Na Zhu

Objectives: Accumulating evidence has confirmed the efficacy and safety of COVID-19 vaccines against SARS-CoV-2 infection. However, the effect of COVID-19 vaccination on immuno-virological parameters in people with HIV (PWH) is uncertain. Methods: A total of 372 PWH treated at Beijing Ditan Hospital were included. Unvaccinated PWH were matched 1:3 with vaccinated PWH using a propensity score matching algorithm. Differences in immuno-virological markers between the matched groups were analyzed. The Wilcoxon signed rank test was used to test for changes in CD4 and CD8 counts and HIV viral load over two months around vaccination. In addition, we investigated the long-term changes in HIV-related markers in different vaccination dose groups and in the entire vaccinated population. Results: Vaccinated PWH had a higher CD4/CD8 ratio (0.64 (0.49, 0.78) vs. 0.80 (0.56, 1.03), p = 0.037) than unvaccinated PWH within a two-month window after the third dose. There were 337 PWH who received COVID-19 vaccination, and 73.9% (n = 249) received three doses of vaccine. We observed a transient increase in CD4 count and CD4/CD8 ratio within a two-month window after vaccination, especially after the second dose (CD4 count: 583.5 (428.5, 706.8) vs. 618.0 (452.0, 744.0), p = 0.018; CD4/CD8 ratio: 0.70 (0.50, 0.91) vs. 0.71 (0.53, 0.96), p < 0.001)) and the third dose (CD4 count: 575.5 (435.5, 717.0) vs. 577.5 (440.8, 754.8), p = 0.001; CD4/CD8 ratio: 0.70 (0.52, 0.93) vs. 0.79 (0.53, 1.00), p < 0.001)). Recent CD4 counts and CD4/CD8 ratios were lower than after COVID-19 but remained higher than before COVID-19 in vaccinated PWH. In addition, COVID-19 vaccination had no negative effect on HIV viral load. Conclusions: A transient increase in CD4 count and CD4/CD8 ratio was observed after COVID-19 vaccination. However, the enhanced cellular immune response induced by vaccination may diminish over time and return to normal levels. There is no adverse effect of vaccination on HIV viral load.

Background and Objectives: The relationship between circulating retinol-binding protein 4 (RBP4) levels and hepatitis C virus (HCV) infection remains unclear. This study aims to systematically assess RBP4 expression in patients with HCV and its correlation with disease severity. Materials and Methods: We searched the Embase, PubMed, and Cochrane databases for relevant studies up to 1 January 2024. This study was registered on PROSPERO (CRD42023489051). Results: Our analysis included eight studies with 2612 participants (1152 controls and 1282 patients with HCV). Overall, RBP4 levels did not significantly differ between patients with HCV and controls (SMD: −0.36; 95% CI: −0.94, 0.23; p = 0.23). However, in a subgroup of Asian subjects, patients with HCV showed significantly lower RBP4 levels (SMD: −0.40; 95% CI: −0.49, −0.31; p = 0.10). Additionally, a negative correlation between RBP4 levels and disease severity was observed across all studied populations. Conclusions: RBP4 levels may vary due to HCV genotype, ethnicity, and environmental factors. In the context of HCV infection, RBP4 levels appear to reflect the severity of disease progression. Our findings indicate that RBP4 could serve as a biomarker for HCV disease progression. Further research is needed to elucidate the complex mechanisms of RBP4 in HCV infection.

The C6orf120 gene is a novel gene whose function has not been fully defined. Previous studies have associated it with various liver pathologies, but its specific role in hepatocellular carcinoma (LIHC) remains unclear. This study aimed to investigate the diagnostic and prognostic value of C6orf120 in LIHC, as well as its potential biological functions. In this preliminary research, we utilized data from various databases and bioinformatics tools, including TCGA, GEO, TIMER2, HPA, GEPIA, Linkeomics, Metascape, CIBERSORT, TargetScan, DIANA-microT, RNAinter, and ENCORI, to analyze the expression patterns and mechanisms of C6orf120 in LIHC. Our bioinformatics analysis revealed that C6orf120 is upregulated in LIHC and may serve as a diagnostic and prognostic biomarker. The aberrant expression of C6orf120 in LIHC was further supported by clinical samples and cell lines. In vitro experiments demonstrated that the knockdown of C6orf120 in HepG2 cells significantly reduced migration capacity without affecting proliferation. Additionally, the downregulation of C6orf120 in LIHC cells appeared to inhibit endothelial cell migration and angiogenesis, which are critical in tumorigenesis and development. In conclusion, our findings suggest that C6orf120 could serve as a novel diagnostic and prognostic biomarker for LIHC and is expected to be a prognostic marker and a potential therapeutic target in the clinical management of LIHC.