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The recent human infection with avian influenza virus revealed that H9N2 influenza virus is the gene donor for H7N9 and H10N8 viruses infecting humans. The crucial role of H9N2 viruses at the animal-human interface might be due to the wide host range, adaptation in both poultry and mammalian, and extensive gene reassortment. As the most prevalent subtype of influenza viruses in chickens in China, H9N2 also causes a great economic loss for the poultry industry, even under the long-term vaccination programs. The history, epidemiology, bio- logical characteristics, and molecular determinants of H9N2 influenza virus are reviewed in this paper. The contribution of H9N2 genes, especially RNP genes, to the infection of humans needs to be investigated in the future.

High-energy Ni-rich layered oxide cathode materials such as LiNi 0.8 Mn 0.1 Co 0.1 O 2 (NMC811) suffer from detrimental side reactions and interfacial structural instability when coupled with sulfide solid-state electrolytes in all-solid-state lithium-based batteries. To circumvent this issue, here we propose a gradient coating of the NMC811 particles with lithium oxy-thiophosphate (Li 3 P 1+x O 4 S 4x ). Via atomic layer deposition of Li 3 PO 4 and subsequent in situ formation of a gradient Li 3 P 1+x O 4 S 4x coating, a precise and conformal covering for NMC811 particles is obtained. The tailored surface structure and chemistry of NMC811 hinder the structural degradation associated with the layered-to-spinel transformation in the grain boundaries and effectively stabilize the cathode|solid electrolyte interface during cycling. Indeed, when tested in combination with an indium metal negative electrode and a Li 10 GeP 2 S 12 solid electrolyte, the gradient oxy-thiophosphate-coated NCM811-based positive electrode enables the delivery of a specific discharge capacity of 128 mAh/g after almost 250 cycles at 0.178 mA/cm 2 and 25 °C. Layered oxide cathode active materials suffer from interfacial structural instability when coupled with sulfide solid-state electrolytes. Here, the authors propose a gradient coating with a lithium oxythiophosphate layer that can stabilize the cathode|solid-state electrolyte interface.

Solid-state batteries (SSBs) are considered to be the next-generation lithium-ion battery technology due to their enhanced energy density and safety. However, the high electronic conductivity of solid-state electrolytes (SSEs) leads to Li dendrite nucleation and proliferation. Uneven electric-field distribution resulting from poor interfacial contact can further promote dendritic deposition and lead to rapid short circuiting of SSBs. Herein, we propose a flexible electron-blocking interfacial shield (EBS) to protect garnet electrolytes from the electronic degradation. The EBS formed by an in-situ substitution reaction can not only increase lithiophilicity but also stabilize the Li volume change, maintaining the integrity of the interface during repeated cycling. Density functional theory calculations show a high electron-tunneling energy barrier from Li metal to the EBS, indicating an excellent capacity for electron-blocking. EBS protected cells exhibit an improved critical current density of 1.2 mA cm −2 and stable cycling for over 400 h at 1 mA cm −2 (1 mAh cm −2 ) at room temperature. These results demonstrate an effective strategy for the suppression of Li dendrites and present fresh insight into the rational design of the SSE and Li metal interface. The high electronic conductivity of solid-state electrolytes leads to Li dendrite growth, thus hindering the commercialization of solid-state batteries. Here, the authors propose a flexible electron-blocking interface to protect garnet electrolytes from the electronic degradation.

Many cellular genes and networks induced in human lung epithelial cells infected with the influenza virus remain uncharacterized. Here, we find that p21 levels are elevated in response to influenza A virus (IAV) infection, which is independent of p53. Silencing, pharmacological inhibition or deletion of p21 promotes virus replication in vitro and in vivo , indicating that p21 is an influenza restriction factor. Mechanistically, p21 binds to the C-terminus of IAV polymerase subunit PA and competes with PB1 to limit IAV polymerase activity. Besides, p21 promotes IRF3 activation by blocking K48-linked ubiquitination degradation of HO-1 to enhance type I interferons expression. Furthermore, a synthetic p21 peptide (amino acids 36 to 43) significantly inhibits IAV replication in vitro and in vivo . Collectively, our findings reveal that p21 restricts IAV by perturbing the viral polymerase complex and activating the host innate immune response, which may aid the design of desperately needed new antiviral therapeutics.

The emergence of human infection with a novel H7N9 influenza virus in China raises a pandemic concern. Chicken H9N2 viruses provided all six of the novel reassortant’s internal genes. However, it is not fully understood how the prevalence and evolution of these H9N2 chicken viruses facilitated the genesis of the novel H7N9 viruses. Here we show that over more than 10 y of cocirculation of multiple H9N2 genotypes, a genotype (G57) emerged that had changed antigenicity and improved adaptability in chickens. It became predominant in vaccinated farm chickens in China, caused widespread outbreaks in 2010–2013 before the H7N9 viruses emerged in humans, and finally provided all of their internal genes to the novel H7N9 viruses. The prevalence and variation of H9N2 influenza virus in farmed poultry could provide an important early warning of the emergence of novel reassortants with pandemic potential.

Background Growing evidence implicates gut microbiota (GM) dysbiosis in Alzheimer’s disease (AD) pathogenesis via the gut-brain axis. Dysbiosis contributes to neuroinflammation, amyloid-β deposition, tau hyperphosphorylation, blood-brain barrier disruption, and cognitive decline. Synbiotics (combinations of probiotics and prebiotics) offer a promising strategy to modulate GM, potentially ameliorating these AD hallmarks through multiple mechanisms including enhanced production of neuroprotective short-chain fatty acids (SCFAs), reduced inflammation, improved gut barrier integrity, and immunomodulation. Objective This review critically evaluates the current evidence on the therapeutic potential of synbiotics for AD. It aims to synthesize findings from preclinical and clinical studies regarding the efficacy of synbiotics in improving cognitive function and AD pathology, elucidate the underlying biological mechanisms including GM modulation, SCFA production, immune regulation, and gut-brain signaling, and identify key challenges and future research directions for translating GM-targeted interventions into effective AD therapies. Conclusion Synbiotics demonstrate significant potential, particularly in early AD, by improving cognitive domains, reducing neuroinflammation and AD biomarkers, and modulating beneficial microbial metabolites. However, challenges include confounding factors, unresolved questions about causality, inconsistent results in advanced disease, and insufficient large-scale human trials. Future success hinges on rigorous longitudinal randomized controlled trials integrating multi-omics approaches, advanced in vitro models, and personalized strategies considering baseline microbiota and host genetics. While not a standalone cure, synbiotics represent a valuable component within multi-target therapeutic approaches aimed at modulating the gut-brain axis to slow AD progression.

As 5G small cells gradually become the main force of 5G indoor deployment, it is necessary to study channel estimators for 5G small base stations, but there has been limited research on high-performance channel estimators in recent years. This study implemented a low-delay, low-overhead, relatively universal channel estimation module by dedicated instruction set acceleration including reference signal estimation, Wiener, 1st order, and 2nd order interpolations in frequency and time domains. The instruction level acceleration is on our vector processor, yet is suitable for other commercial and academic vector processors. Through instruction acceleration, compared with the existing general vector processing instruction sets, the processor performance of the LS estimation module and Wiener filter interpolation in the frequency domain is improved by 50% and 37.5%, respectively. The BER VS SNR measure of time–frequency Wiener filter interpolation achieves 4 db compared with linear interpolation, meaning our instruction level acceleration can be an optimum solution.

Influenza A viruses in animal reservoirs repeatedly cross species barriers to infect humans. Dogs are the closest companion animals to humans, but the role of dogs in the ecology of influenza viruses is unclear. H3N2 avian influenza viruses were transmitted to dogs around 2006 and have formed stable lineages. The long-term epidemic of avian-origin H3N2 virus in canines offers the best models to investigate the effect of dogs on the evolution of influenza viruses. Here, we carried out a systematic and comparative identification of the biological characteristics of H3N2 canine influenza viruses (CIVs) isolated worldwide over 10 years. We found that, during adaptation in dogs, H3N2 CIVs became able to recognize the human-like SAα2,6-Gal receptor, showed gradually increased hemagglutination (HA) acid stability and replication ability in human airway epithelial cells, and acquired a 100% transmission rate via respiratory droplets in a ferret model. We also found that human populations lack immunity to H3N2 CIVs, and even preexisting immunity derived from the present human seasonal influenza viruses cannot provide protection against H3N2 CIVs. Our results showed that canines may serve as intermediates for the adaptation of avian influenza viruses to humans. Continuous surveillance coordinated with risk assessment for CIVs is necessary.

The interaction between influenza A virus (IAV) and host proteins is an important process that greatly influences viral replication and pathogenicity. PB2 protein is a subunit of viral ribonucleoprotein (vRNP) complex playing distinct roles in viral transcription and replication. BAG6 (BCL2-associated athanogene 6) as a multifunctional host protein participates in physiological and pathological processes. Here, we identify BAG6 as a new restriction factor for IAV replication through targeting PB2. For both avian and human influenza viruses, overexpression of BAG6 reduced viral protein expression and virus titers, whereas deletion of BAG6 significantly enhanced virus replication. Moreover, BAG6-knockdown mice developed more severe clinical symptoms and higher viral loads upon IAV infection. Mechanistically, BAG6 restricted IAV transcription and replication by inhibiting the activity of viral RNA-dependent RNA polymerase (RdRp). The co-immunoprecipitation assays showed BAG6 specifically interacted with the N-terminus of PB2 and competed with PB1 for RdRp complex assembly. The ubiquitination assay indicated that BAG6 promoted PB2 ubiquitination at K189 residue and targeted PB2 for K48-linked ubiquitination degradation. The antiviral effect of BAG6 necessitated its N-terminal region containing a ubiquitin-like (UBL) domain (17-92aa) and a PB2-binding domain (124-186aa), which are synergistically responsible for viral polymerase subunit PB2 degradation and perturbing RdRp complex assembly. These findings unravel a novel antiviral mechanism via the interaction of viral PB2 and host protein BAG6 during avian or human influenza virus infection and highlight a potential application of BAG6 for antiviral drug development.

Turkey herpesvirus (HVT) vector vaccine expressing hemagglutinin from the H9N2 AIV, namely HVT-H9, were demonstrated to block H9N2 AIV infection and transmission in chickens. In this study, we evaluated the protection efficiency and production performance of broilers in HVT-H9 field trials in the presence or absence of the H9N2 AIV natural infection. HI titers against H9N2 AIV in broilers harboring maternal antibodies were successfully induced by HVT-H9. In the presence of H9N2 AIV natural infection, immunization with HVT-H9 blocked H9N2 AIV infection and reduced the mortality rate. Importantly, HVT-H9 vaccination slightly increased broiler weight and decreased the feed conversion rate in the absence of the H9N2 AIV natural infection but significantly reduced mortality rates and increased production efficiency during the H9N2 AIV natural infection. In summary, HVT-H9 immunization might block H9N2 AIV infection and improve production efficiency in the field, especially in the presence of H9N2 AIV natural infection. •Immunization with HVT-H9 improved broiler production efficiency especially in the present of the H9N2 epidemic.•HI titers against H9N2 AIV were induced by HVT-H9 in broilers harboring maternal antibodies.•Further confirmations that immunization with HVT-H9 might block H9N2 virus infection and reduces the mortality rate.•It is proposed that cellular immunity induced by HVT-H9 might be the key to preventing and controlling H9N2 infection.