Epstein–Barr virus (EBV) is the first human oncogenic virus to be identified, which evades the body's immune surveillance through multiple mechanisms that allow long-term latent infection. Under certain pathological conditions, EBVs undergo a transition from the latent phase to the lytic phase and cause targeted dysregulation of the host immune system, leading to the development of EBV-related diseases. Therefore, an in-depth understanding of the mechanism of developing an immune response to EBV and the evasion of immune recognition by EBV is important for the understanding of the pathogenesis of EBV, which is of great significance for finding strategies to prevent EBV infection, and developing a therapy to treat EBV-associated diseases. In this review, we will discuss the molecular mechanisms of host immunological responses to EBV infection and the mechanisms of EBV-mediated immune evasion during chronic active infection.

Neonatal medicine advancements have significantly improved preterm infants’ survival rates, yet optimizing their neurodevelopmental outcomes, is challenging. A central factor in these challenges is oxidative stress (OS), arising from an imbalance between free radicals (FRs) production and antioxidant defense mechanisms. In preterm infants, OS is particularly detrimental due to their underdeveloped antioxidant systems, high brain metabolic demands, immature blood-brain barrier (BBB), and increased vulnerability to inflammation and hypoxia. This review focuses on the multifaceted aspects of OS concerning preterm brain injury. It examines developmental, physiological, pathological, and environmental factors contributing to preterm infants’ susceptibility to OS. In addition, the review discusses various pathophysiological mechanisms of preterm brain injury and proposes comprehensive solutions, including the use of antioxidants, nutritional support with a focus on breast milk, tailored oxygen therapy, and the importance of reducing oxidative stressors in the neonatal intensive care unit (NICU) including effective pain management and environmental modifications. The review emphasizes the need for future research focused on developing integrated and individualized treatment approaches for brain injury in preterm infants. Specifically, a deeper understanding and effective management of OS is crucial for enhancing long-term prognoses in this vulnerable group.

Background: Hypoxic-ischemic injury of neurons is a pathological process observed in several neurological conditions, including ischemic stroke and neonatal hypoxic-ischemic brain injury (HIBI). An optimal treatment strategy for these conditions remains elusive. The present study delved deeper into the molecular alterations occurring during the injury process in order to identify potential therapeutic targets. Methods: Oxygen-glucose deprivation/reperfusion (OGD/R) serves as an established in vitro model for the simulation of HIBI. This study utilized RNA sequencing to analyze rat primary hippocampal neurons that were subjected to either 0.5 or 2 h of OGD, followed by 0, 9, or 18 h of reperfusion. Differential expression analysis was conducted to identify genes dysregulated during OGD/R. Time-series analysis was used to identify genes exhibiting similar expression patterns over time. Additionally, functional enrichment analysis was conducted to explore their biological functions, and protein-protein interaction (PPI) network analyses were performed to identify hub genes. Quantitative real-time polymerase chain reaction (qRT-PCR) was used for validation of hub-gene expression. Results: The study included a total of 24 samples. Analysis revealed distinct transcriptomic alterations after OGD/R processes, with significant dysregulation of genes such as Txnip, Btg2, Egr1 and Egr2. In the OGD process, 76 genes, in two identified clusters, showed a consistent increase in expression; functional analysis showed involvement of inflammatory responses and signaling pathways like tumor necrosis factor (TNF), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and interleukin 17 (IL-17). PPI network analysis suggested that Ccl2, Jun, Cxcl1, Ptprc, and Atf3 were potential hub genes. In the reperfusion process, 274 genes, in three clusters, showed initial upregulation followed by downregulation; functional analysis suggested association with apoptotic processes and neuronal death regulation. PPI network analysis identified Esr1, Igf-1, Edn1, Hmox1, Serpine1, and Spp1 as key hub genes. qRT-PCR validated these trends. Conclusions: The present study provides a comprehensive transcriptomic profile of an in vitro OGD/R process. Key hub genes and pathways were identified, offering potential targets for neuroprotection after hypoxic ischemia.

Objective: To study the effect of intestinal microecology on postnatal weight gain of very preterm infants in neonatal intensive care unit (NICU). Methods: Very preterm infants who met the inclusion criteria were enrolled. The subjects were divided into the extrauterine growth retardation (EUGR) group(defined as a body weight less than the 10th percentile of the corresponding gestational age or a weight loss between birth and a given time of > 2SD were considered EUGR) and normal growth group, and the growth was evaluated at 2 and 4 weeks after birth. Meanwhile, the stool samples were taken to perform16S ribosomal RNA (rRNA) high -throughput 16S rRNA sequencing of the intestinal microflora was performed on stool samples. Results: A total of 22 infants were included. There was no significant difference in the alpha diversity indexes indices between the two groups at 2 weeks or 4 weeks after birth. The beta diversity analysis showed that the two groups had similar principal components of the intestinal microflora were similar between the two groups. Linear discriminant analysis (LDA) effect size (LEfSe) showed that 2 weeks after birth, the bacteria with an absolute LDA score (log10) higher than 4 included Streptococcaceae, Streptococcus, Bacteroidetes, Bacteroidales and Stenotrophomonas in the EUGR group and Enterococcaceae and Enterococcus in the control group. At the 4th week after birth, the bacteria with an absolute LDA score (log10) higher than 3 in the EUGR group includedwere Clostriaceae, Eubacteriaceae and Eubacterium. TheBy comparing the composition of the microbial community composition comparison showed, significant differences were found in the principal components of Enterococcus and Streptococcus on the family and genus levels at 2 weeks after birth. No Bifidobacterium was found in either group at 4 weeks after birth. Conclusion: Intestinal microecology is different between infants with EUGR and those with normal growth. The diversity and richness of the intestinal microflora in preterm infants at the NICU are significantly insufficient and change dynamically with time, and the establishment of intestinal homeostasis is obviously delayed.

This study aimed to describe the growth pattern in preterm infants and identify factors influencing catch-up growth. A total of 288 preterm infants were divided into groups based on the degree of prematurity, sex, and size for gestational age. Growth in head circumference, length, weight-for-length, and weight was compared between groups at corrected age of 0, 3, 6, 9, 12, 18, and 24 months. Logistic regression analysis was conducted to determine risk factors for catch-up growth. At a corrected age of 24 months, the proportions of preterm infants with z-scores less than −2 for head circumference, length, weight-for-length, and weight were less than the expected 2.3% at 0.9%, 1.7%, 2.1%, and 1.7%, respectively. The head circumference, length, weight-for-length, and weight z-scores at corrected ages of 24 months were lower in the small for gestational age (SGA) group than in the non-SGA group ( P < .05). The weight-for-length z-scores were higher in the late preterm birth infants than in the very preterm birth infants at a corrected age of 24 months ( P < .05). At a corrected age 24 months, the proportion of male with weight z-scores <−2 was lower than that of female ( P < .05). The differences in proportion of the z-scores (head circumference, length, weight-for-length, and weight) <−2 at a corrected age of 24 months among different gestational age groups and intrauterine growth status groups were not statistically significant ( P > .05). We found that the factors influencing catch-up growth in preterm infants varied at different corrected age stages, and the impact of factors during hospitalization gradually diminished as the infants grew.