China has an ethnically diverse population. Genetic differences may contribute to disparities in the efficiency of HIV transmission. To further characterize this risk, we examined the HIV-related genetic diversity in the predominant Han Chinese and in six minority groups. We searched for the delta32-CCR5 mutation, a common cause of relative HIV resistance in the white population. In addition, CCR5 receptor expression was measured. Blood samples were obtained from adults belonging to the Han, Meng, Zang, Weiwuer, Zhuang, Yi, and Dai ethnic groups. Polymerase chain reaction analysis was performed on genomic DNA samples. Surface expression of CCR5 on peripheral blood mononuclear cells was measured by flow cytometry. One-way ANOVA was used to determine mean statistical differences. Samples from 10 members of each minority were examined. A delta32-CCR5 heterozygote phenotype was detected in one Weiwuer subject, but no mutations were found in the other 69 subjects studied. The mean CCR5 expression of cells harvested from the Dai minority was greater than that of cells from all other minorities studied, for both CD3+CCR5+ and CD4+CCR5+ sets (p < .01, one-way ANOVA). The delta32-CCR5 mutation seems to be rare in most Han Chinese and the minority populations studied. CCR5 expression appears to be greater in the Dai minority than in the other minorities investigated. The mechanism for this increased expression requires further study.

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Ferroptosis is a non-apoptotic form of cell death driven by iron-dependent lipid peroxidation. Recent evidence indicates that inhibiting ferroptosis could alleviate cerebral ischemia/reperfusion (CIR) injury. γ-glutamylcysteine (γ-GC), an intermediate of glutathione (GSH) synthesis, can upregulate GSH in brains. GSH is the co-factor of glutathione peroxidase 4 (GPX4), which is the negative regulator of ferroptosis. In this study, we explored the effect of γ-GC on CIR-induced neuronal ferroptosis and brain injury. We found that γ-GC significantly reduced the volume of cerebral infarction, decreased the loss of neurons and alleviated neurological dysfunction induced by CIR in rats. Further observation showed that γ-GC inhibited the CIR-caused rupture of the neuronal mitochondrial outer membrane and the disappearance of cristae, and decreased Fe2+ deposition and lipid peroxidation in rat cerebral cortices. Meanwhile, γ-GC altered the expression of some ferroptosis-related proteins in rat brains. Mechanistically, γ-GC increased the expression of GSH synthetase (GSS) for GSH synthesis via protein kinase C (PKC)ε-mediated activation of nuclear factor erythroid 2-related factor (Nrf2). Our findings suggest that γ-GC not only serves as a raw material but also increases the GSS expression for GSH synthesis against CIR-induced lipid peroxidation and ferroptosis. Our study strongly suggests that γ-GC has potential for treating CIR injury.