Evaluation of some cellular immune index in HIV infected participants

Abstract

The study was designed to evaluate some cellular immune index of HIV infected participants. For the study, 80 HIV infected participants were recruited for the study. They were aged 15 - 55 years. 45 of these participants were classified as Symptomatic HIV (Stage 11), while the remaining 35 were Asymptomatic HIV (Stage 1). Similarly, 40 HIV seronegative participants served as Control. Blood samples collected from the participants were used HIV screening and confirmation, CD4+ T cell count, absolute lymphocyte count and percent lymphocyte transformation. The CD4+T cell count and percent Lymphocyte Transformation count were significantly lowered in HIV infected participants compared with the HIV Seronegative participants (p<0.05 in each case). Symptomatic HIV seropositive participants also presented with lowered CD4 and percent lymphocyte transformation, compared with the asymptomatic HIV participants (p<0.05 in each case). The lowered CD4+T cell count suggests possible quantitative destruction of cellular immune cells (mainly Th1 cells). While the lowered percent blast formation in HIV infection indicates functional derangement of the cellular immune cells. Meanwhile no significant difference was observed in absolute lymphocyte count among the symptomatic, asymptomatic and control participants (p> 0.05).

Use of plasma albumin, hepatic lipase and lipoprotein lipase enzyme as predictive markers of treatment failure in HIV-1 infected individuals in federal medical center, Lokoja, Nigeria

“…The results of this study suggest that plasma albumin level has the potential to be used as a surrogate prognostic marker for HIV-1 disease monitoring because of a signi icant increase in plasma albumin level at 12 months of therapy. This inding is supported by Ifeanyichukwu et al (2011);Sharma et al (2016) that low plasma albumin in HAART naive participants may be due to acutephase responses in HIV-1 infection leading to a wide range of pathophysiological reactions that resulted in increased levels of in lammatory biomarkers such as tumor necrosis factor (TNF) and interleukin-6 (IL-6), which are responsible for the reduction in hepatic albumin synthesis and increase in albumin leakage to the extravascular space while enhanc-ing the degradation of albumin. In a similar study by Ifeanyichukwu et al (2011), it was shown that HIV-1 infection is accompanied by a robust plasma pro-in lammatory and anti-in lammatory cytokine response in HAART naive individuals.…”

“…This inding is supported by Ifeanyichukwu et al (2011);Sharma et al (2016) that low plasma albumin in HAART naive participants may be due to acutephase responses in HIV-1 infection leading to a wide range of pathophysiological reactions that resulted in increased levels of in lammatory biomarkers such as tumor necrosis factor (TNF) and interleukin-6 (IL-6), which are responsible for the reduction in hepatic albumin synthesis and increase in albumin leakage to the extravascular space while enhanc-ing the degradation of albumin. In a similar study by Ifeanyichukwu et al (2011), it was shown that HIV-1 infection is accompanied by a robust plasma pro-in lammatory and anti-in lammatory cytokine response in HAART naive individuals. The high proin lammatory cytokines were probably produced by monocytes and macrophages to initiate in lammation which is essential for the development of innate immunity, while the increased anti-in lammatory cytokines were stimulated probably to deactivate the activities of the pro-in lammatory cytokines.…”

“…This is because the lipoprotein lipase enzyme is inactive until it becomes bound to its cofactor, apoprotein C II (AP o C II ). And activation of the immune system in HIV-1 infection promotes pro-in lammatory cytokines synthesis and release that leads to the poor synthesis of apoprotein C II from the liver and, in turn, affects the activation of lipoprotein lipase (Ifeanyichukwu et al, 2011). From another study, it has been reported that immune system activation in HIV-1 infection causes a knockdown of AP o A −1 and AP o C II expression due to elevations of interferon-gamma (IFNr) and tumor necrosis factor-α (TNFα) that promotes lipids peroxidation and disturbances in the metabolism of lipids (Cunha et al, 2015); these lead to lipodystrophy, myositis and hepatomegaly.…”

“…Human immunode iciency virus infection has the ability to progressively shut down the host immune system due to the exponential growth of the virus in some infected individuals (Ifeanyichukwu et al, 2011). This may result in the manifestation of acquired immune de iciency syndrome (AIDS) if HIV progression in a host is not check meted (Ifeanyichukwu et al, 2011).…”

“…Despite vigorous researches and prophylactic mea-sures on HIV/AIDS, the infection and the disease conditions continue to threaten the lives of millions of people in Africa (Ifeanyichukwu et al, 2011). The continued surge of HIV/AIDS in Africa can be attributed to the in luence of so many other factors on the pathogenesis of the disease condition.…”