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Successful virological suppression in the face of immunological failure amongst HIV seropositive persons on antiretroviral treatment
Abstract
Background: In the absence of viral load tests as monitoring tool for people living with HIV/AIDS on antiretroviral therapy, CD4 cell count and clinical assessment were depended upon as a monitoring tool. Our clinically healthy clients with immune failure repeatedly for two to three times were switched to second line drugs. Those clinically ill with immune failure with no other known comorbidity were also switched to second line drugs. Studies have shown that some persons living with human immunodeficiency virus (HIV) who did normalise their immune status while on HAART, had viral suppression while others showed blunted immune response despite virologic suppression evidenced by low plasma HIV-1 RNA.1-5 Quality improvement programme later on set up and funded by the PEPFAR US based programme in which 1,520 clients on antiretroviral therapy were randomly selected and subjected to viral load assay. We reviewed the CD4 response of our patients on HAART at baseline and at time of viral load assay, in order to identify discordant patients and thus formulate strategies for more efficient and effective antiretroviral client treatment monitoring.
Materials and Methods: Of the 1,520 clients who had their viral load assayed, we reviewed their CD4 count at baseline and at time of viral load assay. We also reviewed the age, gender distribution and the discordancy rate.
Results: We found a discordant immune response to antiretroviral therapy in 165 (10.9% of 1520) clients whose viral load were assayed. Univariate analysis showed that low CD4 counts less than 100cells/ml at baseline, less than 50% gain in CD4 count more than one year after commencement of antiretroviral therapy and time on antiretroviral therapy more than three years, with P-value of 0.035 were associated with immunological failure.
Conclusion: We therefore concluded that approximately 11 per cent of our clients with immune response failure had successful viral suppression.
Materials and Methods: Of the 1,520 clients who had their viral load assayed, we reviewed their CD4 count at baseline and at time of viral load assay. We also reviewed the age, gender distribution and the discordancy rate.
Results: We found a discordant immune response to antiretroviral therapy in 165 (10.9% of 1520) clients whose viral load were assayed. Univariate analysis showed that low CD4 counts less than 100cells/ml at baseline, less than 50% gain in CD4 count more than one year after commencement of antiretroviral therapy and time on antiretroviral therapy more than three years, with P-value of 0.035 were associated with immunological failure.
Conclusion: We therefore concluded that approximately 11 per cent of our clients with immune response failure had successful viral suppression.
