Department of Microbiology and Immunology
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Browsing Department of Microbiology and Immunology by Author "Amanya, Sharon Bright"
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Item A cross-sectional study of stress and its sources among health professional students at Makerere University, Uganda(Wiley, 2017) Amanya, Sharon Bright; Nakitende, Joyce; Ngabirano, Tom DenisAim: To assess prevalence of stress and its sources among undergraduate health professional students at Makerere University. Design: This was a descriptive cross-sectional study using quantitative methods of data collection. Methods: The study was conducted among 258 undergraduate health professional students (Medical, Dental and, Nursing students) at Makerere University. From each programme, students were recruited proportionately, while being selected conveniently from each year of study. Stress was measured using the General Health Questionnaire 12 and stressors assessed using a questionnaire developed from literature. After obtaining ethics approval, data were collected from consenting students. Data collected were analysed using SPSS statistical program. Results: The prevalence of stress was found to be 57.4% and stressors of academic and psychosocial origin were most frequently reported. The top stressors included; academic curriculum (38%), dissatisfaction with class lectures (30.9%), long distance walk (29.5%), lack of time for recreation (28.9%), performance in examination (28.3%), lack of special guidance from faculty (26.7%) and high parental expectations (26.7%).Item Variations in Trim5α and Cyclophilin A genes among HIV‑1 elite controllers and non controllers in Uganda: a laboratory‑based cross‑sectional study(2020) Amanya, Sharon Bright; Nyiro, Brian; Waswa, Francis; Obura, Bonniface; Nakaziba, Rebecca; Nabulime, Eva; Katabazi, Ashaba Fred; Nabatanzi, Rose; Bayiyana, Alice; Mboowa, Gerald; Kayongo, Alex; Wayengera, Misaki; Obondo, J. SandeBackground: Tripartite Motif Containing 5 alpha (TRIM5α), a restriction factor produced ubiquitously in cells and tissues of the body plays an important role in the immune response against HIV. TRIM5α targets the HIV capsid for proteosomal destruction. Cyclophilin A, an intracellular protein has also been reported to influence HIV infectivity in a cell-specific manner. Accordingly, variations in TRIM5α and Cyclophilin A genes have been documented to influence HIV-1 disease progression. However, these variations have not been documented among Elite controllers in Uganda and whether they play a role in viral suppression remains largely undocumented. Our study focused on identifying the variations in TRIM5α and Cyclophilin A genes among HIV-1 Elite controllers and non-controllers in Uganda. Results: From the sequence analysis, the rs10838525 G > A mutation in exon 2 of TRIM5α was only found among elite controllers (30%) while the rs3824949 in the 5′UTR was seen among 25% of the non-controllers. In the Cyclophilin A promoter, rs6850 was seen among 62.5% of the non-controllers and only among 10% elite controllers. Furthermore, rs17860048 in the Cyclophillin A promoter was predominantly seen among elite controllers (30%) and 12.5% noncontrollers. From gene expression analysis, we noted that the respective genes were generally elevated among elite controllers, however, this difference was not statistically significant (TRIM5α p = 0.6095; Cyclophilin A p = 0.6389). Conclusion: Variations in TRIM5α and Cyclophillin A promoter may influence HIV viral suppression. The rs10838525 SNP in TRIM5α may contribute to viral suppression among HIV-1 elite controllers. The rs6850 in the cyclophillin A gene may be responsible for HIV-1 rapid progression among HIV-1 non-controllers. These SNPs should be investigated mechanistically to determine their precise role in HIV-1 viral suppression.