Immunologic and virological response to ART among HIV infected individuals at a tertiary hospital in Ghana

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Abstract

Background

The need to study the outcome of Antiretroviral Therapy (ART) among Human Immunodeficiency Virus (HIV) infected individuals in Ghana, a sub-Saharan African country crucial in the era of the “Treat All” policy. The aim of this study was to analyze selected determinants of immunological and virological response to ART among HIV infected individuals in a tertiary facility in Cape Coast, Ghana.

Methods

An analytical cross sectional study with a retrospective component was conducted in the Cape Coast Teaching Hospital (CCTH), Central Region. Clients aged 18 years and above attending the HIV Clinics for ART and who were on ART for 6 months or more were recruited. The viral loads, CD4 count and other socio-demographic data were analyzed using STATA version 13 (STATA Corp, Texas USA). Descriptive analysis was done and presented with appropriate measures of central tendencies. In addition, bivariate and multivariate analysis was carried out with p value of 0.05 interpreted as evidence of association between variables.

Results

A total of 440 participants were included in this study with a mean age of 45.5 (±11.6) years. The mean CD4 count at baseline, 6 months on ART and currently at study recruitment were 215.1 cells/mm ³ (±152.6), 386.6 cells/mm ³ (±178.5), and 579.6 cells/mm ³ (±203.0) respectively. After 6 months and 12 months on ART, the number who had achieved viral copies < 1000/ml were 149 (47.0%) and 368 (89.6%) respectively. There was strong evidence of an association between having CD4 count < 350 cells/mm ³ after 6 months on ART and having a diagnosis of tuberculosis since HIV diagnosis (aOR 8.5, 95% CI 1.1–73.0, p = 0.05) and clients having plasma viral load > 1000 copies/ml after 6 months on ART (aOR 2.0, 95% CI 1.2–3.2, p = 0.01).

Conclusion

There was good response to ART among clients, high virological suppression and immunological recovery hence low rates of change to second line ART regimen in this cohort studied. With strict adherence to the national policy on HIV testing, management of positive clients and full implementation of the “Treat All” policy, Ghana could achieve, if nothing at all, the third “90, 90, 90” target by 2020.

Electronic supplementary material

The online version of this article (10.1186/s12879-018-3142-5) contains supplementary material, which is available to authorized users.

Related collections

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Incomplete peripheral CD4+ cell count restoration in HIV-infected patients receiving long-term antiretroviral treatment.

Colleen Kelley, Christina Kitchen, Peter W. Hunt … (2009)

Although antiretroviral therapy has the ability to fully restore a normal CD4(+) cell count (>500 cells/mm(3)) in most patients, it is not yet clear whether all patients can achieve normalization of their CD4(+) cell count, in part because no study has followed up patients for >7 years. Three hundred sixty-six patients from 5 clinical cohorts who maintained a plasma human immunodeficiency virus (HIV) RNA level 1000 copies/mL for at least 4 years after initiation of antiretroviral therapy were included. Changes in CD4(+) cell count were evaluated using mixed-effects modeling, spline-smoothing regression, and Kaplan-Meier techniques. The majority (83%) of the patients were men. The median CD4(+) cell count at the time of therapy initiation was 201 cells/mm(3) (interquartile range, 72-344 cells/mm(3)), and the median age was 47 years. The median follow-up period was 7.5 years (interquartile range, 5.5-9.7 years). CD4(+) cell counts continued to increase throughout the follow-up period, albeit slowly after year 4. Although almost all patients (95%) who started therapy with a CD4(+) cell count 300 cells/mm(3) were able to attain a CD4(+) cell count 500 cells/mm(3), 44% of patients who started therapy with a CD4(+) cell count 500 cells/mm(3) over a mean duration of follow-up of 7.5 years; many did not reach this threshold by year 10. Twenty-four percent of individuals with a CD4(+) cell count <500 cells/mm(3) at year 4 had evidence of a CD4(+) cell count plateau after year 4. The frequency of detectable viremia ("blips") after year 4 was not associated with the magnitude of the CD4(+) cell count change. A substantial proportion of patients who delay therapy until their CD4(+) cell count decreases to <200 cells/mm(3) do not achieve a normal CD4(+) cell count, even after a decade of otherwise effective antiretroviral therapy. Although the majority of patients have evidence of slow increases in their CD4(+) cell count over time, many do not. These individuals may have an elevated risk of non-AIDS-related morbidity and mortality.

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Sustained suppression of the human immunodeficiency virus (HIV) type 1 RNA load with the use of highly active antiretroviral therapy (HAART) results in immunologic improvement, but it is not clear whether the CD4(+) cell count increases to normal levels or whether it reaches a less-than-normal plateau. We characterized the increase in the CD4(+) cell count in patients in clinical practice who maintained sustained viral suppression for up to 6 years. All patients were from the Johns Hopkins HIV Clinical Cohort, a longitudinal observational study of patients receiving primary HIV care in Baltimore, Maryland, who were observed for >1 year while receiving HAART and who had sustained suppression of the HIV RNA load at 350 cells/microL, and we assessed the development of clinical events (death and new acquired immunodeficiency syndrome-defining illness) by Kaplan-Meier analysis. A total of 655 patients were observed for a median of 46 months (range, 13-72 months). The median change from baseline to most recent CD4(+) cell count was +274 cells/microL, with 92% of patients having an increase in CD4(+) cell count. By 6 years, the median CD4(+) cell count was 493 cells/microL among patients with baseline CD4(+) cell counts 350 cells/microL. In addition to baseline CD4(+) cell count, injection drug use and older age were associated with a lesser CD4(+) cell count response, and duration of therapy was associated with a greater CD4(+) cell count response. Only patients with baseline CD4(+) cell counts >350 cells/microL returned to nearly normal CD4(+) cell counts after 6 years of follow-up. Significant increases were observed in all CD4(+) cell count strata during the first year, but there was a lower plateau CD4(+) cell count at lower baseline CD4(+) cell strata. These data suggest that waiting to start HAART at lower CD4(+) cell counts will result in the CD4(+) cell count not returning to normal levels.

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Pathophysiology of CD4+ T-Cell Depletion in HIV-1 and HIV-2 Infections

K. K. Vidya Vijayan, Krithika Priyadarshini Karthigeyan, Srikanth Tripathi … (2017)

The hall mark of human immunodeficiency virus (HIV) infection is a gradual loss of CD4+ T-cells and imbalance in CD4+ T-cell homeostasis, with progressive impairment of immunity that leads ultimately to death. HIV infection in humans is caused by two related yet distinct viruses: HIV-1 and HIV-2. HIV-2 is typically less virulent than HIV-1 and permits the host to mount a more effective and sustained T-cell immunity. Although both infections manifest the same clinical spectrum, the much lower rate of CD4+ T-cell decline and slower progression of disease in HIV-2 infected individuals have grabbed the attention of several researchers. Here, we review the most recent findings on the differential rate of decline of CD4+ T-cell in HIV-1 and HIV-2 infections and provide plausible reasons for the observed differences between the two groups.

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Author and article information

Contributors

Dorcas Obiri-Yeboah:

ORCID: http://orcid.org/0000-0003-4562-9294

00233 264 527 387 , d.obiri-yeboah@uccsms.edu.gh , dobiri-yeboah@ucc.edu.gh

Faustina Pappoe: f.pappoe@uccsms.edu.gh

Ibrahim Baidoo: ibrahimbaidoo@gmail.com

Francis Arthur: arcosus@yahoo.com

Anna Hayfron-Benjamin: ahayfron-benjamin@ucc.edu.gh

Samuel Essien-Baidoo: sessien-baidoo@ucc.edu.gh

Godwin Kwakye-Nuako: gkncarlos@yahoo.com

Stephen Ayisi Addo: saddo@nacp.org.gh

Journal

Journal ID (nlm-ta): BMC Infect Dis

Journal ID (iso-abbrev): BMC Infect. Dis

Title: BMC Infectious Diseases

Publisher: BioMed Central (London )

ISSN (Electronic): 1471-2334

Publication date (Electronic): 21 May 2018

Publication date PMC-release: 21 May 2018

Publication date Collection: 2018

Volume: 18

Electronic Location Identifier: 230

Affiliations

[1 ]ISNI 0000 0001 2322 8567, GRID grid.413081.f, Department of Microbiology and Immunology, School of Medical Sciences, , University of Cape Coast, ; Cape Coast, Ghana

[2 ]Public Health Unit, Cape Coast Teaching Hospital, Cape Coast, Ghana

[3 ]Microbiology Unit, Cape Coast Teaching Hospital, Cape Coast, Ghana

[4 ]ISNI 0000 0001 2322 8567, GRID grid.413081.f, Department of Maternal and Child Health, School of Nursing and Midwifery, , University of Cape Coast, ; Cape Coast, Ghana

[5 ]ISNI 0000 0001 2322 8567, GRID grid.413081.f, Department of Laboratory Technology, , University of Cape Coast, ; Cape Coast, Ghana

[6 ]ISNI 0000 0001 2322 8567, GRID grid.413081.f, Department of Biomedical Sciences, , University of Cape Coast, ; Cape Coast, Ghana

[7 ]National AIDS/STI Control Program, Ghana Health Services, Accra, Ghana

Author information

Dorcas Obiri-Yeboah http://orcid.org/0000-0003-4562-9294

Article

Publisher ID: 3142

DOI: 10.1186/s12879-018-3142-5

PMC ID: 5963173

PubMed ID: 29783953

SO-VID: d8963fdb-cfb9-43e1-8073-ceaa67abf2fc

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.