包含5α的三方基序（TRIM5α），在机体的细胞和组织中普遍产生的限制因子在抗HIV的免疫应答中起重要作用。TRIM5α靶向HIV衣壳进行蛋白酶体破坏。亲环蛋白A,细胞内蛋白也被报道以细胞特异性方式影响HIV感染性。因此，TRIM5α和亲环蛋白A基因的变异已被证明会影响HIV-1疾病的进展。然而,这些变异尚未在乌干达的精英控制者中记录,它们是否在病毒抑制中发挥作用仍未被记录.我们的研究重点是确定乌干达HIV-1精英控制者和非控制者中TRIM5α和亲环蛋白A基因的变化。
从序列分析来看，TRIM5α外显子2中的rs10838525G>A突变仅在精英控制者中发现（30％），而5'UTR中的rs3824949在25％的非控制者中发现。在亲环蛋白A启动子中,在62.5%的非控制者中看到rs6850，只有10%的精英控制者。此外，cyclophillinA启动子中的rs17860048主要出现在精英控制者（30％）和12.5％的非控制者中。从基因表达分析，我们注意到，精英控制者各自的基因普遍升高，然而,差异无统计学意义(TRIM5αp=0.6095;亲环蛋白Ap=0.6389)。
TRIM5α和CyclophillinA启动子的变异可能影响HIV病毒抑制。TRIM5α中的rs10838525SNP可能有助于HIV-1精英控制者中的病毒抑制。环菲青霉素A基因中的rs6850可能是HIV-1非控制者中HIV-1快速发展的原因。应该对这些SNP进行机械研究，以确定它们在HIV-1病毒抑制中的确切作用。
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.
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% non-controllers. 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).
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.
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