dc.contributor.author |
Sokoya, T.
|
|
dc.contributor.author |
Steel, Helen C.
|
|
dc.contributor.author |
Nieuwoudt, M.
|
|
dc.contributor.author |
Rossouw, Theresa M.
|
|
dc.date.accessioned |
2017-11-20T12:45:23Z |
|
dc.date.available |
2017-11-20T12:45:23Z |
|
dc.date.issued |
2017 |
|
dc.description.abstract |
Systemic immune activation has emerged as an essential component of the immunopathogenesis of HIV. It not only leads to faster
disease progression, but also to accelerated decline of overall immune competence. HIV-associated immune activation is
characterized by an increase in proinflammatory mediators, dysfunctional T regulatory cells, and a pattern of T-cell-senescent
phenotypes similar to those seen in the elderly. These changes predispose HIV-infected persons to comorbid conditions that
have been linked to immunosenescence and inflamm-ageing, such as atherosclerosis and cardiovascular disease,
neurodegeneration, and cancer. In the antiretroviral treatment era, development of such non-AIDS-defining, age-related
comorbidities is a major cause of morbidity and mortality. Treatment strategies aimed at curtailing persistent immune
activation and inflammation may help prevent the development of these conditions. At present, the most effective strategy
appears to be early antiretroviral treatment initiation. No other treatment interventions have been found effective in large-scale
clinical trials, and no adjunctive treatment is currently recommended in international HIV treatment guidelines. This article
reviews the role of systemic immune activation in the immunopathogenesis of HIV infection, its causes and the clinical
implications linked to immunosenescence in adults, and the therapeutic interventions that have been investigated. |
en_ZA |
dc.description.department |
Immunology |
en_ZA |
dc.description.librarian |
am2017 |
en_ZA |
dc.description.sponsorship |
The National Research Foundation of South Africa, Unique Grant no. 93944, and DST/NRF Centre of Excellence in Epidemiological Modelling and Analysis (SACEMA). |
en_ZA |
dc.description.uri |
http://www.hindawi.com/journals/mi |
en_ZA |
dc.identifier.citation |
Sokoya, T., Steel, H.C., Nieuwoudt, M. & Rossouw, T.M. 2017, 'HIV as a cause of immune activation and immunosenescence', Mediators of Inflammation, vol. 2017 art. no. 682493, pp. 1-16. |
en_ZA |
dc.identifier.issn |
0962-9351 (print) |
|
dc.identifier.issn |
1466-1861 (online) |
|
dc.identifier.other |
10.1155/2017/6825493 |
|
dc.identifier.uri |
http://hdl.handle.net/2263/63235 |
|
dc.language.iso |
en |
en_ZA |
dc.publisher |
Hindawi Publishing |
en_ZA |
dc.rights |
© 2017 T. Sokoya et al. This is an open access article distributed under the Creative Commons Attribution License. |
en_ZA |
dc.subject |
Systemic immune activation |
en_ZA |
dc.subject |
Antiretroviral treatment (ART) |
en_ZA |
dc.subject |
HIV treatment guidelines |
en_ZA |
dc.subject |
Human immunodeficiency virus (HIV) |
en_ZA |
dc.subject |
T-cell activation |
en_ZA |
dc.subject |
Active antiretroviral therapy |
en_ZA |
dc.subject |
Microbial translocation |
en_ZA |
dc.subject |
Infected patients |
en_ZA |
dc.subject |
Natural SIV hosts |
en_ZA |
dc.subject |
Simian immunodeficiency virus (SIV) |
en_ZA |
dc.subject |
Epstein-Barr virus (EBV) |
en_ZA |
dc.subject |
Toll-like receptors |
en_ZA |
dc.subject |
Tubular epithelial cells |
en_ZA |
dc.subject |
Randomized controlled trial |
en_ZA |
dc.title |
HIV as a cause of immune activation and immunosenescence |
en_ZA |
dc.type |
Article |
en_ZA |