Electromagnetic Interference Shielding Films: Structure Design and Prospects.

The popularity of portable and wearable flexible electronic devices, coupled with the rapid advancements in military field, requires electromagnetic interference (EMI) shielding materials with lightweight, thin, and flexible characteristics, which are incomparable for traditional EMI shielding materials. The film materials can fulfill the above requirements, making them among the most promising EMI shielding materials for next-generation electronic devices. Meticulously controlling structure of composite film materials while optimizing the electromagnetic parameters of the constructed components can effectively dissipate and transform electromagnetic wave energy. Herein, the review systematically outlines high-performance EMI shielding composite films through structural design strategies, including homogeneous structure, layered structure, and porous structure. The attenuation mechanism of EMI shielding materials and the evaluation (Schelkunoff theory and calculation theory) of EMI shielding performance are introduced in detail. Moreover, the effect of structure attributes and electromagnetic properties of composite films on the EMI shielding performance is analyzed, while summarizing design criteria and elucidating the relevant EMI shielding mechanism. Finally, the future challenges and potential application prospects of EMI shielding composite films are prospected. This review provides crucial guidance for the construction of advanced EMI shielding films tailored for highly customized and personalized electronic devices in the future.

The I7L protein of African swine fever virus is involved in viral pathogenicity by antagonizing the IFN-γ-triggered JAK-STAT signaling pathway through inhibiting the phosphorylation of STAT1.

Cell-passage-adapted strains of African swine fever virus (ASFV) typically exhibit substantial genomic alterations and attenuated virulence in pigs. We have indicated that the human embryonic kidney (HEK293T) cells-adapted ASFV strain underwent genetic alterations and the I7L gene in the right variable region was deleted compared with the ASFV HLJ/2018 strain (ASFV-WT). A recent study has revealed that the deletion of the I7L-I11L genes results in attenuation of virulent ASFV in vivo, but the underlying mechanism remains largely unknown. Therefore, we hypothesized that the deletion of the I7L gene may be related to the pathogenicity of ASFV in pigs. We generated the I7L gene-deleted ASFV mutant (ASFV-ΔI7L) and found that the I7L gene deletion does not influence the replication of ASFV in primary porcine alveolar macrophages (PAMs). Using transcriptome sequencing analysis, we identified that the differentially expressed genes in the PAMs infected with ASFV-ΔI7L were mainly involved in antiviral immune responses induced by interferon gamma (IFN-γ) compared with those in the ASFV-WT-infected PAMs. Meanwhile, we further confirmed that the I7L protein (pI7L) suppressed the IFN-γ-triggered JAK-STAT signaling pathway. Mechanistically, pI7L interacts with STAT1 and inhibits its phosphorylation and homodimerization, which depends on the tyrosine at position 98 (Y98) of pI7L, thereby preventing the nuclear translocation of STAT1 and leading to the decreased production of IFN-γ-stimulated genes. Importantly, ASFV-ΔI7L exhibited reduced replication and virulence compared with ASFV-WT in pigs, likely due to the increased production of IFN-γ-stimulated genes, indicating that pI7L is involved in the virulence of ASFV. Taken together, our findings demonstrate that pI7L is associated with pathogenicity and antagonizes the IFN-γ-triggered JAK-STAT signaling pathway via inhibiting the phosphorylation and homodimerization of STAT1 depending on the Y98 residue of pI7L and the Src homology 2 domain of STAT1, which provides more information for understanding the immunoevasion strategies and designing the live attenuated vaccines against ASFV infection.

Colorimetric screening model for identification of menaquinone-7 (MK-7) producing strains.

In this study, a novel colorimetric screening method for identifying menaquinone-7 (MK-7) producing strains was established using potassium permanganate. To our knowledge, this method represents the first direct screening methodology for the identification of MK-7 producing strains. Utilizing this screening method, a new MK-7 producing strain, Bacillus subtilis GSA-184, was identified from the soil of the Tibetan Plateau. Under the optimized fermentation medium (50 g/L glycerol, 30 g/L yeast extract powder, 100 g/L soybean peptone, 1 g/L KH2PO4, and 1 g/L MnSO4), the production of MK-7 was increased to 25.7 mg/L. Additionally, the maximum production of MK-7 reached 36.46 mg/L after 48 h in a 5-L fermenter. Supplementary Information: The online version contains supplementary material available at 10.1007/s13205-024-04097-1.

African swine fever virus modulates the endoplasmic reticulum stress-ATF6-calcium axis to facilitate viral replication.

African swine fever (ASF), caused by African swine fever virus (ASFV), is a devastating infectious disease of domestic pigs and wild boar, which threatens the global pig industry. Endoplasmic reticulum (ER) is a multifunctional signaling organelle in eukaryotic cells that is involved in protein synthesis, processing, posttranslational modification and quality control. As intracellular parasitic organisms, viruses have evolved several strategies to modulate ER functions to favor their life cycles. We have previously demonstrated that the differentially expressed genes associated with unfolded protein response (UPR), which represents a response to ER stress, are significantly enriched upon ASFV infection. However, the correlation between the ER stress or UPR and ASFV replication has not been illuminated yet. Here, we demonstrated that ASFV infection induces ER stress both in target cells and in vivo, and subsequently activates the activating transcription factor 6 (ATF6) branch of the UPR to facilitate viral replication. Mechanistically, ASFV infection disrupts intracellular calcium (Ca2+) homeostasis, while the ATF6 pathway facilitates ASFV replication by increasing the cytoplasmic Ca2+ level. More specifically, we demonstrated that ASFV infection triggers ER-dependent Ca2+ release via the inositol triphosphate receptor (IP3R) channel. Notably, we showed that the ASFV B117L protein plays crucial roles in ER stress and the downstream activation of the ATF6 branch, as well as the disruption of Ca2+ homeostasis. Taken together, our findings reveal for the first time that ASFV modulates the ER stress-ATF6-Ca2+ axis to facilitate viral replication, which provides novel insights into the development of antiviral strategies for ASFV.

Advanced Functional Electromagnetic Shielding Materials: A Review Based on Micro-Nano Structure Interface Control of Biomass Cell Walls.

Research efforts on electromagnetic interference (EMI) shielding materials have begun to converge on green and sustainable biomass materials. These materials offer numerous advantages such as being lightweight, porous, and hierarchical. Due to their porous nature, interfacial compatibility, and electrical conductivity, biomass materials hold significant potential as EMI shielding materials. Despite concerted efforts on the EMI shielding of biomass materials have been reported, this research area is still relatively new compared to traditional EMI shielding materials. In particular, a more comprehensive study and summary of the factors influencing biomass EMI shielding materials including the pore structure adjustment, preparation process, and micro-control would be valuable. The preparation methods and characteristics of wood, bamboo, cellulose and lignin in EMI shielding field are critically discussed in this paper, and similar biomass EMI materials are summarized and analyzed. The composite methods and fillers of various biomass materials were reviewed. this paper also highlights the mechanism of EMI shielding as well as existing prospects and challenges for development trends in this field.

Immune responses induced by a recombinant C-strain of classical swine fever virus expressing the F317L protein of African swine fever virus.

African swine fever (ASF), a highly infectious and devastating disease affecting both domestic pigs and wild boars, owes its etiology to African swine fever virus (ASFV). ASFV encodes more than 165 proteins. However, novel immunogenic proteins remain unknown. This study aimed to determine the antigenicity of the F317L protein (pF317L) of ASFV. The results revealed that pF317L was able to react with convalescent pig sera, indicating that pF317L could be a candidate antigen. The antigenic potential of pF317L expressed by rHCLV-F317L, a recombinant virus in the backbone of C-strain (a lapinized live attenuated classical swine fever virus) was further investigated in rabbits and pigs. The results revealed that antibodies and cell-mediated immune responses against pF317L were induced in either rabbits or pigs inoculated with rHCLV-F317L. Importantly, anti-pF317L antibodies from rabbits or pigs immunized with rHCLV-F317L significantly inhibited ASFV replication in vitro. In conclusion, pF317L demonstrates favorable immunogenic properties, positioning it as a promising candidate for the development of protective antigens in the ongoing endeavor to formulate efficacious ASF vaccine strategies.

Crosstalk between Dysfunctional Mitochondria and Proinflammatory Responses during Viral Infections.

Mitochondria play pivotal roles in sustaining various biological functions including energy metabolism, cellular signaling transduction, and innate immune responses. Viruses exploit cellular metabolic synthesis to facilitate viral replication, potentially disrupting mitochondrial functions and subsequently eliciting a cascade of proinflammatory responses in host cells. Additionally, the disruption of mitochondrial membranes is involved in immune regulation. During viral infections, mitochondria orchestrate innate immune responses through the generation of reactive oxygen species (ROS) and the release of mitochondrial DNA, which serves as an effective defense mechanism against virus invasion. The targeting of mitochondrial damage may represent a novel approach to antiviral intervention. This review summarizes the regulatory mechanism underlying proinflammatory response induced by mitochondrial damage during viral infections, providing new insights for antiviral strategies.

A recombinant pseudorabies virus surface - displaying the classical swine fever E2 protein induces specific antibodies rapidly.

Pseudorabies virus (PRV) and classical swine fever virus (CSFV) are both economically important pathogens threatening the pig industry in many countries. The triple-gene-deleted variant of PRV, herein referred to as rPRVTJ-delgE/gI/TK, has exhibited pronounced efficacy and safety profiles. This underscores its viability as a prospective vaccine vector. However, the generation of specific anti-E2 antibodies necessitates elevated immunization doses and extended durations when the extracellular domain of the E2 protein of CSFV is secreted via the recombinant rPRVTJ-delgE/gI/TK vector. To enhance the presentation of exogenous antigens by antigen-presenting cells (APCs), we engineered the E2 protein expressed on the surface of PRV particles in this study. The recombinant virus expressing the E2 protein with a heterogonous transmembrane domain was generated in the backbone of rPRVTJ-delgE/gI/TK and designated as rPRVTJ-UL44-E2. The E2 gene was fused to the 3' terminus of the UL44 gene utilizing P2A, a self-cleaving peptide sequence. The electron microscopy showed that the E2 protein was anchored on the surface of the viral particles of rPRVTJ-delgE/gI/TK-E2. The insertion of the E2 gene did not alter the native biological characteristics of the viral vector. Rabbits immunized with 107 median tissue culture infective doses (TCID50) of rPRVTJ-UL44-E2 exhibited a rapid seroconversion to anti-E2 specific antibodies within 7 days post-immunization (dpi). All the rabbits immunized with the rPRVTJ-UL44-E2 had generated antibodies specific to E2 prior to the administration of the booster immunization. However, the immunized rabbits were not protected from the CSFV C-strain challenge. Nevertheless, this strategy has notably achieved rapid induction of E2-specific non-neutralizing antibodies. These findings provide insights that the design of rPRVTJ-UL44-E2 requires optimization, thereby indicating a promising avenue for augmenting vaccine-induced immune responses.

GluN2A: A Promising Target for Developing Novel Antidepressants.

BACKGROUND: Depression is a heterogeneous disorder with high morbidity and disability rates that poses serious problems regarding mental health care. It is now well established that N-methyl D-aspartate receptor (NMDAR) modulators are being increasingly explored as potential therapeutic options for treating depression, although relatively little is known about their mechanisms of action. NMDARs are glutamate-gated ion channels that are ubiquitously expressed in the central nervous system (CNS), and they have been shown to play key roles in excitatory synaptic transmission. GluN2A, the predominant Glu2N subunit of functional NMDARs in neurons, is involved in various physiological processes in the CNS and is associated with diseases such as anxiety, depression, and schizophrenia. However, the role of GluN2A in the pathophysiology of depression has not yet been elucidated. METHODS: We reviewed several past studies to better understand the function of GluN2A in depression. Additionally, we also summarized the pathogenesis of depression based on the regulation of GluN2A expression, particularly its interaction with neuroinflammation and neurogenesis, which has received considerable critical attention and is highly implicated in the onset of depression. RESULTS: These evidence suggests that GluN2A overexpression impairs structural and functional synaptic plasticity, which contributes to the development of depression. Consequently, this knowledge is vital for the development of selective antagonists targeting GluN2A subunits using pharmacological and molecular methods. CONCLUSIONS: Specific inhibition of the GluN2A NMDAR subunit is resistant to chronic stress-induced depressive-like behaviors, making them promising targets for the development of novel antidepressants.

Electrochemical Dehydrogenative [3 + 2]/[5 + 2] Annulation of N-Arylacrylamides with γ,σ-Unsaturated Malonates via Direct C(sp3)-H/C(sp2)-H Functionalization.

Herein, we introduce an electrochemical dehydrogenative [3 + 2]/[5 + 2] annulation of easily available N-arylacrylamides with γ,σ-unsaturated malonates through C(sp3)-H/C(sp2)-H functionalization. The employment of inexpensive ferrocene as the redox catalyst allows access to diverse benzo[b]azepin-2-ones in moderate to excellent yields without stoichiometric oxidants. This protocol features broad substrate scope and excellent selectivity, and mechanistic studies indicated that the reaction proceeded through the oxidation of a C(sp3)-H bond to generate an alkyl radical, radical addition across the C═C bond, [3 + 2]/[5 + 2] annulations, and C(sp2)-H functionalization cascades.

Viral replication organelles: the highly complex and programmed replication machinery.

Viral infections usually induce the rearrangement of cellular cytoskeletal proteins and organelle membrane structures, thus creating independent compartments [termed replication organelles (ROs)] to facilitate viral genome replication. Within the ROs, viral replicases, including polymerases, helicases, and ligases, play functional roles during viral replication. These viral replicases are pivotal in the virus life cycle, and numerous studies have demonstrated that the viral replicases could be the potential targets for drugs development. Here, we summarize primarily the key replicases within viral ROs and emphasize the advancements of antiviral drugs targeting crucial viral replicases, providing novel insights into the future development of antiviral strategies.

The multifaceted roles of selective autophagy receptors in viral infections.

Selective autophagy is a protein clearance mechanism mediated by evolutionarily conserved selective autophagy receptors (SARs), which specifically degrades misfolded, misassembled, or metabolically regulated proteins. SARs help the host to suppress viral infections by degrading viral proteins. However, viruses have evolved sophisticated mechanisms to counteract, evade, or co-opt autophagic processes, thereby facilitating viral replication. Therefore, this review aims to summarize the complex mechanisms of SARs involved in viral infections, specifically focusing on how viruses exploit strategies to regulate selective autophagy. We present an updated understanding of the various critical roles of SARs in viral pathogenesis. Furthermore, newly discovered evasion strategies employed by viruses are discussed and the ubiquitination-autophagy-innate immune regulatory axis is proposed to be a crucial pathway to control viral infections. This review highlights the remarkable flexibility and plasticity of SARs in viral infections.

Structural basis for difunctional mechanism of m-AMSA against African swine fever virus pP1192R.

The African swine fever virus (ASFV) type II topoisomerase (Topo II), pP1192R, is the only known Topo II expressed by mammalian viruses and is essential for ASFV replication in the host cytoplasm. Herein, we report the structures of pP1192R in various enzymatic stages using both X-ray crystallography and single-particle cryo-electron microscopy. Our data structurally define the pP1192R-modulated DNA topology changes. By presenting the A2+-like metal ion at the pre-cleavage site, the pP1192R-DNA-m-AMSA complex structure provides support for the classical two-metal mechanism in Topo II-mediated DNA cleavage and a better explanation for nucleophile formation. The unique inhibitor selectivity of pP1192R and the difunctional mechanism of pP1192R inhibition by m-AMSA highlight the specificity of viral Topo II in the poison binding site. Altogether, this study provides the information applicable to the development of a pP1192R-targeting anti-ASFV strategy.

Cellulose nanofibers-based composite film with broadening MXene layer spacing and rapid moisture separation for humidity sensing and humidity actuators.

Based on the basic idea of expanding the interlayer spacing of MXene, utilizing the effect of gallic acid-modified cellulose nanofibers for rapid moisture separation, the flexible sensing and driving composite film with a perfect balance among humidity signal response and mechanical properties was prepared. Inspired by the stacking of autumn fallen leaves, the cellulose nanofibers-based composite films were formed by self-assembly under vacuum filtration of blending gallic acid-modified cellulose nanofibers with MXene. The enhanced mechanical properties (tensile strength 131.1 MPa, puncture load 0.88 N, tearing strength 165.55 N/mm, and elongation at break 16.14 %), humidity sensing (the stable induced voltage 63.7 mV and response/recovery time 3.2/5.1 s), and humidity driving (154.7° bending angle) properties were observed. The synergistic effect of hydrogen bonds, the "pinning effect" arising from the side chains, and the hierarchical layered microstructure contributed to the enhanced performance. This work exemplifies the application of green natural product for preparing intelligent sensing, wearable devices, and biomimetic robots.

MXene-based fibers: Preparation, applications, and prospects.

With the vigorous development and huge demand for portable wearable devices, wearable electronics based on functional fibers continue to emerge in a wide range of energy storage, motion monitoring, disease prevention, electromagnetic interference (EMI) shielding, etc. MXene, as an emerging two-dimensional inorganic compound, has shown great potential in functional fiber manufacturing and has attracted much research attention due to its own good mechanical properties, high electrical conductivity, excellent electrochemical properties and favorable processability. Herein, this paper reviews recent advances of MXene-based fibers. Speaking to MXene dispersions, the properties of MXene dispersions including dispersion stability, rheological properties and liquid crystalline properties are highlighted. The preparation techniques used to produce MXene-based fibers and application progress regarding MXene-based fibers into supercapacitors, sensors, EMI shielding and Joule heaters are summarized. Challenges and prospects surrounding the development of MXene-based fibers are proposed in future. This review aims to provide processing guidelines for MXene-based fiber manufacturing, thereby achieving more possibilities of MXene-based fibers in advanced applications with a view to injecting more vitality into the field of smart wearables.

Multi-Component and Nanoporous Design toward RuO2-Based Electrocatalyst with Enhanced Performance for Acidic Water Splitting.

Developing electrocatalysts with excellent activity and stability for water splitting in acidic media remains a formidable challenge due to the sluggish kinetics and severe dissolution. As a solution, a multi-component doped RuO2 prepared through a process of dealloying-annealing is presented. The resulting multi-doped RuO2 possesses a nanoporous structure, ensuring a high utilization efficiency of Ru. Furthermore, the dopants can regulate the electronic structure, causing electron aggregation around unsaturated Ru sites, which mitigates Ru dissolution and significantly enhances the catalytic stability/activity. The representative catalyst (FeCoNiCrTi-RuO2) shows an overpotential of 167 mV at 10 mA cm-2 for oxygen evolution reaction (OER) in 0.5 m H2SO4 solution with a Tafel slope of 53.1 mV dec-1, which is among the highest performance reported. Moreover, it remains stable for over 200 h at a current density of 10 mA cm-2. This work presents a promising approach for improving RuO2-based electrocatalysts, offering a crucial advancement for electrochemical water splitting.

Advances in the immunoescape mechanisms exploited by alphaherpesviruses.

Alphaherpesviruses, categorized as viruses with linear DNA composed of two complementary strands, can potentially to induce diseases in both humans and animals as pathogens. Mature viral particles comprise of a core, capsid, tegument, and envelope. While herpesvirus infection can elicit robust immune and inflammatory reactions in the host, its persistence stems from its prolonged interaction with the host, fostering a diverse array of immunoescape mechanisms. In recent years, significant advancements have been achieved in comprehending the immunoescape tactics employed by alphaherpesviruses, including pseudorabies virus (PRV), herpes simplex virus (HSV), varicella-zoster virus (VZV), feline herpesvirus (FeHV), equine herpesvirus (EHV), and caprine herpesvirus type I (CpHV-1). Researchers have unveiled the intricate adaptive mechanisms existing between viruses and their natural hosts. This review endeavors to illuminate the research advancements concerning the immunoescape mechanisms of alphaherpesviruses by delineating the pertinent proteins and genes involved in virus immunity. It aims to furnish valuable insights for further research on related mechanisms and vaccine development, ultimately contributing to virus control and containment efforts.

Prospective cohort studies underscore the association of abnormal glycemic measures with all-cause and cause-specific mortalities.

The role of fasting plasma glucose (FPG), glycated hemoglobin (HbA1c), and triglyceride-glucose index (TyG index) in predicting all-cause and cause-specific mortalities remains elusive. This study included 384,420 adults from the Shanghai cohort and the UK Biobank (UKB) cohort. After multivariable adjustment in the Cox models, FPG ≥7.0 mmol/L or HbA1c ≥ 6.5% increased the risk of all-cause mortality, FPG ≥5.6 mmol/L or HbA1c ≥ 6.5% increased CVD-related mortality, and higher or lower TyG index increased all-cause and CVD-related mortalities in the Shanghai cohort; FPG ≥5.6 mmol/L, HbA1c ≥ 5.7%, TyG index <8.31 or ≥9.08 increased the risks of all-cause, CVD-related, and cancer-related mortalities in the UKB cohort. FPG or HbA1c increased the discrimination of the conventional risk model in predicting all-cause and CVD-related mortalities in both cohorts. Thus, increased levels of FPG and HbA1c and U-shaped TyG index increase the risks of all-cause especially CVD-related mortalities.

[Plankton Community Stability and Drive Factor Identification Guizhou Plateau Reservoir].

In order to understand the stability of the zooplankton and phytoplankton communities in the Guizhou plateau reservoir environment, the process of reservoir water quality change affecting the stability of plankton was studied. The changes in the plankton community and water quality in three different nutrient reservoirs （Huaxi Reservoir, Goupitan Reservoir, and Hailong Reservoir） were studied from October 2020 to August 2021. The stability of the zooplankton and phytoplankton communities was studied using time-lag analysis （TLA）. Variance decomposition analysis （VPA） was used to explore the response of the two communities to environmental changes. The driving factors of plankton community changes in reservoirs were also revealed. The results showed that Huaxi Reservoir and Goupitan Reservoir were mesotrophic reservoirs, and Hailong Reservoir was a eutrophic reservoir. The average comprehensive nutrition indices of the three reservoirs were 44.07, 44.68, and 50.25. A total of 51 species of zooplankton rotifers, 39 species of rotifers, three species of copepods, and nine species of cladocera were identified. Among them, the abundance of rotifers was the highest, accounting for 85.96%. A total of seven phyla and 73 species of phytoplankton were identified, including 16 species in the phylum Cyanophyta, 32 species in the phylum Chlorophyta, 16 species in the phylum Diatoma, three species in the phylum Chlorophyta, four species in the phylum Euglenophyta, and one species each in the phyla Cryptophyta and Chrysophyta. Among them, the abundance of cyanobacteria and diatoms was the highest, accounting for 66.2% and 27.35%, respectively. The median absolute deviation （MAD） of the Bray-Curtis distance of zooplankton and phytoplankton community in the three reservoirs were 0.67 and 0.65 in Huaxi Reservoir, 0.80 and 0.69 in Goupitan Reservoir, and 0.85 and 0.47 in Hailong Reservoir, respectively. The larger the value, the greater the variation in the community. The absolute value of the slope of zooplankton was greater than that of phytoplankton in the TLA results, and the absolute values of the slopes were 0.018 and 0.004, respectively. The larger the absolute value of the slope, the faster the community variability. The zooplankton community in the three reservoirs was less stable than the phytoplankton community and more sensitive to environmental changes, and the degree of variation was greater. The higher the degree of eutrophication of the reservoir, the more obvious this phenomenon. VPA showed that the changes in plankton communities in Huaxi Reservoir and Hailong Reservoir were mainly influenced by water temperature and eutrophication factors. The changes in planktonic community in Goupitan Reservoir were mainly influenced by water temperature and chemical factors. The driving factors of Huaxi Reservoir were water temperature, TP, permanganate index, and SD. The driving factors of Goupitan Reservoir were water temperature, NO3-- N, and pH. The driving factors of Hailong Reservoir were water temperature and TP. Nutrients and water temperature were the main factors affecting the stability of plankton communities in reservoirs.

The antibodies against the A137R protein drive antibody-dependent enhancement of African swine fever virus infection in porcine alveolar macrophages.

African swine fever virus (ASFV) is the causative agent of African swine fever (ASF), a highly contagious disease that can kill up to 100% of domestic pigs and wild boars. It has been shown that the pigs inoculated with some ASF vaccine candidates display more severe clinical signs and die earlier than do pigs not immunized. We hypothesize that antibody-dependent enhancement (ADE) of ASFV infection may be caused by the presence of some unidentified antibodies. In this study, we found that the ASFV-encoded structural protein A137R (pA137R) can be recognized by the anti-ASFV positive sera, indicating that the anti-pA137R antibodies are induced in the ASFV-infected pigs. Interestingly, our results demonstrated that the anti-pA137R antibodies produced in rabbits or pigs enhanced viral replication of different ASFV strains in primary porcine alveolar macrophages (PAMs), the target cells of ASFV. Mechanistic investigations revealed that anti-pA137R antibodies were able to promote the attachment of ASFV to PAMs and two types of Fc gamma receptors (FcγRs), FcγRII and FcγRIII, mediated the ADE of ASFV infection. Taken together, anti-pA137R antibodies are able to drive ASFV ADE in PAMs. These findings shed new light on the roles of anti-ASFV antibodies and have implications for the pathophysiology of the disease and the development of ASF vaccines.