Current Issue
Human coronavirus OC43 (HCoV-OC43), a typical type of coronavirus, causes the common cold in humans. Although the HCoV-OC43 virus has been identified for over 60 years, the specific mechanism of viral internalization post-infection remains unclear. In this issue, Li et al. investigate how sorting nexin 10 (SNX10) mediates HCoV-OC43 infection via interacting with the adaptor protein complex 2 μ1 subunit (AP2M1). SNX10 can further promote lysosomal acidification and assist viral genome release. The cover image draws on the story of the Trojan Horse: For a long time, the Greek army (representing the virus) could not break through the walls of Troy (the host cell membrane). They thus feigned retreat and left a huge wooden horse (AP2M1). The Trojans (SNX10) took the house into the city as a trophy. When night fell (mimicking the acidic environment), the Greek soldiers hiding inside the horse rushed out (release the viral genome) and cooperated with the returning army to breach the walls of Troy (Kindly designed and provided by Prof. Shuwen Liu and Dr. Haobin Li). See page 755–768 for details.
HBV and host metabolic crosstalk: Reprogramming pathways for viral replication and pathogenesis
2025, 40(5): 685 doi: 10.1016/j.virs.2025.09.008
Received: 12 June 2025
Accepted: 24 September 2025
Hepatitis B virus (HBV) establishes chronic infection through strategic manipulation of host metabolic networks, driving a spectrum of hepatic pathologies ranging from hepatitis to cirrhosis and hepatocellular carcinoma. Mechanistically, HBV reprograms core metabolic pathways, including glycolysis, tricarboxylic acid (TCA) cycle, oxidative phosphorylation, and lipid homeostasis, to fuel its replication machinery and evade immune surveillance. This review systematically synthesizes current evidence on HBV-induced glucose/lipid metabolic rewiring, with particular emphasis on how viral-host crosstalk at the metabolic interface sustains viral pathogenesis.
Genetic analysis of human adenovirus type 108 circulating in China during 2014-2024
2025, 40(5): 694 doi: 10.1016/j.virs.2025.09.002
Received: 17 April 2025
Accepted: 11 September 2025
Human adenovirus type 108 (HAdV-108) has been detected in multiple countries, including China, and is associated with severe acute respiratory infection (ARI) in children, with reported fatalities. However, studies on HAdV-108 remain limited. This study aimed to investigate the clinical and genetic characteristics of HAdV-108 in ARI children in China. From 2014 to 2024, 6720 respiratory samples were collected from hospitalized children with ARI at ten hospitals across northern and southern China, of which 505 (7.51%) tested positive for HAdV. The whole-genome and three major capsid protein genes were amplified and sequenced for bioinformatics analysis, which revealed that among 317 HAdV-isolated samples, 21 (6.62%) were identified as HAdV-108, ranking third after HAdV-114 and HAdV-7. Clinical analysis of HAdV-108-positive cases showed that the main manifestations were cough and fever. Seven children had gastrointestinal symptoms, and two children without underlying diseases were diagnosed with severe pneumonia. Phylogenetic analysis of whole-genome sequences revealed distinct predominant epidemic branches between domestic and international strains, with one strain obtained in this study forming an independent branch. Hexon protein exhibited the fastest evolution rate, lowest identity, and greatest amino acid variability, while fiber protein displayed the slowest evolution rate, highest identity, and greatest conservation and stability. Compared with the earliest reported HAdV-108 strain, three amino acid deletions were identified in the RGD loop region of penton base protein, resulting in potential structural change. Recombination analysis identified five distinct recombination patterns. In vitro experiments demonstrated that HAdV-108 had proliferation capacity comparable to other species C adenoviruses. In summary, HAdV-108 has persistently circulated in China, causing severe ARIs and concurrent gastrointestinal manifestations. Cluster3 was the predominant epidemic branch in China. HAdV-108 exhibited significant intra-type genetic variation, with random and diverse recombination events.
Long-term surveillance of avian avulavirus in wild birds in China from 2003 to 2020
2025, 40(5): 710 doi: 10.1016/j.virs.2025.09.004
Received: 10 March 2025
Accepted: 17 September 2025
Avian avulavirus (AAVV) is a significant pathogen affecting avian species, but research on its prevalence in wild birds in China has been relatively limited. In this study, active surveillance for AAVV was conducted in wild birds in China from 2003 to 2020. A total of 124,882 samples were collected from 26 provinces, and 220 AAVV-positive samples were identified, encompassing various serotypes including AAVV-1, -4, -6, -8, -9, -13, and -16. Notably, AAVV-9 isolates were reported for the first time in China through this study. Detailed genetic analysis of 148 representative strains revealed that 26 of them exhibited a polybasic amino acid residue at the F gene cleavage site, a molecular marker associated with virulent AAVV strains in chickens. The geographical isolation between the Old and New Worlds has led to the independent evolution of AAVVs in each region, resulting in distinct Eurasian and North American lineages. Our findings predominantly aligned with the Eurasian lineage. However, repeated detections of AAVVs of North American origin in wild birds in China suggests potential viral dispersal between North America and China, which warrants further investigation. Furthermore, geographical reconstruction of AAVV-4 occurrence indicated a possible transmission route from Europe to East Asia. The origin of AAVV-4 remains uncertain due to limited sequence data, underscoring the need for expanded surveillance and highlight the necessity for sustained, long-term epidemiological surveillance efforts.
Epidemiological, phylogenetic, and pathogenicity analysis of H4 subtype avian influenza viruses in China, 2011-2022
2025, 40(5): 722 doi: 10.1016/j.virs.2025.09.005
Received: 07 May 2025
Accepted: 19 September 2025
The H4 subtype of avian influenza virus (AIV) is prevalent worldwide, but only receives little attention due to its low pathogenicity in poultry. Consequently, it remains largely unclear whether H4 AIVs pose a potential threat to the poultry industry and public health. During the period from 2011 to 2022, we conducted an active surveillance programm. A total of 154,762 swab samples were collected across various provinces, and 427 H4 viruses were detected, resulting in a positivity rate of 0.28%. All H4 viruses were isolated from poultry, primarily from ducks in live poultry markets. We further investigated the genetic evolutionary characteristics and pathogenicity of 20 H4Nx viruses isolated in our program. Phylogenetic analysis revealed that the 20 H4Nx viruses belonged to the Eurasian lineage and exhibited significant genetic diversity, with 19 distinct genotypes identified. Molecular characterization indicated that these viruses were low-pathogenicity AIVs with limited binding affinity to human receptors, yet they contained mutations associated with enhanced viral replication and pathogenicity in mammals. Pathogenicity tests conducted in ducks demonstrated that H4 viruses were weakly pathogenic, exhibiting limited replication and transmission capabilities. However, some viruses were able to replicate effectively in mice and induce weight loss. For instance, DK/AH/AG61/11(H4N6) can replicate efficiently in MDCK cells, indicating a potential threat to mammals. These findings underscore the importance of ongoing surveillance of H4 AIVs to better understand their evolution and transmission dynamics and to prevent potential public health risks.
Phylogenomics and structural modelling feature accelerated evolution of Oropouche virus: 1955 to 2024
2025, 40(5): 735 doi: 10.1016/j.virs.2025.09.009
Received: 12 May 2025
Accepted: 28 September 2025
A large multi-country outbreak of Oropouche virus (OROV), a segmented negative-sense RNA virus, is emerging in Latin America. By analyzing publicly available whole-genome sequences spanning 1955 to 2024, this study reveals accelerated spatiotemporal evolution of OROV, cooperatively driven by genome mutagenesis and segment reassortment. The strains responsible for the 2023-2024 outbreak are universally reassortants, but form two divergent lineages, namely the Brazil and western Amazon basin lineages. This epidemic spreading is primarily fueled by localized transmission within countries and cross-border spread. Phylogenomic analysis further suggests that the S segment of the viral genome originated in Brazil around the 1740s, underwent diversification into five distinct clusters by the 1970s, and experienced rapid proliferation during 2020-2024. In contrast, the L segment originated in Peru around the 1630s and evolved into two independent clusters by the 1850s. Divergent evolutionary pressures have driven distinct patterns of amino acid changes in viral proteins between the Brazil and the western Amazon basin lineages. These mutations are predicted to alter the protein structures and bear functional consequences for viral fitness and transmission. These findings provide critical insights into the evolutionary dynamics of OROV and underscore the necessity of genome surveillance to track the transmission pathways and spatiotemporal evolution.
Seasonal dynamics of hedgehog-borne ticks and severe fever with thrombocytopenia syndrome virus in Beijing's urban parks
2025, 40(5): 748 doi: 10.1016/j.virs.2025.10.005
Received: 17 March 2025
Accepted: 15 October 2025
Severe fever with thrombocytopenia syndrome virus (SFTSV), an emerging tick-borne pathogen, has caused a rising number of human cases in the urban-rural fringe of Beijing since 2021. This study explores the seasonal dynamics of hedgehog-associated ticks and SFTSV transmission in urban parks of Beijing. Surveys across six parks revealed distinct activity patterns: adult Haemaphysalis longicornis peaked in summer, while nymphs dominated spring and autumn. All collected H. longicornis belonged to parthenogenetic populations. A near-complete SFTSV genome (C4 strain) was identified in a tick collected from Taoranting Park, suggesting multiple viral introductions into Beijing. Serological analysis showed that > 50% of hedgehogs carried SFTSV-neutralizing antibodies in spring; yet seropositivity declined markedly in summer and autumn, indicating recurrent infections and implicating hedgehogs as potential reservoirs. These findings reveal an urban SFTSV transmission cycle maintained by hedgehogs and parthenogenetic H. longicornis, emphasizing the urgency of enhanced surveillance and public health interventions to curb urban zoonotic risks.
SNX10 enhances HCoV-OC43 infection by facilitating viral entry and inhibiting virus-triggered autophagy
2025, 40(5): 755 doi: 10.1016/j.virs.2025.07.005
Received: 22 March 2025
Accepted: 07 July 2025
The ongoing coronavirus epidemic, including the novel coronavirus (SARS-CoV-2), continues to pose a significant threat to global public health. Host targets address multiple stages of the viral life cycle and provide diverse opportunities for therapeutic interventions. This study identified sorting nexin 10 (SNX10) as a facilitator of replication of human coronavirus OC43 (HCoV-OC43), underscoring its potential as a novel antiviral target. The knockout of SNX10 significantly suppressed HCoV-OC43 replication both in vivo and in vitro. Immunoprecipitation-mass spectrometry (IP-MS) analysis identified the adaptor protein complex 2 subunit μ1 (AP2M1) as a direct interactor of SNX10. Specifically, SNX10 facilitates phosphorylation of the AP2M1, thereby enhancing clathrin-mediated viral endocytosis. Furthermore, subsequent binding and internalization assays revealed that SNX10 knockout significantly inhibits viral entry into host cells. Conversely, the reconstitution of SNX10 fully restored viral entry, thereby confirming the critical and indispensable role of SNX10 in pathogen internalization. Simultaneously, SNX10 was identified as a key factor that promotes endosomal acidification by modulating pH levels, which in turn facilitated the release of the viral genome. Notably, the ablation of SNX10 was found to trigger autophagy activation during infection, thereby maintaining intracellular homeostasis. Additionally, it exerted autonomous antiviral effects through lysosomal degradation pathways. Collectively, these findings demonstrate SNX10 serves as a pivotal regulator of the viral life cycle and underscore its therapeutic potential as a multi-faceted antiviral candidate target capable of simultaneously inhibiting viral internalization, viral genomic release, and host-pathogen equilibrium.
Antigenic and structural insights into Langya henipavirus attachment glycoprotein
2025, 40(5): 769 doi: 10.1016/j.virs.2025.08.005
Received: 31 December 2024
Accepted: 29 August 2025
The invasion of host cells by the henipavirus is facilitated through the interaction between viral attachment (G) and fusion (F) glycoproteins with receptors on the cell surface. Langya henipavirus (LayV) was newly identified in China in 2022. The G proteins of LayV and Mojiang virus (MojV) exhibit high amino acid homology (86%), while they are located in a unique evolutionary clade within the Henipavirus genus. In this study, the crystal structure of the LayV G protein was resolved at a 3.37 Å resolution, revealing a head domain with six β-propeller-like domains distinct from other henipavirus G proteins, such as those of Nipah virus (NiV) and Hendra virus (HeV). Furthermore, the prominent loop in the center cavity of the LayV G protein showed unique structural features. In the ELISA and SPR assays, the LayV G protein was unable to bind to the existing henipavirus-neutralizing antibodies or the ephrin-B2 receptor. Immunogenicity studies in mice demonstrated robust antibody responses elicited by the LayV G protein. These antibodies exhibited strong reactivity against both LayV and MojV G proteins. However, only weak cross-reactivity was observed with other henipaviruses. Moreover, eight monoclonal antibodies targeting the LayV G protein were generated, two of which exhibited broad binding activity across different henipavirus G proteins. These findings underscore the need for tailored vaccines and therapeutics for LayV and related novel henipaviruses
Ubiquitously expressed transcript isoform 2 (UXT-V2) restricts HSV-2 replication by targeting glycoprotein B for degradation through ubiquitin-proteasome pathway
2025, 40(5): 778 doi: 10.1016/j.virs.2025.08.004
Received: 28 April 2025
Accepted: 27 August 2025
Herpes simplex virus 2 (HSV-2) is a major pathogen causing neonatal herpes and increasing the risk of human immunodeficiency virus 1 (HIV-1) infection. However, the mechanisms underlying host restriction of HSV-2 infection are still not fully understood. The ubiquitously expressed transcript isoform 2 (UXT-V2), an α-type prefoldin protein, functions as a versatile transcription factor associated with numerous human tumors, but its role in viral infection remains unclear. In this study, we found that ectopic expression of UXT-V2 significantly inhibited HSV-2 replication, while knockout of endogenously expressed UXT-V2 promoted HSV-2 proliferation. Further analysis revealed that UXT-V2 restricts HSV-2 replication independent of its role in regulating NF-κB. In the context of HSV-2 infection or in viral glycoprotein B (gB)-transfected cells, UXT-V2 facilitates K48-linked ubiquitination of gB, leading to its degradation via the proteasome pathway, thereby inhibiting viral replication. Furthermore, we identified that UXT-V2 interacts with gB, recruiting the E3 ligase TRIM21 to facilitate K48-linked ubiquitination of gB. HSV-2, in turn, reduces the abundance of UXT-V2 proteins both in vitro and in mice, highlighting the complexity of HSV-2-host interactions. Collectively, our findings, for the first time, demonstrate an anti-HSV-2 role of UXT-V2, unveiling a novel host immune defense mechanism involved in regulating glycoprotein homeostasis.
A safe and broad-spectrum SARS-CoV-2 mRNA vaccine with a new delivery system for in-situ expression
2025, 40(5): 793 doi: 10.1016/j.virs.2025.09.001
Received: 09 June 2025
Accepted: 01 September 2025
Since the outbreak of COVID-19 in late 2019, the cumulative number of confirmed cases worldwide has surpassed 778 million, and the number of deaths has exceeded 7 million, posing a significant threat to human life and health while inflicting enormous losses on the global economy. At the stage where sequential immunization is recommended, there is a pressing demand for mRNA vaccines that can be rapidly adapted to new sequences, are easy to industrialize, and exhibit high safety and effectiveness. We developed a lipid nanoparticle (LNP) system, designated as WNP, which facilitates essentially in situ expression at the injection site and results in lower levels of pro-inflammatory factors in the liver, thus enhancing its safety compared to liver-targeted alternatives. Furthermore, in light of the swiftly mutating characteristic of SARS-CoV-2, a study has used cross-lineage chimeras and mutation patch strategies to design an antigen that is highly immunogenic and can stimulate the production of a broad range of effective antibodies. Therefore, we used the same antigenic configuration of RBD including five key mutation sites (K417T, L452R, T478K, E484K, and N501Y) to achieve optimal broad-spectrum efficacy. Our results indicate that WNP can elicit a humoral immunity response that is as robust as that of SM-102, a stronger cellular immune response, and provide a certain protective effect. On top of that, WNP can be applied to the development of vaccines targeting other pathogens and will contribute to a quicker response to the spillovers of unknown mammalian viruses.
The pathogenic role and genomic characteristics of Epstein-Barr virus in vitreoretinal lymphoma
2025, 40(5): 804 doi: 10.1016/j.virs.2025.09.007
Received: 22 July 2025
Accepted: 24 September 2025
Epstein-Barr virus (EBV) infection is well-known for its association with lymphoproliferative disorders and various lymphomas, causing significant global morbidity and mortality. EBV-positive vitreoretinal lymphoma (VRL) is exceedingly rare. As a result, the pathogenic role and genomic characteristics of EBV in VRL remain poorly understood. In this study, we employed droplet digital PCR (ddPCR) combined with EBV-specific immunofluorescence assay to detect EBV in the vitreous fluid of fifty-three VRL patients. We found that approximately 28% (15/53) of the patients were EBV positive. Analysis of clinical data showed that EBV-positive VRL patients had shorter progression-free survival (PFS) compared to EBV-negative patients (P = 0.004). Additionally, through integration of EBV-targeted sequencing and PCR-based deep sequencing, we found that all five VRL-derived EBV genomes formed a distinct cluster within one phylogenetic branch. Meanwhile, several non-synonymous mutations were exclusively detected in the VRL group, including S229T in latent membrane protein 1 (LMP1) and G2248R in the Epstein-Barr virus BamHI-PraL fragment 1 (BPLF1). In conclusion, our findings suggest that EBV as a risk factor associated with poor prognosis in VRL, and we provide a genome-wide view of EBV sequence variations from VRL patients. This may offer insights into the pathogenic role of EBV in VRL and could potentially assist in the diagnosis and treatment of this disease.
Synthetic genomics-based generation of the tick-borne encephalitis virus Siberian subtype prototype strain and E51K-attenuated variant for vaccine development and antiviral screening
2025, 40(5): 812 doi: 10.1016/j.virs.2025.09.010
Received: 01 April 2025
Accepted: 30 September 2025
Tick-borne encephalitis virus (TBEV) is a re-emerging pathogen in Kazakhstan, where the increasing risk of its spread underscores the need for improved healthcare preparedness, including the development of local vaccines. However, the absence of reference TBEV strains in the country presented a major challenge. To address this, we generated a prototype strain (Vasilchenko) of the Siberian TBEV genotype, predominant in Kazakhstan, using synthetic genome and molecular infectious clone technology. A DNA-launched TBEV molecular clone was assembled from DNA fragments, enabling virus rescue upon plasmid transfection. During the propagation of the post-transfection virus in cell culture, a single amino acid substitution (E51K) in the envelope protein emerged, resulting in a 100-fold increase in the titer of the mutant variant. In vivo, this mutation significantly attenuated virulence: while wild-type TBEV caused 100% mortality in BALB/c mice, the E51K variant was non-lethal and exhibited reduced viremia, suggesting impaired neuroinvasiveness. To further exploit this attenuated, high-titer virus, we developed a GFP-expressing reporter TBEV variant. Using this reporter system, we demonstrated that favipiravir possesses antiviral activity against TBEV, with inhibitory concentrations within a pharmacologically relevant range. In conclusion, synthetic genomics enabled the generation of a reference TBEV strain to replenish Kazakhstan's collections. The E51K mutation enhances viral replication in vitro while attenuating pathogenicity in vivo, and the derived reporter virus is suitable for antiviral compound screening.
African swine fever virus MGF360-9L degrades DDX20 through the Rab1A-dependent autophagy pathway to antagonize its antiviral effect
2025, 40(5): 822 doi: 10.1016/j.virs.2025.10.001
Received: 15 April 2025
Accepted: 13 October 2025
African swine fever (ASF) is an acute, hemorrhagic, and highly contagious disease in pigs caused by the African swine fever virus (ASFV). Our previous studies have demonstrated that deletion of the MGF360-9L gene weakens ASFV virulence in pigs, yet the underlying mechanism remains unclear. To investigate the mechanism of MGF360-9L regulating ASFV pathogenicity, the relationship between MGF360-9L and host proteins was identified by mass spectrometry. We found that host protein DEAD-box helicase 20 (DDX20) interacted with and colocalized with MGF360-9L. Overexpression of DDX20 inhibited ASFV replication, whereas knockdown of DDX20 had the opposite effects. Moreover, DDX20 inhibited ASFV replication by promoting the activation of type I interferon signaling. Surprisingly, DDX20 was gradually degraded following ASFV infection. Mechanistically, MGF360-9L promoted the autophagic degradation of DDX20 by recruiting autophagy-related protein Ras-related protein Rab-1A (Rab1A). Silencing Rab1A suppressed ASFV replication, while overexpression of Rab1A exhibited the opposite effects. Furthermore, Rab1A, MGF360-9L and DDX20 could form a complex to facilitate the degradation of DDX20. Knockdown of Rab1A impaired MGF360-9L-mediated degradation of DDX20 during ASFV infection. In summary, our study demonstrates that MGF360-9L targets DDX20 for autophagy degradation to antagonize its antiviral function and facilitate ASFV replication. This finding broadens our understanding of the regulatory network between ASFV and its host, and provides new insights into the pathogenesis and immune evasion mechanisms of ASFV.
Efficacy and safety of switching from lopinavir/ritonavir-based regimens to bictegravir/emtricitabine/tenofovir alafenamide in people living with HIV: A multicenter retrospective study
2025, 40(5): 835 doi: 10.1016/j.virs.2025.10.003
Received: 15 January 2025
Accepted: 14 October 2025
In China, approximately 13% of people living with human immunodeficiency virus (HIV) (PLWH) are receiving lopinavir/ritonavir (LPV/r)-based regimens. These PLWH typically have a history of either treatment failure or intolerance to first-line efavirenz-based regimens. Given the considerable pill burden and adverse effects associated with LPV/r, treatment optimization is important for this population. This multicenter retrospective study aimed to evaluate the efficacy and safety of switching from LPV/r-based regimens to the single-tablet regimen of bictegravir/emtricitabine/tenofovir alafenamide (BIC/FTC/TAF). Virological suppression rates (HIV-RNA < 40 copies/mL) were primarily compared between the 48-week periods before and after switching to BIC/FTC/TAF. CD4 counts and metabolic data were also assessed. A total of 461 PLWH were recruited between January 2021 and December 2023, with 92.2% being male, a median age of 38 years, and a median antiretroviral therapy duration of 8 years. Prior to initiating LPV/r, 23.0% (106/461) had documented virological failure. During LPV/r treatment, 18.9% (20/106) of these individuals experienced viral rebound. Among all participants, the overall virological suppression rates significantly increased from 94.6% (pre-switch) to 98.6% (post-switch) (P < 0.001). Notably, among participants with prior virological failure, suppression rates improved significantly from 81.1% to 97.2% (P < 0.001), whereas no significant difference was observed in those without such history (from 98.6% to 99.2%, P = 0.764). The median triglyceride level decreased from 2.4 mmol/L to 1.8 mmol/L (P < 0.001), while no difference in CD4 counts was observed. These findings demonstrate that BIC/FTC/TAF is an effective and metabolically favorable treatment option for PLWH switching from LPV/r based regimens, regardless of whether they have a prior history of virological failure.
Oncolytic Newcastle disease virus promotes tumor cell death via the anoikis effector Bit1 translocation
2025, 40(5): 842 doi: 10.1016/j.virs.2025.10.004
Received: 30 May 2025
Accepted: 15 October 2025
Anoikis is a specialized form of programmed cell death triggered by the detachment of cells from the extracellular matrix (ECM). Tumor cells that develop resistance to anoikis acquire the ability to detach, migrate, and colonize distant sites, ultimately leading to the formation of metastatic tumors. Bit1 (Bcl-2 inhibitor of transcription 1), a key effector of anoikis, is released into the cytoplasm upon loss of cell attachment and activates a caspase-independent pathway of apoptosis. Newcastle disease virus (NDV), a pathogen that poses a significant threat to the poultry industry, has also emerged as a promising oncolytic virus capable of selectively targeting and killing tumor cells. However, whether NDV can induce the death of anoikis-resistant tumor cells by activating Bit1 remains unclear. In this study, we utilized physical methods to induce cell suspension as a positive control for anoikis and further examined the expression and cellular localization of Bit1 following NDV infection in tumor cells. The results indicated that both viral infection and cell suspension resulted in partial cell death, accompanied by the translocation of Bit1 from the mitochondria to the cytoplasm and a reduction in its protein levels. Notably, Bit1 expression was found not to significantly affect viral replication. These findings suggest that NDV infection promotes tumor cell death by activating Bit1 translocation, mirroring the effects observed during cell suspension-induced anoikis. In addition, in vivo experiments demonstrated that NDV effectively inhibits the metastasis and growth of melanoma in mice, and that overexpression of Bit1 in tumor cells accelerates this process. This study provides novel insights into NDV-induced tumor cell death and identifies potential targets for understanding the mechanisms of oncolytic virus action.
Black swans as sentinel species for the emergence of clade 2.3.4.4b highly pathogenic avian influenza (H5N1) in Shanghai, China, 2024
2025, 40(5): 853 doi: 10.1016/j.virs.2025.07.008
Received: 21 May 2025
Accepted: 17 July 2025
Highlights
1. A novel reassortant H5N1 virus detected in 15 sick black swans in Shanghai, China.
2. Novel H5N1 virus in black swans suggests wild-domestic bird reassortant from East Asia.
3. Susceptible black swans could serve as ideal sentinel species for HPAI early detection.
1. A novel reassortant H5N1 virus detected in 15 sick black swans in Shanghai, China.
2. Novel H5N1 virus in black swans suggests wild-domestic bird reassortant from East Asia.
3. Susceptible black swans could serve as ideal sentinel species for HPAI early detection.
Antisera and antivirals targeting the conserved domains in SARS-CoV-2 S2 subunit are effective against ACE2-using MERSr-CoVs with spillover potential
2025, 40(5): 856 doi: 10.1016/j.virs.2025.09.003
Received: 28 June 2025
Accepted: 12 September 2025
Highlights
1. S2 subunit remains high conserved throughout coronavirus evolution.
2. BA.5/BF.7-infection induces weak cross-immune response against MERS-related coronaviruses (MERSr-CoVs) in humans.
3. HR1LS based on conserved S2 elicits strong cross-immune response to MERSr-CoVs in mice.
4. Conserved domains in S2 represent ideal targets for pan-CoV vaccines and antivirals.
1. S2 subunit remains high conserved throughout coronavirus evolution.
2. BA.5/BF.7-infection induces weak cross-immune response against MERS-related coronaviruses (MERSr-CoVs) in humans.
3. HR1LS based on conserved S2 elicits strong cross-immune response to MERSr-CoVs in mice.
4. Conserved domains in S2 represent ideal targets for pan-CoV vaccines and antivirals.
First identification of Tusavirus in calf intestinal tissue suggests interspecies transmission and genomic variation
2025, 40(5): 860 doi: 10.1016/j.virs.2025.09.006
Received: 20 May 2025
Accepted: 24 September 2025
Highlights
1. This is the first identification of Tusavirus in calf tissue in China, expanding its host species and geographical range.
2. Genomic analysis reveals conservation, with nucleotide insertions in the VP1 gene and deletions in both VP1 and VP2 genes.
3. Phylogenetic analysis shows close evolutionary linkage between bovine and ovine TuV strains.
1. This is the first identification of Tusavirus in calf tissue in China, expanding its host species and geographical range.
2. Genomic analysis reveals conservation, with nucleotide insertions in the VP1 gene and deletions in both VP1 and VP2 genes.
3. Phylogenetic analysis shows close evolutionary linkage between bovine and ovine TuV strains.
