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HIV Seropositivity: HELP
Articles by Lynn Morris
Based on 3 articles published since 2008
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Between 2008 and 2019, Lynn Morris wrote the following 3 articles about HIV Seropositivity.
 
+ Citations + Abstracts
1 Clinical Trial Sequential Immunization with gp140 Boosts Immune Responses Primed by Modified Vaccinia Ankara or DNA in HIV-Uninfected South African Participants. 2016

Churchyard, Gavin / Mlisana, Koleka / Karuna, Shelly / Williamson, Anna-Lise / Williamson, Carolyn / Morris, Lynn / Tomaras, Georgia D / De Rosa, Stephen C / Gilbert, Peter B / Gu, Niya / Yu, Chenchen / Mkhize, Nonhlanhla N / Hermanus, Tandile / Allen, Mary / Pensiero, Michael / Barnett, Susan W / Gray, Glenda / Bekker, Linda-Gail / Montefiori, David C / Kublin, James / Corey, Lawrence. ·Aurum Institute for Health Research, Klerksdorp, South Africa. · School of Public Health, University of Witwatersrand, Johannesburg, South Africa. · Advancing Care and Treatment for TB and HIV, Medical Research Council Collaborating Centre, Klerksdorp, South Africa. · University of Kwa-Zulu Natal, Durban, South Africa. · Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA, United States of America. · Institute of Infectious Disease and Molecular Medicine, Division of Medical Virology, University of Cape Town, Cape Town, South Africa; National Health Laboratory Services, Observatory, Cape Town, South Africa. · National Institute for Communicable Diseases, National Health Laboratory Services, Sandringham, Johannesburg, South Africa. · Duke Human Vaccine Institute, Duke University Medical Center, Durham, NC, United States of America. · Department of Laboratory Medicine, University of Washington, Seattle, WA, United States of America. · Vaccine Research Program, Division of AIDS, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, United States of America. · Novartis Vaccines and Diagnostics, Cambridge, MA, United States of America. · South African Medical Research Council, Cape Town, South Africa. · Perinatal HIV Research Unit, Faculty of Health Sciences, University of the Witwatersrand, Braamfontein, Johannesburg, South Africa. · Desmond Tutu HIV Centre, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Cape Town, South Africa. · Laboratory for AIDS Vaccine Research and Development, Duke University Medical Center, Durham, NC, United States of America. ·PLoS One · Pubmed #27583368.

ABSTRACT: BACKGROUND: The safety and immunogenicity of SAAVI DNA-C2 (4 mg IM), SAAVI MVA-C (2.9 x 109 pfu IM) and Novartis V2-deleted subtype C gp140 (100 mcg) with MF59 adjuvant in various vaccination regimens was evaluated in HIV-uninfected adults in South Africa. METHODS: Participants at three South African sites were randomized (1:1:1:1) to one of four vaccine regimens: MVA prime, sequential gp140 protein boost (M/M/P/P); concurrent MVA/gp140 (MP/MP); DNA prime, sequential MVA boost (D/D/M/M); DNA prime, concurrent MVA/gp140 boost (D/D/MP/MP) or placebo. Peak HIV specific humoral and cellular responses were measured. RESULTS: 184 participants were enrolled: 52% were female, all were Black/African, median age was 23 years (range, 18-42 years) and 79% completed all vaccinations. 159 participants reported at least one adverse event, 92.5% were mild or moderate. Five, unrelated, serious adverse events were reported. The M/M/P/P and D/D/MP/MP regimens induced the strongest peak neutralizing and binding antibody responses and the greatest CD4+ T-cell responses to Env. All peak neutralizing and binding antibody responses decayed with time. The MVA, but not DNA, prime contributed to the humoral and cellular immune responses. The D/D/M/M regimen was poorly immunogenic overall but did induce modest CD4+ T-cell responses to Gag and Pol. CD8+ T-cell responses to any antigen were low for all regimens. CONCLUSIONS: The SAAVI DNA-C2, SAAVI MVA-C and Novartis gp140 with MF59 adjuvant in various combinations were safe and induced neutralizing and binding antibodies and cellular immune responses. Sequential immunization with gp140 boosted immune responses primed by MVA or DNA. The best overall immune responses were seen with the M/M/P/P regimen. TRIAL REGISTRATION: ClinicalTrials.gov NCT01418235.

2 Clinical Trial Reactivity of routine HIV antibody tests in children who initiated antiretroviral therapy in early infancy as part of the Children with HIV Early Antiretroviral Therapy (CHER) trial: a retrospective analysis. 2015

Payne, Helen / Mkhize, Nonhlanhla / Otwombe, Kennedy / Lewis, Joanna / Panchia, Ravindre / Callard, Robin / Morris, Lynn / Babiker, Abdel / Violari, Avy / Cotton, Mark F / Klein, Nigel J / Gibb, Diana M. ·Institute of Child Health, University College London, London, UK. Electronic address: helenpayne@doctors.org.uk. · Centre for HIV and Sexually Transmitted Infections, National Institute for Communicable Diseases of the National Health Laboratory Services, Johannesburg, South Africa. · Perinatal HIV Research Unit, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa. · Centre for Maths and Physics in the Life Sciences and Experimental Biology, University College London, London, UK. · Institute of Child Health, University College London, London, UK; Centre for Maths and Physics in the Life Sciences and Experimental Biology, University College London, London, UK. · Clinical Trials Unit, Medical Research Council, London, UK. · Children's Infectious Diseases Clinical Research Unit, Department of Paediatrics and Child Health, Stellenbosch University, Cape Town, South Africa. · Institute of Child Health, University College London, London, UK. ·Lancet Infect Dis · Pubmed #26043884.

ABSTRACT: BACKGROUND: Early antiretroviral therapy (ART) and virological suppression can affect evolving antibody responses to HIV infection. We aimed to assess frequency and predictors of seronegativity in infants starting early ART. METHODS: We compared HIV antibody results between two of three treatment groups of the Children with HIV Early Antiretroviral Therapy (CHER) trial, done from July, 2005, until July, 2011, in which infants with HIV infection aged 5·7-12·0 weeks with a percentage of CD4-positive T lymphocytes of at least 25% were randomly assigned to immediate ART for 96 weeks (ART-96W) or deferred ART until clinical or immunological progression (ART-Def). We measured antibody from all available stored samples for ART-96W and ART-Def at trial week 84 using three assays: fourth-generation enzyme immunoassay HIV antigen-antibody combination, HIV-1 and HIV-2 rapid antibody test, and quantitative anti-gp120 IgG ELISA. We also assessed odds of seropositivity with respect to age of ART initiation and cumulative viral load. The CHER trial was registered with ClinicalTrials.gov, number NCT00102960. FINDINGS: The median age of the infants from when samples were taken (184 samples from 268 infants) was 92 weeks (IQR 90·6-93·4). More specimens from the ART-96W group were seronegative than from the ART-Def group by enzyme immunoassay (ART-96W 49 [46%] of 107 vs ART-Def eight [11%] of 75; p<0·0001) and rapid antibody test (54 [53%] of 101 vs eight [11%] of 74; p<0·0001). Median anti-gp120 IgG concentration was lower in the ART-96W group (230 μg/μL [IQR 133-13 129]) than in the ART-Def group (6870 μg/μL [1706-53 645]; p<0·0001). If ART was started between 12 and 24 weeks of age, odds of seropositivity were increased 13·7 times (95% CI 3·1-60·2; p=0·001) compared with starting it between 0 and 12 weeks. All children starting ART aged older than 24 weeks were seropositive. Cumulative viral load to week 84 correlated with anti-gp120 IgG concentrations (coefficient 0·54; p<0·0001) and increased odds of seropositivity (odds ratio 1·59 [95% CI 1·1-2·3]) adjusted for ART initiation age. INTERPRETATION: About half of children starting ART before 12 weeks of age were HIV seronegative by almost 2 years of age. HIV antibody tests cannot be used to reconfirm HIV diagnosis in children starting early ART. Long-term effects of seronegativity need further study. Clear guidelines are needed for retesting alongside improved diagnostic tests. FUNDING: Wellcome Trust, Medical Research Council, and National Institutes of Health.

3 Article Evolution of an HIV glycan-dependent broadly neutralizing antibody epitope through immune escape. 2012

Moore, Penny L / Gray, Elin S / Wibmer, C Kurt / Bhiman, Jinal N / Nonyane, Molati / Sheward, Daniel J / Hermanus, Tandile / Bajimaya, Shringkhala / Tumba, Nancy L / Abrahams, Melissa-Rose / Lambson, Bronwen E / Ranchobe, Nthabeleng / Ping, Lihua / Ngandu, Nobubelo / Abdool Karim, Quarraisha / Abdool Karim, Salim S / Swanstrom, Ronald I / Seaman, Michael S / Williamson, Carolyn / Morris, Lynn. ·Centre for HIV and STI, National Institute for Communicable Diseases of the National Health Laboratory Service, Johannesburg, South Africa. ·Nat Med · Pubmed #23086475.

ABSTRACT: Neutralizing antibodies are likely to play a crucial part in a preventative HIV-1 vaccine. Although efforts to elicit broadly cross-neutralizing (BCN) antibodies by vaccination have been unsuccessful, a minority of individuals naturally develop these antibodies after many years of infection. How such antibodies arise, and the role of viral evolution in shaping these responses, is unknown. Here we show, in two HIV-1-infected individuals who developed BCN antibodies targeting the glycan at Asn332 on the gp120 envelope, that this glycan was absent on the initial infecting virus. However, this BCN epitope evolved within 6 months, through immune escape from earlier strain-specific antibodies that resulted in a shift of a glycan to position 332. Both viruses that lacked the glycan at amino acid 332 were resistant to the Asn332-dependent BCN monoclonal antibody PGT128 (ref. 8), whereas escaped variants that acquired this glycan were sensitive. Analysis of large sequence and neutralization data sets showed the 332 glycan to be significantly under-represented in transmitted subtype C viruses compared to chronic viruses, with the absence of this glycan corresponding with resistance to PGT128. These findings highlight the dynamic interplay between early antibodies and viral escape in driving the evolution of conserved BCN antibody epitopes.