, P., Uccelli, M. C., As, Bertelli, Rizzardini, At, G., Migliorino, At, M., Abeli, At, C., Manconi, P. E., Au, Piano, Au, P., Ferraro, Av, T., Scerbo, Av, A., Pizzigallo, Aw, E., Ricci, Aw, F., Santoro, Ax, D., Pusterla, Ax, L., Carnevale, Ay, G., Galloni, Ay, D., Viganò, Az, P., Mena, Az, M., Ghinelli, Ba, F., Sighinolfi, Ba, L., Leoncini, Bb, F., Mazzotta, Pozzi, Bb, M., Caputo, Lo, Bb, S., Angarano, Bc, G., Grisorio, Bc, B., Ferrara, Bc, S., Grima, Bd, P., Tundo, Pagano, Be, G., Piersantelli, Be, N., Alessandrini, Be, A., Piscopo, Be, R., Toti, Bf, M., Chigiotti, Bf, S., Soscia, Bg, F., Tacconi, Bg, L., Orani, Bh, A., Perini, Bh, P., Nigro, Bh, M., Scasso, Bi, A., Vincenti, Scalzini, Bj, A., Fibbia, Bj, G., Moroni, Bk, M., Lazzarin, Bk, A., Cargnel, Vigevani, G. M., Bk, Caggese, Bk, L., Tordato, Bk, F., Novati, Bk, R., Galli, Merli, Bk, S., Pastecchia, Bk, C., Moioli, Esposito, Bl, R., Abrescia, Bm, N., Chirianni, Bm, A., Izzo, Bm, C., Piazza, Bm, M., Marco, De, Montesarchio, Bm, V., Manzillo, Bm, E., Nappa, Bm, S., Colomba, Bn, A., Abbadessa, Bn, V., Prestileo, Bn, T., Mancuso, Bn, S., Ferrari, Bo, C., Pzzaferri, Bo, P., Filice, Bp, G., Minoli, Bp, L., Bruno, Bp, R., Maserati, Bp, S., Tinelli, Bp, C., Pauluzzi, Bq, S., Baldelli, Bq, F., Petrelli, Br, E., Cioppi, Br, A., Alberici, Bs, F., Ruggieri, Bs, A., Menichetti, Bt, F., Martinelli, Bt, C., Stefano, De, Bu, C., Gala, La, Bu, A., Zauli, Bv, T., Ballardini, Bv, G., Magnani, Bw, G., Ursitti, M. A., Bw, Arlotti, Bx, M., Ortolani, Bx, P., Ortona, By, L., Dianzani, By, F., Ippolito, By, G., Antinori, Bz, A., Antonucci, Bz, G., D'Elia, Bz, S., Narciso, Bz, P., Petrosillo, Bz, N., Vullo, Bz, V., Luca, De, Del, Forno, Bz, L., Zaccarelli, Bz, M., Longis, De, Ciardi, D'Offizi, Noto, Lichtner, Capobianchi, M. R., Bz, Girardi, Bz, E., Pezzotti, Rezza, Mura, M. S., Ca, Mannazzu, Ca, M., Caramello, Cb, P., Sinicco, Cb, A., Soranzo, M. L., Cb, Gennero, Cb, L., Sciandra, Cb, M., Salassa, Cb, B., Grossi, P. A., Cc, Basilico, Cc, C., Poggio, Cd, A., Bottari, Cd, G., Raise, Ce, E., Pasquinucci, Ce, S., Lalla, De, Cf, F., Tositti, Cf, G., Resta, Cg, F., Chimienti, Cg, A., Lepri, Cozzi, Ch, A., Bachmann, Fb, S., Battegay, Fb, M., Bernasconi, Fb, E., Bucher, Fb, H., Bürgisser, Fb, P., Cattacin, Egger, Erb, Fierz, Fb, W., Fischer, Flepp, Fontana, Fb, A., Francioli, Furrer, H. J., Fb, Gorgievski, Günthard, Hirschel, Fb, B., Kaiser, Fb, L., Kind, Fb, C., Klimkait, Fb, T., Lauper, Fb, U., Opravil, Paccaud, Fb, F., Pantaleo, Fb, G., Perrin, Piffaretti, J. C., Fb, Rickenbach, Rudin, Schüpbach, Fb, J., Speck, Fb, R., Tarr, Telenti, Trkola, Vernazza, Yerly, Wolf, De, Ci, F., Van, Sighem, A. I., Ci, Van, Valkengoed, Ci, I., Gras, Ci, L., Bronsveld, Ci, W., Veldkamp, Ci, A., Prins, J. M., Cj, Bos, J. C., Cj, Schattenkerk, Eeftinck, J. K. M., Cj, Godfried, M. H., Cj, Lange, J. M. A., Cj, Lowe, S. H., Cj, van der Meer, J. T. M., Cj, Nellen, F. J. B., Cj, Pogany, Cj, K., van der Poll, Cj, T., Ruys, T. A., Cj, Sankatsing, Cj, S., van der Valk, Cj, M., Van, Vonderen, M. G. A., Cj, Wit, F. W. M. N., Cj, Van, Eeden, Cj, A., Ten, Veen, J. H., Cj, Van, Dam, P. S., Cj, Hillebrand, Haverkort, M. E., Cj, Brinkman, Frissen, P. H. J., Cj, Weigel, H. M., Cj, Mulder, J. W., Cj, Van, Gorp, E. C. M., Cj, Meenhorst, P. L., Cj, Mairuhu, A. T. A., Cj, Veenstra, Cj, J., Danner, S. A., Cj, Van, Agtmael, M. A., Cj, Claessen, F. A. P., Cj, Geerlings, S. E., Cj, Perenboom, R. M., Cj, Jurriaans, Back, N. K. T., Cj, Cuijpers, Rietra, P. J. G. M., Cj, Roozendaal, K. J., Cj, Pauw, Cj, W., Van, Zanten, A. P., Cj, Smits, P. H. M., Cj, Von, Blomberg, B. M. E., Cj, Savelkoul, Cj, P., Zaaijer, Cj, H., Beijnen, Crommentuyn, K. M. L., Cj, Huitema, A. D. R., Cj, Kappelhoff, Cj, B., Maat, De, M. M. R., Cj, Richter, Ck, C., van der Berg, Ck, J., Van, Leusen, Ck, R., Swanink, Vriesendorp, Cl, R., Jeurissen, F. J. F., Cl, Kauffmann, R. H., Cm, Koger, E. L. W., Cm, Franck, P. F. H., Cm, Lampe, A. S., Cm, Jansen, C. L., Cm, Bravenboer, Cn, B., Ten, Napel, C. H. H., Co, Mudrikova, Co, T., Hendriks, Co, R., Sprenger, H. G., Cp, Miesen, W. M. A. J., Cp, Schirm, Cp, J., Benne, Cp, D., Ten, Kate, R. W., Cq, Veenendaal, Cq, D., Van, Houte, D. P. F., Cr, Leemhuis, M. P., Cr, Pole, Cr, M., Storm, Cr, H., Van, Zeijl, J. H., Cr, Kroon, F. P., Cs, Schippers, E. F., Cs, Kroes, A. C. M., Cs, Claas, H. C. J., Cs, Schreij, Ct, G., van de Geest, Ct, S., Verbon, Ct, A., Bruggeman, C. A. M. V. A., Ct, Goossens, V. J., Ct, Koopmans, P. P., Cu, Telgt, Cu, M., van der Ven, A. J. A. M., Cu, Burger, D. M., Cu, Hugen, P. W. H., Cu, Galama, J. M. D., Cu, Poort, Y. A. G. M., Cu, van der Ende, M. E., Cv, Gyssens, I. C., Cv, Marie, De, Cv, S., Nouwen, J. L., Cv, Niesters, M. G., Cv, Osterhaus, A. D. M. E., Cv, Schutten, Cv, M., Juttmann, J. R., Cw, Buiting, A. G. M., Cw, Swaans, C. A. M., Cw, Schneider, M. M. E., Cx, Bonten, M. J. M., Cx, Borleffs, J. C. C., Cx, Hoepelman, I. M., Cx, Jaspers, C. A. J. J., Cx, Schouten, Cx, I., Schurink, C. A. M., Cx, Boucher, C. A. B., Cx, Schuurman, Cx, R., Blok, W. L., Cy, Groeneveld, P. H. P., Cz, Boel, Da, E., Jansz, A. F., Da, Dabis, Db, F., Thiebaut, Db, R., Chêne, Db, G., Lawson, Ayayi, Db, S., Meyer, Dc, L., Boufassa, Dc, F., Hamouda, Dd, O., De, P., De, G., Touloumi, Df, G., Hatzakis, Df, A., Karafoulidou, Katsarou, Df, O., Brettle, Dg, R., Del, Amo, Dh, J., Del, Romero, Van, Asten, Di, L., Van, Benthem, Di, B., Di, M., Coutinho, Di, R., Kirk, Dj, O., Pedersen, Dj, C., Hernández, Aguado, Dk, I., Pérez, Hoyos, Dk, S., Eskild, Dl, A., Bruun, J. N., Dl, Sannes, Dl, M., Lee, Dm, C., Johnson, A. M., Dn, Babiker, Dn, A., Darbyshire, Dn, J., Gill, Dn, N., Porter, Dn, K., Do, P., Vanhems, Do, M., Cooper, Dp, D., Kaldor, Dpdq, J., Ashton, Dp, L., Dq, D., Dq, L., Vizzard, Dq, J., Muga, Dr, R., Ds, P., Dt, J., Cayla, Du, J., Garcia de Olalla, Du, P., Day, N. E., Dv, Angelis, De, Dv, D., Fb, K., Dw, A., Dw, S., Dw, J., Tyrer, Dw, F., Beral, Fb, V., Fb, N., Raffanti, Becker, Scarsella, Braun, Most, Balu, Gilbert, Fleenor, Ising, Dieterich, Fb, D., Fusco, Losso, Dx, M., Duran, Dx, A., Vetter, Dy, N., Clumeck, Dz, N., Wit, De, Dz, S., Kabeya, Dz, K., Poll, Dz, B., Colebunders, Dz, R., Machala, Ea, L., Rozsypal, Ea, H., Nielsen, Eb, J., Lundgren, Eb, O., Olsen, C. H., Eb, Gerstoft, Katzenstein, Eb, T., Hansen, A. B. E., Eb, Skinhøj, Eb, P., Eb, C., Zilmer, Ec, K., Rauka, Ec, M., Katlama, Ed, C., De, Sa, Ed, M., Viard, J. P., Ed, Saint, Marc, Ed, T., Ed, P., Pradier, Dietrich, Ee, M., Manegold, Ee, C., Van, Lunzen, Ee, J., Stellbrink, H. J., Ee, Miller, Ee, V., Goebel, F. D., Ee, Salzberger, Ee, B., Rockstroh, Kosmidis, Ef, J., Gargalianos, Ef, P., Sambatakou, Ef, H., Perdios, Panos, Ef, G., Filandras, Ef, A., Banhegyi, Eg, D., Mulcahy, Eh, F., Yust, Ei, I., Burke, Ei, M., Pollack, Ei, S., Hassoun, Ei, J., Sthoeger, Ei, Z., Maayan, Vella, Ej, S., Chiesi, Ej, A., Ej, C., Pristerá, Ej, R., Ej, F., Gabbuti, Bedini, Ej, E., Ej, V., Santopadre, Ej, P., Franci, Ej, M., Castagna, Viksna, Ek, L., Rozentale, Ek, B., Chaplinskas, El, S., Hemmer, Em, R., Staub, Em, T., En, J., Maeland, En, A., Ormaasen, En, V., Knysz, Eo, B., Gasiorowski, Eo, J., Horban, Eo, A., Prokopowicz, Eo, D., Wiercinska, Drapalo, Boron, Kaczmarska, Pynka, Eo, M., Beniowski, Trocha, Eo, H., Smiatacz, Eo, T., Antunes, Ep, F., Mansinho, Ep, K., Maltez, Duiculescu, Eq, D., Streinu, Cercel, Eq, A., Mokrás, Er, M., Staneková, Er, D., González, Lahoz, Es, J., Diaz, Es, B., García, Benayas, Es, T., Martin, Carbonero, Es, L., Soriano, Es, V., Clotet, Jou, Es, A., Conejero, Tural, Es, C., Gatell, J. M., Es, Miró, Zamora, Blaxhult, Et, A., Karlsson, Pehrson, Et, P., Eu, P., Eu, B., Schiffer, Eu, V., Eu, H., Chentsova, Ev, N., Barton, Ew, S., A. M., Ew, Mercey, Ew, D., Phillips, Ew, A., Youle, Ew, M., M. A., Ew, Mocroft, Murphy, Weber, Ew, J., Scullard, Ew, G., Fisher, Ew, R., Loveday, Ew, C., Ex, B., Ruiz, Ex, L., Helm, E. B., Fb, Carlebach, Mösch, Müller, Haberl, Korn, Stephan, Bickel, Gute, Locher, Lutz, Klauke, Doerr, H. W., Fb, Stürmer, Dauer, Jennings, Alexander, Braitstein, Chan, Cote, Gataric, Harrigan, P. R., Fb, Harris, Bonner, Montaner, O'Shaughnessy, Yip, Chaloner, Gumley, Ransom, Sabin, C. A., Fb, Lipman, Ey, J., Read, Ey, R., Ez, F., Riccio, Fa, G., Borghi, AII - Amsterdam institute for Infection and Immunity, APH - Amsterdam Public Health, Infectious diseases, Global Health, Other departments, Public and occupational health, General Internal Medicine, Center of Experimental and Molecular Medicine, Ledergerber, B, Lundgren, Jd, Walker, A, Sabin, C, Justice, A, Reiss, P, Mussini, C, Wit, F, Monforte, Ad, Weber, R, Fusco, G, Staszewski, S, Law, M, Hogg, R, Lampe, F, Gill, Mj, Castelli, F, Phillips, An, Fusco, Gp, Rooney, P, Taylor, S, Couldwell, D, Austin, D, Block, M, Clemons, J, Finlayson, R, Petoumenos, K, Quan, D, Smith, D, O'Connor, C, Gorton, C, Allen, D, Mulhall, B, Mutimer, K, Keeffe, N, Cooper, D, Carr, A, Miller, J, Pell, C, Ellis, D, Baker, D, Kidd, J, Mcfarlane, R, Liang, Mt, Brown, K, Huffam, S, Savage, J, Morgan, S, Knibbs, P, Sowden, D, Orth, D, Lister, G, Chuah, J, Fankhauser, W, Dickson, B, Bradford, D, Wilson, C, Ree, H, Magon, H, Anderson, J, Moore, R, Russell, D, Mcgovern, G, Mcnair, R, Bal, J, Fairley, K, Roth, N, Eu, B, Strecker, S, Wood, H, Mijch, A, Hoy, J, Pierce, A, Mccormack, C, Watson, K, Medland, N, Daye, J, Mallal, S, French, M, Skett, J, Maxwel, D, Cain, A, Montroni, M, Scalise, G, Costantini, A, Giacometti, A, Tirelli, U, Nasti, G, Pastore, G, Ladisa, N, Perulli, Ml, Suter, F, Arici, C, Chiodo, F, Gritti, Fm, Colangeli, V, Fiorini, C, Guerra, L, Carosi, G, Cadeo, Gp, Minardi, C, Vangi, D, Rizzardini, G, Migliorino, G, Manconi, Pe, Piano, P, Ferraro, T, Scerbo, A, Pizzigallo, E, Ricci, F, Santoro, D, Pusterla, L, Carnevale, G, Galloni, D, Vigano, P, Mena, M, Ghinelli, F, Sighinolfi, L, Leoncini, F, Mazzotta, F, Pozzi, M, Lo Caputo, S, Angarano, G, Grisorio, B, Ferrara, S, Grima, P, Tundo, P, Pagano, G, Piersantelli, N, Alessandrini, A, Piscopo, R, Toti, M, Chigiotti, S, Soscia, F, Taccooni, L, Orani, A, Perini, P, Scasso, A, Vincenti, A, Scalzini, A, Fibbia, G, Moroni, M, Lazzarin, A, Cargnel, A, Vigevani, Gm, Caggese, L, Tordato, F, Novati, R, Galli, A, Merli, S, Pastecchia, C, Moioli, C, Esposito, R, Abrescia, N, Chirianni, A, Izzo, C, Piazza, M, De Marco, M, Montesarchio, V, Manzillo, E, Nappa, S, Colomba, A, Abbadessa, V, Prestileo, T, Mancuso, S, Ferrari, C, Pzzaferri, P, Filice, G, Minoli, L, Bruno, R, Maserati, R, Pauluzzi, S, Baldelli, F, Petrelli, E, Cioppi, A, Alberici, F, Ruggieri, A, Menichetti, F, Martinelli, C, De Stefano, C, La Gala, A, Zauli, T, Ballardini, G, Magnani, G, Ursitti, Ma, Arlotti, M, Ortolani, P, Ortona, L, Dianzani, F, Ippolito, G, Antinori, A, Antonucci, G, D'Elia, S, Narciso, P, Petrosillo, N, Vullo, V, De Luca, A, Del Forno, L, Zaccarelli, M, De Longis, P, Ciardi, M, D'Offizi, G, Noto, P, Lichtner, M, Capobianchi, Mr, Girardi, E, Pezzotti, P, Rezza, G, Mura, M, Mannazzu, M, Caramello, P, Sinicco, A, Soranzo, Ml, Gennero, L, Sciandra, M, Salassa, B, Grossi, Pa, Basilico, C, Poggio, A, Bottari, G, Raise, E, Pasquinucci, S, De Lalla, F, Tositti, G, Resta, F, Chimienti, A, Lepri, Ac, Bachmann, S, Battegay, M, Bernasconi, E, Bucher, H, Burgisser, P, Cattacin, S, Egger, M, Erb, P, Fierz, W, Fischer, M, Flepp, M, Fontana, A, Francioli, P, Furrer, Hj, Gorgievski, M, Hirschel, B, Kaiser, L, Kind, C, Klimkait, T, Lauper, U, Opravil, M, Paccaud, F, Pantaleo, G, Perrin, L, Piffaretti, Jc, Rickenbach, M, Rudin, C, Schupbach, J, Speck, R, Tarr, P, Telenti, A, Trkola, A, Vernazza, P, Yerly, S, de Wolf, F, van Sighem, Ai, van Valkengoed, I, Gras, L, Bronsveld, W, Prins, Jm, Bos, Jc, Schattenkerk, Jkme, Godfried, Mh, Lange, Jma, Lowe, Sh, van der Meer, Jtm, Nellen, Fjb, Pogany, K, van der Poll, T, Ruys, Ta, Sankatsing, S, van der Valk, M, van Vonderen, Mga, Wit, Fwmn, van Eeden, A, ten Veen, Jh, van Dam, P, Hillebrand Haverkort, Me, Brinkman, K, Frissen, Phj, Weigel, Hm, Mulder, Jw, van Gorp, Ecm, Meenhorst, Pl, Mairuhu, Ata, Veenstra, J, Danner, Sa, Van Agtmael, Ma, Claessen, Fap, Geerlings, Se, Perenboom, Rm, Richter, C, van der Berg, J, van Leusen, R, Vriesendorp, R, Jeurissen, Fjf, Kauffmann, Rh, Koger, Elw, Bravenboer, B, ten Napel, Chh, Mudrikova, T, Sprenger, Hg, Miesen, Wmaj, ten Kate, Rw, van Houte, Dpf, Leemhuis, Mp, Pole, M, Kroon, Fp, Schippers, Ef, Schreij, G, van de Geest, S, Verbon, A, Koopmans, Pp, Telgt, M, van der Ven, Ajam, van der Ende, Me, Gyssens, Ic, de Marie, S, Nouwen, Jl, Juttmann, Jr, Schneider, Mme, Bonten, Mjm, Borleffs, Jcc, Hoepelman, Im, Jaspers, Cajj, Schouten, I, Schurink, Cam, Blok, Wl, Groenveld, Php, Jurriaans, S, Back, Nkt, Cuijpers, T, Rietra, Pjgm, Roozendaal, Kj, Pauw, W, van Zanten, Ap, Smits, Phm, von Blomberg, Bme, Savelkoul, P, Zaaijer, H, Swanink, C, Franck, Pfh, Lampe, A, Jansen, Cl, Hendriks, R, Schirm, J, Benne, D, Veenendaal, D, Storm, H, van Zeijl, Jh, Kroes, Acm, Claas, Hcj, Bruggeman, Camva, Goossens, Vj, Galama, Jmd, Poort, Yagm, Niesters, Mg, Osterhaus, Adme, Schutten, M, Buiting, Agm, Swaans, Cam, Boucher, Cab, Schuurman, R, Boel, E, Jansz, Af, Veldkamp, A, Beijnen, Jh, Crommentuyn, Kml, Huitema, Adr, Kappelhoff, B, de Maat, Mmr, Burger, Dm, Hugen, Pwh, Dabis, F, Thiebaut, R, Chene, G, Lawson Ayayi, S, Meyer, L, Boufassa, F, Hamouda, O, Touloumi, G, Hatzakis, A, Karafoulidou, A, Katsarou, O, Brettle, R, Del Amo, J, del Romero, J, van Asten, L, van Benthem, B, Prins, M, Coutinho, R, Kirk, O, Pedersen, C, Aguado, Ih, Perez Hoyos, S, Eskild, A, Bruun, Jn, Sannes, M, Lee, C, Johnson, Am, Babiker, A, Darbyshire, J, Gill, N, Porter, K, Vanhems, P, Kaldor, J, Ashton, L, Vizzard, J, Muga, R, Gill, J, Cayla, J, de Olalla, Pg, Day, Ne, De Angelis, D, Walker, S, Tyrer, F, Beral, V, Raffanti, S, Becker, S, Scarsella, A, Braun, J, Most, B, Balu, R, Gilbert, L, Fleenor, R, Ising, T, Dieterich, D, Fusco, J, Losso, M, Duran, A, Vetter, N, Clumeck, N, De Wit, S, Kabeya, K, Poll, B, Colebunders, R, Machala, L, Rozsypal, H, Nielsen, J, Lundgren, J, Olsen, Ch, Gerstoft, J, Katzenstein, T, Hansen, Abe, Skinhoj, P, Zilmer, K, Rauka, M, Katlama, C, De Sa, M, Viard, Jp, Saint Marc, T, Pradier, C, Dietrich, M, Manegold, C, van Lunzen, J, Stellbrink, Hj, Miller, V, Goebel, Fd, Salzberger, B, Rockstroh, J, Kosmidis, J, Gargalianos, P, Sambatakou, H, Perdios, J, Panos, G, Filandras, A, Banhegyi, D, Mulcahy, F, Yust, I, Burke, M, Pollack, S, Hassoun, J, Sthoeger, Z, Maayan, S, Vella, S, Chiesi, A, Pristera, R, Gabbuti, A, Bedini, A, Montesarchio, E, Santopadre, P, Franci, P, Castagna, Antonella, Viksna, L, Rozentale, B, Chaplinskas, S, Hemmer, R, Staub, T, Bruun, J, Maeland, A, Ormaasen, V, Knysz, B, Gasiorowski, J, Horban, A, Prokopowicz, D, Wiercinska Drapalo, A, Boron Kaczmarska, A, Pynka, M, Beniowski, M, Trocha, H, Smiatacz, T, Antunes, F, Mansinho, K, Maltez, F, Duiculescu, D, Streinu Cercel, A, Mokras, M, Stanekova, D, Gonzalez Lahoz, J, Diaz, B, Garcia Benayas, T, Martin Carbonero, L, Soriano, V, Clotet, B, Jou, A, Conejero, J, Tural, C, Gatell, Jm, Miro, Jm, Zamora, L, Blaxhult, A, Karlsson, A, Pehrson, P, Schiffer, V, Furrer, H, Chentsova, N, Barton, S, Mercey, D, Phillips, A, Youle, M, Johnson, Ma, Mocroft, A, Murphy, M, Weber, J, Scullard, G, Fisher, M, Loveday, C, Ruiz, L, Helm, Eb, Carlebach, A, Mosch, M, Muller, A, Haberl, A, Korn, S, Stephan, C, Bickel, M, Gute, P, Locher, L, Lutz, T, Klauke, S, Doerr, Hw, Sturmer, M, Dauer, B, Jennings, B, Alexander, C, Braitstein, P, Chan, K, Cote, H, Gataric, N, Harrigan, Pr, Harris, M, Bonner, S, Montaner, J, O'Shaughnessy, M, Wood, E, Yip, B, Chaloner, C, Gumley, H, Ransom, D, Sabin, Ca, Lipman, M, Johnson, M, Read, R, Paraninfo, G, Casari, S, Pan, A, Patroni, A, Torti, C, Quiros Roldan, E, Tomasoni, L, Moretti, F, Nasta, P, Uccelli, Mc, Bertelli, D, Nigro, M, Migliorino, M, Abeli, C, Maggiolo, F, Novati, S, Tinelli, C, Riccio, G, Borghi, V, and Esposito, R.

Subjects
Male, HAART, Human immunodeficiency virus (HIV), CD4 cell count, HIV Infections, CLINICAL PROGRESSION, medicine.disease_cause, THERAPY, HAART REGIMEN, Cohort Studies, Risk Factors, Adult, Anti-Retroviral Agents, CD4 Lymphocyte Count, Cohort Studies, Female, Follow-Up Studies, HIV Infections, HIV Protease Inhibitors, HIV-1, Humans, Male, Middle Aged, Proportional Hazards Models, Reverse Transcriptase Inhibitors, Risk Factors, Treatment Failure, Viral Load, Medicine, Treatment Failure, Mortality rate, Medicine (all), INHIBITOR, General Medicine, Middle Aged, HUMAN IMMUNODEFICIENCY VIRUS TYPE 1 (HIV-1), BLIND CONTROLLED-TRIAL, medicine.anatomical_structure, Anti-Retroviral Agents, Cohort, HUMAN-IMMUNODEFICIENCY-VIRUS, Reverse Transcriptase Inhibitors, Female, Off Treatment, Viral load, Cohort study, Adult, medicine.medical_specialty, Settore MED/17 - Malattie Infettive, T cell, Internal medicine, Humans, COHORT, Proportional Hazards Models, business.industry, Proportional hazards model, DISEASE PROGRESSION, HIV Protease Inhibitors, HIV-INFECTED INDIVIDUALS, CD4 Lymphocyte Count, VIRAL LOAD, Immunology, HIV-1, business, Follow-Up Studies
Abstract

Background Treatment strategies for patients in whom HIV replication is not suppressed after exposure to several drug classes remain unclear. We aimed to assess the inter-relations between viral load, CD4-cell count, and clinical outcome in patients who had experienced three-class virological failure.Methods We undertook collaborative joint analysis of 13 HIV cohorts from Europe, North America, and Australia, involving patients who had had three-class virological failure (viral load >1000 copies per mL for >4 months). Regression analyses were used to quantify the associations between CD4-cell-count slope, HIV-1 RNA concentration, treatment information, and demographic characteristics. Predictors of death were analysed by Cox's proportional-hazards models.Findings 2488 patients were included. 2118 (85%) had started antiretroviral therapy with single or dual therapy. During 5015 person-years of follow-up, 276 patients died (mortality rate 5.5 per 100 person-years; 3-year mortality risk 15.3% (95% Cl 13.5-17.3). Risk of death was strongly influenced by the latest CD4-cell count with a relative hazard of 15.8 (95% CI 9.28-27.0) for counts below 50 cells per muL versus above 200 cells per muL. The latest viral load did not independently predict death. For any given viral load, patients on treatment had more favourable CD4-cell-count slopes than those off treatment. For patients on treatment and with stable viral load, CD4-cell counts tended to be increasing at times when the current viral load was below 10 000 copies per mL or 1.5 log(10) copies per mL below off-treatment values.Interpretation In patients for whom viral-load suppression to below the level of detection is not possible, achievement and maintenance of a CD4-cell count above 200 per muL becomes the primary aim. Treatment regimens that maintain the viral load below 10 000 copies per mL or at least provide 1.5 log(10) copies per mL suppression below the off-treatment value do not seem to be associated with appreciable CD4-cell-count decline.

Published
2004

18. Lack of decline in hepatitis C virus incidence among HIV-positive men who have sex with men during 1990-2014.

Author

van Santen DK, van der Helm JJ, Del Amo J, Meyer L, D'Arminio Monforte A, Price M, Béguelin CA, Zangerle R, Sannes M, Porter K, Geskus RB, and Prins M

Subjects
Australia epidemiology, Canada epidemiology, Europe epidemiology, Hepatitis C transmission, Homosexuality, Male, Humans, Incidence, Male, Regression Analysis, Risk Factors, Time Factors, HIV Infections complications, Hepatitis C complications, Hepatitis C epidemiology
Abstract

Background & Aims: Hepatitis C virus (HCV) incidence among HIV-positive men who have sex with men (MSM) has increased since 2000, although there are regional differences. We aimed to 1) estimate trends in HCV incidence among HIV-positive MSM, 2) assess the association between incidence and geographical region, age and HIV-related measurements and, 3) assess temporal changes from HIV seroconversion to HCV infection., Methods: Data was used from MSM with well-estimated dates of HIV seroconversion from the CASCADE Collaboration (1990-2014). Smoothly varying trends in HCV incidence over time were allowed, using restricted cubic splines. The association of calendar year, age, CD4 count (lagged), HIV RNA (lagged), geographical region and HIV infection stage (recent vs. chronic) with HCV incidence were assessed using Poisson regression., Results: Of 5,941 MSM, 337 acquired HCV during follow-up. HCV incidence significantly increased from 0.7/1,000 person-years in 1990 to 18/1,000 person-years in 2014. Recent calendar years, younger age, recent HIV infection and higher HIV RNA levels were significantly associated with HCV incidence, while CD4 count was not. Trends differed by geographical region; while incidence appeared to have stabilized in Western Europe and remained stable in Southern Europe, it continued to increase in Northern Europe in recent years. Time from HIV to HCV infection significantly decreased over time (p<0.001)., Conclusions: HCV has continued to spread among HIV-positive MSM in recent years, but trends differ by geographical region. Interventions to decrease the risk of HCV acquisition and increase early diagnosis are warranted., Lay Summary: Hepatitis C virus infection continues to spread among HIV-positive men who have sex with men, especially among younger individuals. However, trends seem to differ by European region in recent years. Furthermore, men who have sex with men with a higher HIV RNA load were more likely to get infected with the hepatitis C virus. During recent HIV infection, MSM appear to be at higher risk of acquiring hepatitis C., (Copyright © 2017 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.)

Published
2017
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19. Evaluation of rapid progressors in HIV infection as an extreme phenotype.

Author

Olson AD, Guiguet M, Zangerle R, Gill J, Perez-Hoyos S, Lodi S, Ghosn J, Dorrucci M, Johnson A, Sannes M, Moreno S, and Porter K

Subjects
Adult, CD4 Lymphocyte Count, CD4-Positive T-Lymphocytes virology, Cohort Studies, Confidence Intervals, Disease Progression, Europe, Female, Follow-Up Studies, HIV Infections blood, HIV Infections virology, Humans, Male, Proportional Hazards Models, CD4-Positive T-Lymphocytes immunology, HIV Infections immunology, HIV-1
Abstract

Design: Rapid CD4 cell loss represents an HIV phenotype used to identify causal variants of accelerated disease progression. The optimal rate and threshold for identifying this extreme phenotype in recently infected individuals is unclear., Methods: Using a cohort of patients with known dates of HIV-1 seroconversion (SC), CASCADE (Concerted Action on SeroConversion on AIDS and Death in Europe), we identified proportions experiencing nadir CD4 cell levels within 1 year of SC, and assessed their mean AIDS-free survival time at 10-year follow-up and hazard of AIDS/death, compared with those whose CD4 remained >500 cells per cubic millimeter. Follow-up was censored at December 31, 1996 to avoid bias due to combination antiretroviral therapy initiation., Results: Of 4876 individuals, 2.8%, 7.3%, and 24.9% experienced ≥1 CD4 <100, 200, and 350 cells per cubic millimeter, respectively, within 1 year of SC. Minimum CD4 levels of 30, 166, 231, and 506 cells per cubic millimeter were experienced during this period by 1%, 5%, 10%, and 50% of individuals, respectively. Mean (95% confidence interval) AIDS-free survival at 10 years follow-up was 2.9 (2.3 to 3.6), 5.5 (5.0 to 6.1), 6.7 (6.5 to 7.0), 7.4 (7.2 to 7.6), and 8.1 (7.9 to 8.3), for those with minimum counts ≤100, 100-200, 200-350, 350-500, >500 cells per cubic millimeter, respectively. Using counts of >500 cells per cubic millimeter as reference, the hazard ratios (95% confidence interval) of AIDS/death were 15.0 (11.9 to 18.9), 3.6 (2.9 to 4.5), 2.1 (1.8 to 2.4), and 1.5 (1.3 to 1.7), respectively. The hazard ratio increased to 37.5 (26.5 to 53.1) when a minimum CD4 count <100 was confirmed within 1 year of SC., Conclusion: At least 1 CD4 ≤100 cells per cubic millimeter within the first year of SC identifies a rare group of individuals at high risk of disease progression and could form the basis for defining the rapid progressor phenotype.

Published
2014
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20. Natural history of HIV-control since seroconversion.

Author

Madec Y, Boufassa F, Porter K, Prins M, Sabin C, d'Arminio Monforte A, Amornkul P, Bartmeyer B, Sannes M, Venet A, Lambotte O, and Meyer L

Subjects
Adult, Australia, CD4 Lymphocyte Count, Canada, Europe, Female, Humans, Kaplan-Meier Estimate, Male, Proportional Hazards Models, RNA, Viral blood, Risk Factors, Time Factors, Viral Load, HIV Infections virology, HIV Seropositivity virology, HIV-1, Viremia virology
Abstract

Objectives: HIV-controllers spontaneously maintain HIV viremia at an undetectable level. We aimed to describe the delay to control from seroconversion, the duration of control, and risk factors for losing control., Methods: HIV-controllers were identified from a pooled dataset of 24 seroconverter cohorts from Europe, Australia, and Canada (CASCADE). HIV-controllers had at least five consecutive viral loads less than 400/500 copies/ml, while antiretroviral therapy naive, for at least 5 years after seroconversion. End of control was defined as two consecutive viral loads above 2000 copies/ml. Duration of control was described using Kaplan-Meier estimates; factors associated with duration of control were identified using a Cox model. CD4⁺ cell count evolution during control was described using a mixed model., Results: Of 9896 eligible seroconverters, we identified 140 (1.4%) HIV-controllers, the largest database of HIV-controllers followed from seroconversion. For 64 with viral load measured within 24 months from seroconversion, median delay to control was 16.7 (interquartile range: 7.8-37.9) months. Probability of maintaining control 20 years after seroconversion was 0.74 [95% confidence interval (CI): 0.64-0.85]. Occurrence of blips followed by return to undetectability did not increase the risk of loss of control [hazard ratio: 0.81 (95% CI: 0.10-6.70)]. However, CD4⁺ cell loss during control was significantly accelerated in individuals with blips., Conclusion: In most individuals, control occurred rapidly after seroconversion; however, more than 3 years were required to achieve control in 25% of HIV-controllers. Control may be sustained even when CD4⁺ cell levels are below 500 cells/μl, opening important new perspectives to understand the physiopathology underlying control., (© 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins)

Published
2013
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21. Immunovirologic control 24 months after interruption of antiretroviral therapy initiated close to HIV seroconversion.

Author

Lodi S, Meyer L, Kelleher AD, Rosinska M, Ghosn J, Sannes M, and Porter K

Subjects
Adult, Anti-Retroviral Agents administration & dosage, Antiretroviral Therapy, Highly Active, Databases, Factual, Female, HIV Infections immunology, HIV Infections virology, HIV Seropositivity immunology, HIV Seropositivity virology, Humans, Male, Middle Aged, Prospective Studies, Treatment Outcome, Viral Load, Anti-Retroviral Agents therapeutic use, HIV Infections drug therapy, HIV Seropositivity drug therapy, HIV-1 immunology
Abstract

Background: There is interest in whether a short course of combination antiretroviral therapy (cART) at the time of human immunodeficiency virus (HIV) seroconversion could induce long-term immunologic control after its interruption. We aimed to determine the time of virologic rebound after interruption of treatment initiated close to HIV seroconversion and to identify potential cases of posttreatment controllers (PTCs) in the CASCADE (Concerted Action on Seroconversion to AIDS and Death in Europe) Collaboration., Methods: Prospective cohort study nested within the CASCADE database of routinely collected data about patients with HIV with well-estimated date of HIV seroconversion from Europe, Canada, and Australia in the post-cART era. Participants were individuals who interrupted successful cART initiated within 3 months of HIV seroconversion. The main outcome was loss of PTC status, defined as the earlier date of virologic rebound (first of 2 consecutive measurements showing HIV RNA levels >50 copies/mL) or reinitiation of any ART after cART interruption., Results: Median time to loss of PTC status in 259 eligible individuals was 1.7 months. Eleven patients did not experience virologic rebound by 24 months after treatment interruption., Conclusion: Most patients experience virologic rebound soon after cART interruption; however, although PTCs are rare, the results of this study confirm their existence.

Published
2012
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22. The hepatitis C epidemic among HIV-positive MSM: incidence estimates from 1990 to 2007.

Author

van der Helm JJ, Prins M, del Amo J, Bucher HC, Chêne G, Dorrucci M, Gill J, Hamouda O, Sannes M, Porter K, and Geskus RB

Subjects
Adult, Epidemics, Europe epidemiology, HIV Seropositivity transmission, HIV Seropositivity virology, Hepacivirus classification, Hepatitis C transmission, Hepatitis C virology, Homosexuality, Male statistics & numerical data, Humans, Incidence, Male, Phylogeny, Sexual Behavior, HIV Seropositivity epidemiology, Hepacivirus isolation & purification, Hepatitis C epidemiology
Abstract

Background: Outbreaks of acute hepatitis C virus (HCV) infection among HIV-infected MSM have been described since 2000. However, phylogenetic analysis suggests that the spread of HCV started around 1996. We estimated the incidence of HCV in HIV-infected MSM with well estimated dates of HIV seroconversion from 1990 to 2007., Methods: Data from 12 cohorts within the Concerted Action on SeroConversion to AIDS and Death in Europe (CASCADE) Collaboration were used. HCV incidence was estimated using standard incidence methods and methods for interval-censored data. We accounted for the fact that routine HCV data collection in each cohort started in different calendar years., Results: Of 4724 MSM, 3014 had an HCV test result and were included. Of these, 124 (4%) had only positive HCV test results, 2798 (93%) had only negative results and 92 (3%) had both. In 1990, HCV incidence ranged from 0.9 to 2.2 per 1000 person-years, depending on the analysis strategy used. HCV incidence increased up to 1995 when it was estimated to range between 5.5 and 8.1 per 1000 person-years. From 2002 onwards, it increased substantially to values between 16.8 and 30.0 per 1000 person-years in 2005 and between 23.4 and 51.1 per 1000 person-years in 2007., Conclusion: Our data support phylodynamic findings that HCV incidence had already increased among HIV-infected MSM from the mid-1990s. However, the main expansion of the HCV epidemic started after 2002. Incidence estimates obtained from cohort studies may help identify changes in the spread of important infections earlier and should guide routine testing policies to minimize further disease burden.

Published
2011
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23. Overestimation of human immunodeficiency virus type 1 load caused by the presence of cells in plasma from plasma preparation tubes.

Author

Kran AM, Jonassen TØ, Sannes M, Jakobsen K, Lind A, Maeland A, and Holberg-Petersen M

Subjects
Blood Cells virology, Humans, Diagnostic Errors, HIV-1 isolation & purification, Plasma virology, Specimen Handling methods, Viral Load methods
Abstract

The human immunodeficiency virus type 1 (HIV-1) load is an important marker of disease progression and treatment efficacy in patients with HIV-1 infection. In recent years, an increase in the number of samples with detectable HIV-1 RNA has been reported among patients with previously suppressed viral loads, affecting clinical patient care and leading to repeat measurements of viral load and drug resistance. This rise seems to have coincided with the increased use of plasma preparation tubes (PPTs) for sample collection, and we have aimed to explain why PPTs might yield elevated HIV-1 RNA levels. The impacts of different sample-processing procedures on HIV-1 RNA levels were compared retrospectively. Prospectively, the presence of different cells and cell-associated HIV-1 nucleic acids in paired plasma samples from PPTs centrifuged before (PPT1) and after (PPT2) transportation to the laboratory was compared. A retrospective analysis of 4,049 patient samples with <1,000 HIV-1 RNA copies/ml showed elevated HIV-1 RNA levels in plasma from PPT1 compared with the levels from PPT2 and standard EDTA-containing tubes. Prospective data revealed cell-associated HIV-1 nucleic acids and abundant blood cells in plasma from PPT1 but not from the corresponding PPT2. The levels of HIV-1 RNA correlated with the lymphocyte counts in plasma in PPT1. Cells could be removed by the recentrifugation of PPT1 before analysis. In conclusion, the transportation of PPTs after centrifugation may render cells in the plasma fraction containing cell-associated HIV-1 nucleic acids that contribute significantly to the HIV-1 RNA copy numbers in patients with low viral loads.

Published
2009
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24. Changes in the risk of death after HIV seroconversion compared with mortality in the general population.

Author

Bhaskaran K, Hamouda O, Sannes M, Boufassa F, Johnson AM, Lambert PC, and Porter K

Subjects
Adolescent, Adult, Antiretroviral Therapy, Highly Active, Cohort Studies, Europe epidemiology, Female, HIV Seropositivity drug therapy, Humans, Male, Middle Aged, Mortality trends, Poisson Distribution, Proportional Hazards Models, Risk, Survival Analysis, HIV Seropositivity mortality
Abstract

Context: Mortality among human immunodeficiency virus (HIV)-infected individuals has decreased dramatically in countries with good access to treatment and may now be close to mortality in the general uninfected population., Objective: To evaluate changes in the mortality gap between HIV-infected individuals and the general uninfected population., Design, Setting, and Population: Mortality following HIV seroconversion in a large multinational collaboration of HIV seroconverter cohorts (CASCADE) was compared with expected mortality, calculated by applying general population death rates matched on demographic factors. A Poisson-based model adjusted for duration of infection was constructed to assess changes over calendar time in the excess mortality among HIV-infected individuals. Data pooled in September 2007 were analyzed in March 2008, covering years at risk 1981-2006., Main Outcome Measure: Excess mortality among HIV-infected individuals compared with that of the general uninfected population., Results: Of 16,534 individuals with median duration of follow-up of 6.3 years (range, 1 day to 23.8 years), 2571 died, compared with 235 deaths expected in an equivalent general population cohort. The excess mortality rate (per 1000 person-years) decreased from 40.8 (95% confidence interval [CI], 38.5-43.0; 1275.9 excess deaths in 31,302 person-years) before the introduction of highly active antiretroviral therapy (pre-1996) to 6.1 (95% CI, 4.8-7.4; 89.6 excess deaths in 14,703 person-years) in 2004-2006 (adjusted excess hazard ratio, 0.05 [95% CI, 0.03-0.09] for 2004-2006 vs pre-1996). By 2004-2006, no excess mortality was observed in the first 5 years following HIV seroconversion among those infected sexually, though a cumulative excess probability of death remained over the longer term (4.8% [95% CI, 2.5%-8.6%] in the first 10 years among those aged 15-24 years)., Conclusions: Mortality rates for HIV-infected persons have become much closer to general mortality rates since the introduction of highly active antiretroviral therapy. In industrialized countries, persons infected sexually with HIV now appear to experience mortality rates similar to those of the general population in the first 5 years following infection, though a mortality excess remains as duration of HIV infection lengthens.

Published
2008
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25. [HIV/AIDS--from lethal syndrome to chronic disease].

Author

Bruun JN, Skeie L, Maeland A, Dudman SG, Sannes M, and Ormaasen V

Subjects
Anti-HIV Agents therapeutic use, Cause of Death, Chronic Disease, Drug Therapy, Combination, Follow-Up Studies, Humans, Prognosis, Prospective Studies, Risk Factors, Acquired Immunodeficiency Syndrome complications, Acquired Immunodeficiency Syndrome drug therapy, Acquired Immunodeficiency Syndrome immunology, Acquired Immunodeficiency Syndrome mortality, HIV Infections complications, HIV Infections drug therapy, HIV Infections immunology, HIV Infections mortality
Abstract

Background: At its discovery in 1981, AIDS was a fatal syndrome that rapidly led to death. Combination treatment with at least three drugs has radically improved the prognosis., Material and Methods: The study includes all HIV-patients controlled at the Department of Infectious Diseases, Ullevål University Hospital from 1982 to 2005. Development of immune deficiency, morbidity and causes of death were registered prospectively. Possible connections between death and HIV-infection and treatment were evaluated., Results: 1632 patients were followed at our department. 32 % of these patients have died. The number of patients who died annually during the 5 years from 1986 to 1990 was 47 % and this was reduced to 11 % in 2001 - 05. Many patients still die because they either present too late for treatment or have received insufficient treatment. 22 patients have died during the last 10 years irrespective of starting treatment with at least 3 antiretroviral drugs: 7 died from cancers, 6 from treatment failure, one from unknown cause and 8 from other causes. The 6 patients who died from treatment failure had very low CD4 counts and serious opportunistic infections that could not be treated effectively at the time of diagnosis., Interpretation: Patients who start and adhere to treatment with 3 HIV-medications have a good prognosis, but they may still have an increased risk of non-AIDS defining cancers and cardiovascular disease. HIV/AIDS has become a chronic disease with a good prognosis.

Published
2006

26. Changes over calendar time in the risk of specific first AIDS-defining events following HIV seroconversion, adjusting for competing risks.

Author

Babiker A, Darbyshire J, Pezzotti P, Porter K, Rezza G, Walker SA, Beral V, Coutinho R, Del Amo J, Gill N, Lee C, Meyer L, Tyrer F, Dabis F, Thiebaut R, Lawson-Aye S, Boufassa F, Hamouda O, Fischer K, Pezzotti P, Rezza G, Touloumi G, Hatzakis A, Karafoulidou A, Katsarou O, Brettle R, del Romero J, Prins M, van Benthem B, Kirk O, Pederson C, Hernández Aguado I, Pérez-Hoyos S, Eskild A, Bruun JN, Sannes M, Sabin C, Lee C, Johnson AM, Phillips AN, Francioli P, Vanhems P, Egger M, Rickenbach M, Cooper D, Kaldor J, Ashton L, Vizzard J, Muga R, Day NE, and De Angelis D

Subjects
AIDS-Related Opportunistic Infections mortality, Acquired Immunodeficiency Syndrome mortality, Acute Disease, Adolescent, Adult, Aged, Aged, 80 and over, Cause of Death, Cohort Studies, Disease Progression, Female, HIV Wasting Syndrome mortality, Humans, Male, Middle Aged, Proportional Hazards Models, Risk Assessment, Risk Factors, Time Factors, Acquired Immunodeficiency Syndrome immunology, HIV Seropositivity, HIV-1 immunology
Abstract

Background: Although studies have reported large reductions in the risks of AIDS and death since the introduction of potent anti-retroviral therapies, few have evaluated whether this has been similar for all AIDS-defining diseases. We wished to evaluate changes over time in the risk of specific AIDS-defining diseases, as first events, using data from individuals with known dates of HIV seroconversion., Methods: Using a competing risks proportional hazards model on pooled data from 20 cohorts (CASCADE), we evaluated time from HIV seroconversion to each first AIDS-defining disease (16 groups) and to death without AIDS for four calendar periods, adjusting for exposure category, age, sex, acute infection, and stratifying by cohort. We compared results to those obtained from a cause-specific hazards model., Results: Of 6,941, 2,021 (29%) developed AIDS and 437 (6%) died without AIDS. The risk of AIDS or death remained constant to 1996 then reduced; relative hazard = 0.89 (95% CI: 0.77-1.03); 0.90 (95% CI: 0.81-1.01); and 0.32 (95% CI: 0.28-0.37) for 1979-1990, 1991-1993, and 1997-2001, respectively, compared to 1994-1996. Significant risk reductions in 1997-2001 were observed in all but two AIDS-defining groups and death without AIDS in a competing risks model (with similar results from a cause-specific model). There was significant heterogeneity in the risk reduction across events; from 96% for cryptosporidiosis, to 17% for death without AIDS (P < 0.0001)., Conclusion: These findings suggest that studies reporting a stable trend for particular AIDS diseases over the period 1979-2001 may not have accounted for the competing risks among other events or lack the power to detect smaller trends.

Published
2002
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27. Normal CD4 T-cell receptor repertoire in tonsillar tissue despite perturbed repertoire in peripheral blood in HIV-1 infected individuals.

Author

Mugnaini EN, Syversen AM, Sannes M, Freng A, and Brinchmann JE

Subjects
Adult, B-Lymphocytes immunology, CD4 Antigens blood, CD4-Positive T-Lymphocytes immunology, CD8-Positive T-Lymphocytes immunology, Cell Count, Flow Cytometry, HIV Infections blood, Humans, Immunoglobulin Variable Region immunology, Receptors, Antigen, T-Cell blood, Receptors, Antigen, T-Cell metabolism, CD4 Antigens metabolism, Complementarity Determining Regions, HIV Infections immunology, Palatine Tonsil immunology
Abstract

Objective: To compare the T-cell receptor (TCR) repertoire of T-cell subsets in peripheral blood and lymphoid tissue from HIV-1 infected individuals., Design: Biopsies of tonsillar tissue and samples of peripheral blood were obtained from 10, mostly treatment-naive, HIV-1-infected individuals. CD4 and CD8 T-cell subsets were quantified, the TCR repertoire was analysed within 'naive' and 'memory' subsets, and results compared between identical subsets in tonsillar tissue and blood., Methods: Cell subsets were quantified by flow cytometry. CD4 T cells and CD8 T cells were isolated by immunomagnetic beads. Populations were in most cases further subdivided by immunomagnetic selection on the basis of CD45RO expression. TCR repertoire was studied by spectratyping of the TCR beta variable (BV) complementarity determining region 3 (CDR3) transcripts., Results: Amongst CD4 T cells, an abnormal TCR repertoire was found in median 25% (range, 0-88%) of BV families in peripheral blood, but in 0% (0-7%) in tonsillar tissue (P<0.05). Large peaks suggestive of expanded clones were common within CD8 T-cells, both in peripheral blood and tonsillar tissue. However, the expanded clones were rarely identical in the two compartments. Expanded CDR3 peaks, suggesting the presence of clonally expanded cells, were observed within both CD45RO+ and CD45RO- cells from all T-cell subsets, but, again they were mainly of different lengths., Conclusion: CD4 T cells were preserved in number and TCR repertoire in tonsillar tissue compared with blood in HIV-1 infected individuals. T-cells collected from the peripheral blood may not be representative of those residing in lymphoid tissue.

Published
1999
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28. In vivo expansion coincident with excessive in vitro cell death within the memory subset of CD8+ T cells in HIV type 1 infection.

Author

Mugnaini EN, Haaheim LL, Sannes M, and Brinchmann JE

Subjects
Antigens, CD metabolism, CD28 Antigens metabolism, Humans, Receptors, Antigen, T-Cell, alpha-beta immunology, T-Lymphocyte Subsets, Apoptosis, CD8-Positive T-Lymphocytes immunology, HIV Infections immunology, HIV-1, Immunologic Memory
Abstract

In HIV-1-infected individuals the CD8+ T cell subset is considerably expanded. This has been shown to be caused predominantly by an increase in the number of CD8+CD28- T cells. To characterize further the subsets of CD8+ T cells, we have performed analyses of cell surface phenotype, T cell receptor Vbeta usage, and ability to survive in unstimulated cultures. CD8+CD28- T cells frequently expressed CD45RA. Nonetheless, coincident expression of CD95 (Fas) and high levels of integrins suggested that these cells were immunologically experienced. Contrary to what has been observed in CD8+CD28- T cells from uninfected individuals, a common hierarchy of Vbeta usage was found in CD8+CD28- T cells from HIV-1-infected individuals, which was adhered to by all the study participants, and which was shown to be similar to that observed within CD8+CD28+ T cells. Cells from the memory subsets of CD8+ T cells showed a high incidence of spontaneous death in unstimulated cultures, indicating that these cells have received signals for death by apoptosis in vivo. In contrast, most naive CD8+CD28+CD45RA+ cells survived. The CD8+CD28- memory subset is expanded in vivo despite evidence for coincident excessive cell death in vitro. Our results are consistent with the notion that frequent transitions occur from the memory CD8+CD28+CD45RA- T cell subset to the end-stage CD8+CD28- subset during HIV-1 infection.

Published
1999
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29. Demonstration of identical expanded clones within both CD8+CD28+ and CD8+CD28- T cell subsets in HIV type 1-infected individuals.

Author

Mugnaini EN, Spurkland A, Egeland T, Sannes M, and Brinchmann JE

Subjects
Adult, Amino Acid Sequence, Cell Differentiation immunology, Clone Cells, HIV Infections metabolism, Humans, Molecular Sequence Data, Receptor-CD3 Complex, Antigen, T-Cell analysis, T-Lymphocyte Subsets chemistry, CD28 Antigens blood, CD8 Antigens blood, HIV Infections immunology, HIV-1 immunology, T-Lymphocyte Subsets cytology, T-Lymphocyte Subsets immunology
Abstract

In HIV-1-infected individuals, the CD8+CD28- T cell subset is considerably expanded and is frequently the largest subset of T cells found in peripheral blood. It has been assumed, but not proven, that CD8+CD28- T cells derive from CD8+CD28+ T cells in vivo. To further study the ontogeny of CD8+CD28- T cells, we have performed analyses of the complementarity determining region 3 (CDR3) of the TCRB of CD8+CD28+ and CD8+CD28- T cells from the peripheral blood of HIV-1-infected individuals. When cells from the same individual were compared, expanded peaks in CDR3 length analysis within a given BV family were frequently observed at the same location in both CD8+ subsets (p < 0.001). Sequencing of cDNA corresponding to dominant peaks revealed the presence of identical expanded CD8+ T cell clones within both the CD28+ and CD28- subsets on eight of nine attempts. Our results show that CD8+CD28+ and CD8+CD28- T cells are phenotypic variants of the same lineage, most likely evolving from CD8+CD28+ to end-stage CD8+CD28- T cells.

Published
1998
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30. Risk of toxoplasmic encephalitis in AIDS patients: indications for prophylaxis.

Author

Dunlop O, Rootwelt V, Sannes M, Goplen AK, Abdelnoor M, Skaug K, Baklien K, Skar A, Melby K, Myrvang B, and Bruun JN

Subjects
AIDS-Related Opportunistic Infections etiology, CD4 Lymphocyte Count, Encephalitis etiology, Humans, Immunoglobulin G blood, Retrospective Studies, Toxoplasmosis, Cerebral etiology, AIDS-Related Opportunistic Infections prevention & control, Encephalitis prevention & control, Toxoplasmosis, Cerebral prevention & control
Abstract

To establish the indications for primary prophylaxis against toxoplasmic encephalitis in the Norwegian HIV-positive population, we estimated the incidence of toxoplasmic encephalitis, and related the degree of immunodeficiency and the presence of IgG antibodies against Toxoplasma gondii (T. gondii) to the development of toxoplasmic encephalitis. This retrospective study includes all HIV-positive patients at our hospital from April 1983 to October 1994 (n = 705). A total of 238 patients had AIDS, which represents almost 90% of all AIDS patients in Oslo. Autopsy was done in over 70% of the patients who died during this period; 19 patients developed toxoplasmic encephalitis (8.0%). The median CD4 cell count was 75 x 10(6) cell/I (range 0-280) at the time of diagnosis of toxoplasmic encephalitis. T. gondii serology was studied in 698 (99.0%) of the patients, and was found positive for 17.8%. Of the patients with toxoplasmic encephalitis 18/19 had IgG antibodies against T. gondii and of the 40 AIDS patients who had anti-T. gondii IgG, 18 (45%) developed toxoplasmic encephalitis. We conclude that there is indication for prophylactic treatment of HIV positive patients who have IgG antibodies against T. gondii and who have fewer than 200 x 10(6) CD4 cells/I.

Published
1996
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