Correlation of serum level of inflammatory markers with CD4 count in HAART naïve HIV patient and patient on HAART

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The objective of the study was to evaluate the correlation of the inflammatory markers with absolute CD4 count in on HAART and HAART naïve HIV patients. one hundred and fifty participants, comprising of 50 on-treatment and 50 treatment naïve HIV patients, and 50 sero-negative subjects were recruited for the study. Serum CRP, IL-6 and TNF- α were measured using ELISA, CD4 count analysis was done using the BD FACS count and hematology parameters were measured using an XS-500i automatic blood cell analyzer (Sysmex Corporation Co. Ltd, Japan). IL-6 and TNF- α concentrations in HIV-seropositive group were significantly higher than those in seronegative group, and mutually correlated. No significant differences in serum IL-6, CRP and TNF-α level between on HAART, and HAART naïve, groups were observed. Median levels of proinflammatory cytokines (IL-6, CRP and TNF-Alpha) significantly increased with decreasing CD4 count. Subjects with CD4 count less than 200 cells/mm3 were associated with significantly higher median levels of IL-6, CRP and TNF-Alpha compared to those with CD4 count of 500 cells/mm3 and more. The data observed indicated an association between CD8 and CD3 and between the ratio of CD4/CD8 and the ratio of CD4/CD3. A significant and negative correlation of CD8 was observed with the ratio of CD4/CD8 and CD4/CD3 and TNF-alpha with Hb; HCT and RBC but not WBC in all the studied participants. A negative correlation between TNF-alpha and Hb, HCT, RBC and WBC count and also between TNF-alpha and the ratio of CD4/CD8 among HAART naïve HIV participants were observed. Meanwhile Hb, HCT, RBC and WBC were not significantly associated with both IL-6 and CRP. Regardless of the source and initial stimulus, continued immune activation and inflammation results in the over-production of IL-6, CRP and TNF-α and thus create an oxidised environment replication of new virion of HIV. The attack of these viruses will decrease CD4 T cell which will speed up the progression of HIV pathogenesis.
A thesis submitted to the department of molecular medicine, Kwame Nkrumah University of Science and Technology in fulfilment of the requirement for the degree of Master of Science in Immunology, 2016.