African swine fever virus (ASFV) is the causative agent of the epidemic of African swine fever (ASF), with virulent strains having a mortality rate of up to 100% and presenting devastating impacts on animal farming. Since ASF was first reported in China in 2018, ASFV still exists and poses a potential threat to the current pig industry. Low-virulence and genotype I strains of ASFV have been reported in China, and the prevention and control of ASF is more complicated. Insufficient understanding of the interaction of ASFV with the host immune system hinders vaccine development. Physical barriers, nonspecific immune response and acquired immunity are the three barriers of the host against infection. To escape the innate immune response, ASFV invades monocytes/macrophages and dendritic cells, thereby inhibiting IFN expression, regulating cytokine expression and the body’s inflammatory response process. Meanwhile, in order to evade the adaptive immune response, ASFV inhibits antigen presentation, induces the production of non-neutralizing antibodies, and inhibits apoptosis. Recently, significant advances have been achieved in vaccine development around the world. Live attenuated vaccines (LAVs) based on artificially deleting specific virulence genes can achieve 100% homologous protection and partial heterologous protection. The key of subunit vaccines is identifying the combination of antigens that can effectively provide protection and selecting carriers that can effectively deliver the antigens. In this review, we introduce the epidemic trend of ASF and the impact on the pig industry, analyze the interaction mechanism between ASFV and the body’s immune system, and compare the current status of potential vaccines in order to provide a reference for the development of effective ASF vaccines.

The host cell cytoskeleton plays a critical role in the SARS-CoV-2 life cycle, though the underlying mechanisms remain poorly understood. This study investigates the interaction between the SARS-CoV-2 spike (S) protein and the cytoskeleton-associated ezrin-radixin-moesin (ERM) proteins through biochemical and structural characterization. A previously unidentified ERM-binding motif on the SARS-CoV-2 S protein is identified, revealing that S-ERM interactions are specifically conserved among highly pathogenic coronaviruses, including SARS-CoV, MERS-CoV, and SARS-CoV-2. Functionally, these interactions facilitate S packaging into virions by directing it to assembly sites, utilizing ERM’s affinity for negatively curved membranes, akin to its role in cell surface protrusions. Silencing ERM expression significantly reduces SARS-CoV-2 titer, highlighting its essential role in viral propagation. Additionally, leveraging the established role of COPI-mediated trafficking in S localization, a compound is developed to disrupt S-COPI binding, promoting S secretion to the cell surface and effectively reducing viral titers. Our findings revealed a critical host–pathogen interaction that drives S incorporation into virions and identified ERM proteins as key facilitators of coronavirus assembly. Furthermore, our study suggests an antiviral strategy by targeting the S-COPI trafficking pathway. These insights advanced our understanding of coronavirus–host interactions and provided a potential therapeutic approach against SARS-CoV-2 and other highly pathogenic coronaviruses.

To investigate the relationship between posterior vitreous detachment (PVD) status and fibrovascular membrane (FVM) angio-fibrotic transformation following anti-VEGF therapy in advanced proliferative diabetic retinopathy (PDR), and their combined impact on disease progression and visual outcomes. This prospective real-world study enrolled 165 treatment-naïve PDR patients with vitreous hemorrhage (VH) and FVM who received intravitreal anti-VEGF injection followed by panretinal photocoagulation(PRP) when possible. PVD status and FVM characteristics were monitored during a median follow-up of 13.0 months. Cox proportional hazards and Kaplan-Meier analyses evaluated factors influencing visual prognosis and timing of surgical intervention. FVM fibrosis occurred in 43% of patients, with distinct PVD-dependent patterns: predominantly in complete PVD cases, moderately in partial PVD, and rarely without PVD. Multivariate analysis identified macular involvement as the strongest risk factor for poor visual outcomes (HR=3.65), while PVD (HR=0.37) and FVM fibrosis (HR=0.023) were strongly protective. Patients with both PVD and FVM fibrosis maintained stable vision longest (median 28.5 months) and demonstrated significantly longer surgery-free survival (28.3 months) compared to those without either condition (3.2 months, p<0.0001), who frequently presented with vitreoschisis and recurrent VH disproportionate to visible FVM grade. PVD status critically determines the clinical manifestation and prognosis of post-anti-VEGF FVM fibrosis in PDR. This PVD-dependent pattern challenges the conventional view that FVM fibrosis inevitably leads to “Crunch syndrome” and creates a risk stratification framework that can guide individualized surgical timing decisions, potentially improving functional outcomes in advanced PDR.