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Photocatalytic CO 2 reduction (PCR) is able to convert solar energy into chemicals, fuels, and feedstocks, but limited by the deficiencies of photocatalysts in steering photon-to-electron conversion and activating CO 2 , especially in pure water. Here we report an efficient, pure water CO 2 -to-CO conversion photocatalyzed by sub-3-nm-thick BiOCl nanosheets with van der Waals gaps (VDWGs) on the two-dimensional facets, a graphene-analog motif distinct from the majority of previously reported nanosheets usually bearing VDWGs on the lateral facets. Compared with bulk BiOCl, the VDWGs-rich atomic layers possess a weaker excitonic confinement power to decrease exciton binding energy from 137 to 36 meV, consequently yielding a 50-fold enhancement in the bulk charge separation efficiency. Moreover, the VDWGs facilitate the formation of VDWG-Bi-V O •• -Bi defect, a highly active site to accelerate the CO 2 -to-CO transformation via the synchronous optimization of CO 2 activation, *COOH splitting, and *CO desorption. The improvements in both exciton-to-electron and CO 2 -to-CO conversions result in a visible light PCR rate of 188.2 μmol g −1 h −1 in pure water without any co-catalysts, hole scavengers, or organic solvents. These results suggest that increasing VDWG exposure is a way for designing high-performance solar-fuel generation systems. Efficient CO 2 photoreduction in pure water remains challenging. Here, the authors propose to use van der Waals gaps-rich BiOCl atomic layers with low exciton binding energy and abundant surface oxygen vacancies for CO 2 to CO conversion.

Strain engineering offers an attractive strategy for improving intrinsic catalytic performance of a heterogeneous catalyst. Herein, we successfully create strain into layered indium sulfide (In 2 S 3 ) at atomic scale via introducing oxygen coordination and sulfur vacancy using a wet-chemistry method. The atomically strained In 2 S 3 exhibits greatly enhanced CO 2 photoreduction performance, achieving a CO 2 to CO conversion rate of 5.16 μmol g catalyst −1  h −1 under visible light illumination in ambient air. In-situ spectroscopic measurements together with theoretical calculations indicate that the atomically strained In 2 S 3 features lattice disordered defects on surface, which provides rich uncoordinated catalytic sites and induces structural distortion, resulting in modified band structure that promotes CO 2 adsorption/activation and boosts photogenerated charge carriers’ separation during CO 2 photoreduction. This work provides a new approach for the rational design of atomically strained photocatalysts for CO 2 reduction in ambient air. Achieving visible-light-driven CO 2 photoreduction in ambient air is significant yet challenging. Here, the authors introduce strain into layered In 2 S 3 at atomic scale for promoted CO 2 activation and boosted photogenerated charge carrier separation in atmospheric CO 2 photoreduction.

Efficient molecular oxygen activation is crucial for catalytic oxidation reaction, but highly depends on the construction of active sites. In this study, we demonstrate that dual adjacent Fe atoms anchored on MnO 2 can assemble into a diatomic site, also called as MnO 2 -hosted Fe dimer, which activates molecular oxygen to form an active intermediate species Fe(O = O)Fe for highly efficient CO oxidation. These adjacent single-atom Fe sites exhibit a stronger O 2 activation performance than the conventional surface oxygen vacancy activation sites. This work sheds light on molecular oxygen activation mechanisms of transition metal oxides and provides an efficient pathway to activate molecular oxygen by constructing new active sites through single atom technology. Efficient oxygen activation is crucial for catalytic oxidation reaction, but highly depends on the construction of active sites. Here, dual adjacent Fe atoms anchored on MnO 2 can assemble into a diatomic site, which activates molecular oxygen to form an active intermediate species Fe(O = O)Fe for CO oxidation.

In China, H9N2 subtype avian influenza outbreak is firstly reported in Guangdong province in 1992. Subsequently, the disease spreads into vast majority regions nationwide and has currently become endemic there. Over vicennial genetic evolution, the viral pathogenicity and transmissibility have showed an increasing trend as year goes by, posing serious threat to poultry industry. In addition, H9N2 has demonstrated significance to public health as it could not only directly infect mankind, but also donate partial or even whole cassette of internal genes to generate novel human-lethal reassortants like H5N1, H7N9, H10N8 and H5N6 viruses. In this review, we mainly focused on the epidemiological dynamics, biological characteristics, molecular phylogeny and vaccine strategy of H9N2 subtype avian influenza virus in China to present an overview of the situation of H9N2 in China.

Newcastle disease (ND) is one of the most economically devastating infectious diseases affecting the poultry industry. Virulent Newcastle disease virus (NDV) can cause high mortality and severe tissue lesions in the respiratory, gastrointestinal, neurological, reproductive and immune systems of poultry. Tremendous progress has been made in preventing morbidity and mortality caused by ND based on strict biosecurity and wide vaccine application. In recent decades, the continual evolution of NDV has resulted in a total of twenty genotypes, and genetic variation may be associated with disease outbreaks in vaccinated chickens. In some countries, the administration of genotype-matched novel vaccines in poultry successfully suppresses the circulation of virulent NDV strains in the field. However, virulent NDV is still endemic in many regions of the world, especially in low- and middle-income countries, impacting the livelihood of millions of people dependent on poultry for food. In ND-endemic countries, although vaccination is implemented for disease control, the lack of genotype-matched vaccines that can reduce virus infection and transmission as well as the inadequate administration of vaccines in the field undermines the effectiveness of vaccination. Dissection of the profiles of existing ND vaccines is fundamental for establishing proper vaccination regimes and developing next-generation vaccines. Therefore, in this article, we provide a broad review of commercial and experimental ND vaccines and promising new platforms for the development of next-generation vaccines.

Influenza A virus is a negative-sense single-stranded RNA virus that belongs to Orthomyxoviridae family. Based on the antigenic characteristics of hemagglutinin (HA) and neuraminidase (NA) influenza viruses are classified into multiple subtypes. H9N2 belongs to the low pathogenic Avian Influenza Viruses (AIVs) and is one of the widely spread viruses in poultry, which can pose a threat to humans by directly infecting or providing internal genes for various zoonotic avian influenza strains. It has the potential to directly or indirectly participate in becoming an AIV that causes a human pandemic. When the virus enters a host, the innate immune system is activated first by pattern recognition receptors. The cytokines produced at the site of infection recruit innate immune cells and antigen-presenting cells and those cells subsequently transmit antigenic signals to adaptive immune cells (i.e. B cells and T cells), to trigger specific humoral and cellular immune responses. As a result, humoral and cellular immunity can clear virus and infected cells via antibody-mediated neutralization and cytotoxicity, respectively. Understanding how chicken immune systems respond to H9N2 is a top priority for effectively controlling the virus's spread and designing vaccines. In this review, we comprehensively discuss the role of the chicken immune system in defending against H9N2, and clarify the current limitations in understanding chicken immune responses to H9N2 virus, thereby providing potential directions for future research as research on the chicken respiratory mucosal immune system has been stagnant for more than 20 years especially on how the mucosal immune system in chicken responds to avian influenza.

The eukaryotic translation elongation factor 1 (eEF1) family exhibits critical roles in RNA viral infection beyond its canonical function in protein synthesis. This review analyzes the structural characteristics of eEF1A and the eEF1B complex, and their regulatory mechanisms during viral infection. eEF1A impacts viral replication by stabilizing viral RNA-dependent RNA polymerase (RdRp) complexes, modulating genomic RNA synthesis, and facilitating viral assembly through cytoskeletal regulation. eEF1B subunits contribute through enhancing viral mRNA translation, regulating nuclear transport of viral components, and mediating post-translational modifications. The high conservation of eEF1 proteins across species and their involvement in multiple stages of viral replication establish them as promising broad-spectrum antiviral targets. Current eEF1-targeting compounds like plitidepsin demonstrate efficacy against diverse viral families, though therapeutic development faces challenges in balancing antiviral activity with host toxicity. This review provides a theoretical foundation for developing novel antiviral strategies targeting host–virus interaction interfaces and offers insights into addressing emerging infectious diseases.

Pathological events in a wide range of diseases, from severe infections to sterile inflammatory disorders. PMR serves as the terminal step that releases large quantities of damage-associated molecular patterns (DAMPs)—intracellular molecules that act as danger signals once outside the cell. These DAMPs can trigger strong inflammatory responses, and in many cases, may precipitate a cytokine storm, a hyperactive immune reaction that often amplifies tissue injury beyond the initial insult. For decades, scientists generally believed that PMR resulted from membrane pore-forming cell death, such as pyroptosis or necroptosis, which causes osmotic imbalance and passive membrane swelling. However, in recent years, it was discovered that Nerve Injury-Induced Protein 1 (NINJ1) mediates PMR through active oligomerization. This review first uses pathogen infection as a classical model to explore how multiple cell death pathways converge on plasma membrane rupture (PMR). Subsequently, we elaborate on the structure and function of NINJ1 as a core executor of PMR. Finally, we broaden our perspective from infection to other non-infectious but equally PMR-driven major diseases, and systematically evaluate the commonalities and prospects of NINJ1-targeted therapeutic strategies across different pathological scenarios. It is hoped that this will provide new insights for future researchers in this field.

Influenza A virus (IAV) contains a genome with eight single-stranded, negative-sense RNA segments that encode 17 proteins. During its assembly, all eight separate viral RNA (vRNA) segments are incorporated into virions in a selective manner. Evidence suggested that the highly selective genome packaging mechanism relies on RNA-RNA or protein-RNA interactions. The specific structures of each vRNA that contribute to mediating the packaging of the vRNA into virions have been described and identified as packaging signals. Abundant research indicated that sequences required for genome incorporation are not series and are varied among virus genotypes. The packaging signals play important roles in determining the virus replication, genome incorporation and genetic reassortment of influenza A virus. In this review, we discuss recent studies on influenza A virus packaging signals to provide an overview of their characteristics and functions.

Nature-inspired high-spin Fe IV  = O generation enables efficient ambient methane oxidation. By engineering sulfur-bridged dual ≡Fe II …Fe II ≡ sites on pyrite (FeS 2 ) mimicking soluble methane monooxygenase, we achieve O 2 -driven formation of high-spin (S = 2) surface Fe IV  = O species at room temperature and pressure. Strategic removal of bridging S atoms creates active sites that facilitate O 2 activation via transient ≡Fe-O-O-Fe≡ intermediates, promoting homolytic O − O bond cleavage. The resulting Fe IV  = O exhibits an asymmetrically distorted coordination environment that reduces the crystal field splitting and favors the occupation of higher energy d-orbitals with unpaired electrons. Impressively, this configuration can efficiently convert CH 4 to CH 3 OH through an oxygen transfer reaction with a synthetic efficiency of TOF = 27.4 h −1 and selectivity of 87.0%, outperforming most ambient O 2 -driven benchmarks under comparable conditions and even surpassing many H 2 O 2 -mediated systems. This study offers a facile method to synthesize high-spin surface Fe IV  = O and highlights the importance of metal spin state tailoring on non-enzymatic methane activation. High-spin Fe(IV) = O sites efficiently activate methane but are challenging to synthesize. This study develops dual Fe(II) sites on FeS 2 , generating high-spin Fe(IV) = O from O 2 , achieving superior methane-to-methanol conversion under mild conditions.