Immunological profiles in HIV positive patients with or without opportunistic infections and the influence of highly active antiretroviral therapy: a systematic review and update

Abstract

Background: Immune abnormalities are occasioned during HIV infection consequently predisposing opportunistic infections. In part, these derangements result from impaired expression of a number of immunologically important cytokines. However, exact mechanisms behind HIV infectivity on immune system maturation and cytokine production is not well elucidated, more specifically during treatment with HAART. As such, this review compiles data from various studies with the aim of understanding alterations in cytokine network during the course of HIV infection, while assessing the impact of antiretroviral treatment towards cytokine expression. Methods: Studies describing cytokine profiles among HIV infected cohorts with or without opportunistic infections (from January, 1990-March, 2016) were carefully inspected from various databases including; PubMed, Hinary, Medline search, Cochrane, and Google scholar for material bearing potential relevance pertaining to our review. Results: Based on our search strategy a total of 849 research articles were initially identified. However, upon further scrutinisation 830 were excluded since they failed to fulfill all rations for inclusion after reviewing. Overall 19 studies were selected for final review which satisfied our criteria of inclusion. Discussion: Highly active antiretroviral therapy promotes immune integrity by normalizing progenitor cell function and enhancing CD4+ and CD8+ T cell proliferation and activity. These actions co-operatively prolong survival and quality of life among HIV infected persons while keeping opportunistic infections at bay. Cytokine secretion is vital for T-cell function especially towards control of viral infections as they mediate effector roles as well as support immune system expansion. Elevated cytokine levels during the course of HIV infection can have positive or negative effect on viral load control or CD4+ T cell lymphocyte homeostasis. For instance, TNF-α and IL-4 aid viral replication while IFN-γ is implicated in control viral replication. Conclusion: Both HIV infection and antiretroviral treatment influence levels of circulating inflammatory cytokines. However, further investigations are warranted to define exact mechanisms of HIV disease progression coupled with cytokine expression for improving therapeutic options for HIV infected patients.