Browsing by Author "Weber, Jonathan"

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    Duration of HIV-1 Viral Suppression on Cessation of Antiretroviral Therapy in Primary Infection Correlates with Time on Therapy
    (PLoS ONE, 2013) Stöhr, Wolfgang; Fidler, Sarah; McClure, Myra; Weber, Jonathan; Cooper, David; Ramjee, Gita; Kaleebu, Pontiano; Tambussi, Giuseppe; Schechter, Mauro; Babiker, Abdel; Phillips, Rodney E.; Porter, Kholoud; Frater, John
    A minority of HIV-1 positive individuals treated with antiretroviral therapy (ART) in primary HIV-1 infection (PHI) maintain viral suppression on stopping. Whether this is related to ART duration has not been explored. Design: And Methods: Using SPARTAC trial data from individuals recruited within 6 months of seroconversion, we present an observational analysis investigating whether duration of ART was associated with post-treatment viraemic control. Kaplan-Meier estimates, logistic regression and Cox models were used. 165 participants reached plasma viral loads (VL) 12 weeks compared to ≤12 weeks (p=0.061). Cumulative probabilities of remaining 12 weeks. In multivariable regression, ART for >12 weeks was independently associated with a lower probability of being ≥400 copies/ml within 12 weeks of ART stop (OR=0.11 (95%CI=0.03,0.34), p
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    Effect of Human Immunodeficiency Virus (HIV) Type 1 Envelope Subtypes A and D on Disease Progression in a Large Cohort of HIV-1–Positive Persons in Uganda
    (The Journal of Infectious Diseases, 2002) Kaleebu, Pontiano; French, Neil; Mahe, Cedric; Yirrell, David; Watera, Christine; Lyagoba, Fred; Nakiyingi, Jessica; Rutebemberwa, Alleluiah; Morgan, Dilys; Weber, Jonathan; Gilks, Charles; Whitworth, Jimmy
    The effect of human immunodeficiency virus (HIV) type 1 envelope subtypes A and D on disease progression was investigated in 1045 adults in Uganda. At enrollment and every 6 months, a clinical history, examination, and laboratory investigations that included CD4 cell counts were done. HIV-1 envelope subtype was assessed mainly by peptide serology supplemented by heteroduplex mobility assay and DNA sequencing. A multivariate analysis of survival was performed to assess the prognostic value of HIV-1 subtype on death. A marginal general linear model also determined the effect of subtype on CD4 cell count during follow-up. Subtype D was associated with faster progression to death (relative risk, 1.29; 95% confidence interval, 1.07–1.56; P ¼ .009) and with a lower CD4 cell count during follow-up (P ¼ .001), compared with subtype A, after adjusting for CD4 cell count at enrollment. In Africa, envelope subtype D is associated with faster disease progression, compared with subtype A
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    Relation Between Chemokine Receptor Use, Disease Stage, and HIV-1 Subtypes A and D Results From a Rural Ugandan Cohort
    (JAIDS Journal of Acquired Immune Deficiency Syndromes, 2007) Kaleebu, Pontiano; Nankya, Immaculate L.; Yirrell, David L.; Shafer, Leigh Anne; Kyosiimire-Lugemwa, Jacqueline; Lule, Daniel B.; Morgan, Dilys; Beddows, Simon; Weber, Jonathan; Whitworth, James A. G.
    To determine whether there are differences in coreceptor use in subjects infected with HIV-1 envelope subtypes A and D that could explain the differences in progression rates between these subtypes in a rural Ugandan cohort. HIV-1 was subtyped in env by V3 sequencing or heteroduplex mobility assay. Coreceptor use was determined by the ability of the isolates to replicate in U87 CD4+ cells expressing different coreceptors. The Fisher exact test was used to examine the relation between coreceptor use and subtype, clinical stage, and V3 charge. The Kruskall-Wallis nonparametric test was used to examine the association between median CD4 cell counts, coreceptor use, and subtype. Logistic regression was used to examine predicted coreceptor use at different CD4 groupings. Isolates from 66 participants were analyzed. Thirty-one were infected with subtype A, and 35 were infected with subtype D. Although this work was based on a small sample size, we found statistically significant differences. The probability of having an X4 virus was higher in subtype D infections than in subtype A infections among those with a non-AIDS clinical status (Fisher exact test, P = 0.040). Logistic regression analysis, in which we predicted X4 use by subtype and stratified by CD4 group, confirmed these findings among those with a CD4 count .200 cells/mL (likelihood ratio test, P = 0.003). R5 viruses were associated with higher median CD4 cell counts than X4 or X4/R5 (Kruskall-Wallis test, P = 0.0045). AV3 charge of +5 and greater was highly associated with X4 virus (Fisher exact test, P = 0.006). These subtype differences in coreceptor use may partially explain the faster progression rates we have previously