Articles in press have been peer-reviewed and accepted, which are not yet assigned to volumes/issues, but are citable by Digital Object Identifier (DOI).
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2026, 41(3): 493-512.
doi: 10.1016/j.virs.2025.12.006
Received: 01 April 2025
Accepted: 04 December 2025
Published: 15 December 2025
Crimean-Congo hemorrhagic fever (CCHF), caused by Crimean-Congo hemorrhagic fever virus (CCHFV), is endemic in Africa, Asia, and Europe. However, CCHF epidemiology and epizootiology have been poorly defined in Europe. Here, we summarize the current knowledge of CCHFV distribution in (non-Russian) Europe, including countries previously not considered to be at risk. We collected data on CCHF cases, human/vertebrate animal anti-CCHFV seroprevalence, CCHFV vector (Hyalomma tick), and CCHFV isolation from ticks and classified countries into five risk levels using a One Health approach. From 1944 through Feb 2025, more than 2000 recorded CCHF cases were identified in Europe, mostly from southern/eastern countries/regions, primarily Bulgaria (at least 1623), Kosovo (at least 339), Ukraine (at least 336), Croatia (at least 200), Albania (at least 146), and Republic of Moldova (at least 60). Albania, Bulgaria, Greece, Kosovo, and Spain were categorized as level 1 (reported CCHF cases, presence of robust surveillance systems). North Macedonia, Portugal, and Ukraine/Crimea were assigned to level 2 (reported CCHF cases in the absence of robust established surveillance). Bosnia and Herzegovina, Croatia, France, Hungary, Italy, Montenegro, Republic of Moldova, Romania, and Slovenia were assigned to level 3 due to evidence of CCHFV circulation in absence of recent CCHF cases. Thirty-four countries were assigned to level 4 (presence of Hyalomma ticks) or level 5 (no data). This work provides information on CCHFV distribution and burden with list of at-risk areas to inform international and local public health agencies to establish or strengthen surveillance systems.
2026, 41(3): 513-522.
doi: 10.1016/j.virs.2026.05.011
Received: 05 September 2025
Accepted: 29 May 2026
Published: 03 June 2026
Enterovirus (EV) infections represent a significant global and national health concern in children, leading to various complications. Although most children with EV infections generally have a favorable prognosis, a small proportion may still develop severe complications. This study aimed to analyze the epidemiological characteristics, disease spectrum, and disease burden of EV infections in China. A total of 163,714 hospitalized children with EV infections from 37 member hospitals of the Futang Research Center of Pediatric Development were identified between Jan 1st, 2016 and Dec 31st, 2023, accounting for 1.49% of all pediatric hospitalizations. Most cases occurred in infants aged 28 days to ≤ 1 year (42.29%) and toddlers aged 1 to ≤ 3 years (39.93%), with a male predominance (male-to-female ratio, 1.62 : 1). Severe cases of EV infections can be life-threatening and increase the burden of disease. The median LOS for EV infections were 5 days, with an average hospitalization cost of $587.37. EV infections can affect multiple organs, including the heart, brain, and respiratory system and were associated with severe complications, including myocarditis, encephalitis, and meningitis. These findings underscore the substantial disease burden of EV infections and highlight the need for targeted prevention strategies in young children.
2026, 41(3): 523-531.
doi: 10.1016/j.virs.2026.06.001
Received: 12 December 2025
Accepted: 29 May 2026
Published: 03 June 2026
Tick-borne viruses (TBVs) pose significant emerging threats to public and veterinary health worldwide. In Pakistan, the potential threats posed by TBVs extend far beyond Crimean-Congo hemorrhagic fever virus (CCHFV), which causes outbreaks and severe hemorrhaging with a high fatality rate among humans each year. However, the full extent of the tick-borne virome remains largely unexplored. This study presents the metagenomic profiling of viruses in livestock-associated ticks from Pakistan. Eighty-seven ticks belonging to the genera Ixodes, Rhipicephalus, Haemaphysalis, and Hyalomma species from livestock in Punjab. These ticks were subsequently grouped into 11 pools for RNA sequencing. Our analysis revealed extensive viral diversity, identifying sequences related to 31 viruses spanning at least 11 families. New strains of Jingmen tick virus (JMTV), Brown dog tick phlebovirus 2 (BDTPV-2), and Liman tick virus (LMTV) were characterized, confirming their presence in the region. Serological surveys performed among 319 livestock, 253 humans, and 214 rats detected antibodies against these viruses, indicating host exposure. Notably, the presence of JMTV-neutralizing antibodies was confirmed in two livestock animals, one human, and one rat, providing evidence of productive infection. Our findings significantly expand the known diversity and distribution of TBVs in Pakistan, establish the preliminary baseline of the tick virome in the country, and provide serological evidence of cross-species exposure to emerging TBVs. This study highlights the underestimated risk of tick-borne viral zoonoses in Pakistan and underscores the urgent need for enhanced surveillance and risk assessment.
2026, 41(3): 532-542.
doi: 10.1016/j.virs.2026.05.009
Received: 22 February 2026
Accepted: 27 May 2026
Published: 03 June 2026
Mollusca, the second-largest animal phylum, includes many aquaculture species used as important food resources for humans. While DNA viruses that threaten molluscan aquaculture have received much attention, molluscan RNA viromes are still understudied. Here, using a multi-stage RdRP discovery pipeline combining six-frame translation, profile-based homology search, and phylogenetic validation, 203 RNA viruses spanning five viral phyla and fifteen viral orders were identified, based on 223 molluscan metatranscriptomes covering eight classes. Phylogenetic analysis, combined with structural modeling, revealed a significant increase in the number of Pisuviricota-related lineages. Extensive modular evolution in viral genomes was observed, including gene rearrangements and co-evolution of capsid and RdRP genes. Host prediction linked 76% of the RNA viruses to a range of eukaryotes. These findings expand the diversity of RNA viruses associated with molluscs and shed light on their phylogenetic relationships, highlighting that molluscs might serve as an important reservoir of diverse RNA viruses infecting a range of eukaryotic hosts.
2026, 41(3): 543-560.
doi: 10.1016/j.virs.2026.03.001
Received: 03 September 2025
Accepted: 06 March 2026
Published: 12 March 2026
Hepatitis B virus (HBV) has been implicated in hepatocellular carcinoma (HCC) progression, partly through regulation of the tumor suppressor phosphatase and tensin homolog (PTEN). Although transcriptional regulation of PTEN by HBV is well characterized, its post-transcriptional regulation remains poorly understood. Because RNA 5-methylcytosine (m5C) modification influences post-transcriptional gene control and cancer development, we investigated whether HBV modulates PTEN through m5C. Methylated RNA immunoprecipitation (MeRIP)-quantitative polymerase chain reaction showed a marked reduction in m5C on PTEN mRNA in HBV-producing cells. MeRIP sequencing further identified decreased m5C within the PTEN coding sequence region (chr10:89717747-89717771) in HBV-producing HepAD38/tetracycline-off cells, with chr10:89717756 emerging as a critical site where HBV suppresses m5C enrichment and PTEN expression. Mechanistically, the m5C “writer” NOP2/Sun RNA methyltransferase 2 (NSUN2) and the “reader” Y-box binding protein 1 (YBX1) stabilized PTEN mRNA in an m5C-dependent manner. HBV disrupted this pathway, decreasing PTEN mRNA stability via NSUN2- and YBX1-mediated m5C. Overexpression of NSUN2 or YBX1 attenuated HBV-driven proliferation, migration, and invasion, and these effects were partially reversed by the PTEN inhibitor VO-Ohpic. The small hepatitis B surface antigen and hepatitis B X protein downregulated NSUN2 and YBX1, linking viral proteins to PTEN suppression. Further, HBV is associated with reduced NSUN2 expression in HBV transgenic (HBV-Tg) mice, HBV-infected primary human hepatocytes as well as HBV-positive clinical HCC specimens, supporting the physiological and clinical relevance of this finding. Together, these findings identify the NSUN2/YBX1/PTEN axis as a potential therapeutic target in HBV-associated HCC.
2026, 41(3): 561-573.
doi: 10.1016/j.virs.2026.05.001
Received: 11 January 2026
Accepted: 09 May 2026
Published: 14 May 2026
Antiretroviral therapy (ART) has significantly extended the life expectancy of people with HIV (PWH), rendering population ageing and immunosenescence prominent clinical priorities. T-cell senescence is linked to mitochondrial dysfunction and drives age-related immune remodelling, yet how HIV infection and ageing jointly shape CD4+ and CD8+ T-cell immunophenotypes and mitochondrial remodelling remains unclear. This cross-sectional study included 61 PWH on suppressive ART for ≥ 12 months and 61 age- and sex-matched HIV-negative men who have sex with men, stratified into younger (≤ 35 years) and older (≥ 50 years) groups. Multiparameter flow cytometry was used to profile CD4+ and CD8+ T-cell differentiation, stemness, activation/exhaustion, and metabolic phenotypes, together with mitochondrial mass and membrane potential. We found that ageing and HIV infection were associated with T-cell remodelling, characterized by expanded late-differentiated phenotypes and reduced stem-like, homeostatic and costimulatory CD4+ and CD8+ T-cell subsets, as indicated by upregulated CD57 and CX3CR1 and downregulated CD45RA+CD31+, FOXO1, and CD28. Notably, younger PWH had an ageing-like CD4+ T-cell profile, with higher CD57, CX3CR1 and TIGIT expression than younger HIV-negative individuals. In contrast, HIV-related CD8+ T-cell perturbations (KLRG1, CXCR3, NKG2C and CD95) were more pronounced in older PWH. PWH exhibited increased mitochondrial mass and membrane potential in both total and senescent-like CD4+ and CD8+ T cells, particularly in CD8+ T cells from older PWH. In CD4+ T cells, KLRG1 and CX3CR1 expression correlated positively with age, and inversely with CD4+ T-cell counts and CD4/CD8 ratio. By contrast, FOXO1 expression in CD8+ T cells was inversely associated with age, late-differentiation markers, and ART duration in PWH. Overall, age is a major driver of T-cell immunosenescence, and HIV infection modulates and exacerbates these alterations. Mitochondrial stress, FOXO1 downregulation and immune network remodelling support a multifaceted model of HIV-associated immune ageing that may contribute to heterogeneous immune reconstitution in PWH, highlighting potential targets to mitigate immune ageing.
2026, 41(3): 574-585.
doi: 10.1016/j.virs.2026.05.002
Received: 07 January 2026
Accepted: 12 May 2026
Published: 14 May 2026
Respiratory syncytial virus (RSV) bronchiolitis is the leading cause of hospitalization in infancy and exhibits pronounced age-dependent clinical heterogeneity. Fever becomes increasingly prevalent with age, yet whether febrile representation reflects a uniform inflammatory and immune phenotype across infancy remains unclear. In this prospective cohort of infants hospitalized with RSV bronchiolitis, we performed an integrated analysis of clinical features, pharyngeal microbiome composition, host transcriptomic profiles, and host-microbe interaction networks, with particular attention to age-related variation in fever-associated patterns. Clinically, fever prevalence exhibited a strong age-dependent increase across infancy. Correspondingly, canonical correspondence analysis identified age and fever as dominant gradients related to variation in both pharyngeal microbiome composition and host gene expression. Although no significant age-dependent correlations were observed at the global microbial and host transcriptomic levels in the fever-age interaction model, distinct patterns of microbial and host responses related to fever were observed across different age groups. Specifically, ranked gene set enrichment analysis indicated that febrile infants in early infancy showed relative attenuation of host defense-related programs, whereas older infants showed stronger enrichment of antiviral and inflammatory effector pathways, with more selective regulatory and signaling-associated patterns in late infancy. Integrated host-microbe network analysis further delineated a coherent developmental trajectory of fever-associated interaction architectures, evolving from densely interconnected regulatory networks in early infancy to modular, selectively coupled, host-centered configurations with advancing age. Together, febrile responses in RSV bronchiolitis should not be interpreted as a uniform biological phenotype across infancy and support age-aware interpretation of fever in pediatric RSV infection.
2026, 41(3): 586-601.
doi: 10.1016/j.virs.2026.05.004
Received: 12 November 2025
Accepted: 21 May 2026
Published: 27 May 2026
Mitochondrial homeostasis is intricately linked to the pathogenesis of many viral infections. The maintenance of mitochondrial homeostasis and normal cellular functions relies heavily on the delicate balance of mitochondrial dynamics. However, the precise impact of porcine epidemic diarrhea virus (PEDV) infection on mitochondrial dynamics and subsequent pathological processes is largely unexplored. In this study, through both in vivo and in vitro infections, we have demonstrated that PEDV infection induces mitochondrial fission and leakage of mtDNA by upregulating Drp1 expression, and identified Smad3 as a crucial transcription factor responsible for regulating Drp1 expression. By establishing an inflammatory model using PEDV-infected cells, we have identified Drp1-mediated mtDNA release as an upstream event triggering TLR9/NF-κB pathway activation during PEDV infection. These findings provide novel insights into the relationship between PEDV infection and host inflammatory responses from the perspective of mitochondrial dynamics.
2026, 41(3): 602-611.
doi: 10.1016/j.virs.2026.05.008
Received: 13 March 2026
Accepted: 27 May 2026
Published: 29 May 2026
African swine fever (ASF), caused by the African swine fever virus (ASFV), is characterized by high mortality in infected pigs. ASFV infection triggers severe inflammatory response in the host, which is a crucial contributor to the high lethality of this disease. However, the underlying mechanism by which ASFV infection induces inflammatory response is still poorly understood. In this study, we found that UV-inactivated ASFV induces interleukin-1β (IL-1β) production, suggesting that certain structural proteins incorporated in the virion possess the ability to trigger inflammatory response. Further investigations demonstrated that deletion of the ASFV A137R gene significantly inhibited the ASFV-induced upregulation of the mRNA transcription of various proinflammatory genes and phosphorylation of p65 and IκBα. Furthermore, the purified pA137R protein promoted the mRNA transcription of these proinflammatory genes and phosphorylation of p65 and IκBα. Additionally, pA137R protein interacted with the NACHT and LRR domains of NLRP3 through its N terminal 1-99 amino acid domain, thereby promoting the oligomerization of NLRP3 and ASC and subsequently facilitating NLRP3 inflammasome assembly. Collectively, our findings identify ASFV pA137R protein as a key proinflammatory determinant of ASFV, which not only advances our understanding of the molecular mechanisms underlying ASFV-induced inflammatory response but also provides new insights into ASFV pathogenesis.
2026, 41(3): 612-623.
doi: 10.1016/j.virs.2026.06.005
Received: 05 December 2025
Accepted: 05 June 2026
Published: 09 June 2026
Coronavirus envelope (E) proteins are small, highly conserved viroporins essential for virion assembly and pathogenicity. Despite extensive characterization of their ion channel activity, how host cells sense and dispose of excessive viral membrane proteins remains poorly understood. Here we show that expression of the MERS-CoV E protein triggers pronounced ER stress and autophagy activation in human cells. The E protein is selectively degraded through an RNF26-dependent autophagy-lysosome pathway, and inhibition of autophagy or loss of RNF26 function leads to E accumulation and sustained unfolded protein response. Mechanistically, RNF26, an ER-anchored E3 ubiquitin ligase, promotes RING-dependent clearance of the viral protein through an ER protein quality control-associated pathway linked to autophagy and ER stress adaptation. Disruption of this process establishes a self-amplifying ER stress-autophagy feedback loop that exacerbates proteotoxicity. These findings define a membrane homeostatic conflict between viral viroporins and the host defense machinery, and identify RNF26 as a potential therapeutic target for mitigating viroporin-induced cytotoxicity through host-directed intervention.
2026, 41(3): 624-637.
doi: 10.1016/j.virs.2026.06.007
Received: 09 March 2026
Accepted: 10 June 2026
Published: 13 June 2026
H9N2 avian influenza viruses (AIVs), which are enzootic in poultry and possess spillover potential to humans, represent a considerable global public health threat. Since 2021, we have observed an unprecedented decline in the ability of H9N2 viruses to agglutinate chicken red blood cells (CRBCs), a change that impairs effective detection in routine surveillance. Substituting CRBCs with turkey or guinea pig erythrocytes in hemagglutination assays effectively restored virus detectability. Through integrated bioinformatic and biological approaches, we identified that this phenotype is associated with specific amino acid substitutions at residues 131 and 132 of the 130-loop in the hemagglutinin (HA) protein. The HA motif 131/132-NT emerged in 2015 and rapidly increased in frequency, becoming the dominant pattern since 2021 in chickens and humans. Critically, the 131/132-NT motif attenuated viral binding affinity to short-chain α2,6-linked sialic acid receptors, explaining the loss of agglutination with CRBCs. Animal experiments further demonstrated that viruses carrying the HA 131/132-NT mutations maintained strong infectivity in chickens but altered tissue tropism in mice, showing reduced replication in the lungs. Collectively, our findings reveal a potential surveillance gap caused by reduced hemagglutination activity of H9N2 viruses, which may compromise the sensitivity of CRBC-based detection and potentially lead to under-detection of circulating viruses. Incorporating turkey or guinea pig red blood cells into surveillance protocols is therefore recommended to enhance detection sensitivity.
2026, 41(3): 638-650.
doi: 10.1016/j.virs.2026.06.008
Received: 12 April 2026
Accepted: 09 June 2026
Published: 13 June 2026
Host restriction factors and viral evasion strategies involved in the virus-host arms races remain to be discovered. Through an initial membrane protein-targeted CRISPR-Cas9 screening, we identified Acyl-CoA synthetase long-chain family member 3 (ACSL3) as a restriction factor against influenza A virus (IAV). Clinical transcriptomic analysis shows that ACSL3 is upregulated in peripheral blood mononuclear cells from mildly ill patients with influenza. Ectopic expression and loss-of-function validation demonstrate the physiological role of ACSL3 in restricting viral proliferation of diverse IAV subtypes (H1N1, H3N2, H3N8) in vitro and in vivo. Mechanistically, ACSL3 potentiates the antiviral unfolded protein response (UPR) by engaging the endoplasmic reticulum (ER) stress sensors IRE1α and PERK, thereby enhancing the IRE1α-XBP1-s driven inflammation and inhibiting the PERK-ATF4-CHOP mediated apoptosis. Conversely, IAV triggers the lysosomal degradation of ACSL3 and thus reprograms UPR to promote an immunologically silent apoptosis for viral egress and dissemination. Our findings establish ACSL3 as a molecular switch balancing the UPR-mediated antiviral response, and reveal a targeted viral evasion strategy in the virus-host interplay.
2026, 41(3): 651-661.
doi: 10.1016/j.virs.2026.05.006
Received: 03 February 2026
Accepted: 22 May 2026
Published: 29 May 2026
Enterovirus A71 (EV-A71) is the primary pathogen causing severe hand-foot-and-mouth disease (HFMD) in young children, with T-cell immune dysfunction closely linked to severe clinical outcomes. However, the molecular mechanisms underlying EV-A71-mediated T-cell impairment remain unclear, and no specific therapies are currently available. Here, we investigated the interaction between EV-A71 and T cells, and explored potential targeted therapeutic strategies. Our results showed that EV-A71 efficiently infects T cell lines (Jurkat, EL-4) and primary mouse CD3+ T cells in a dose- and time-dependent manner, inducing T-cell death and upregulating pro-inflammatory cytokines (IL-1β, IL-6, TNF-α). Mechanistically, EV-A71 infection triggers GSDME-dependent pyroptosis in T cells via caspase-3 activation, rather than GSDMD-dependent pyroptosis, as evidenced by genetic ablation and inhibitor experiments. Methylcobalamin (MeCbl), a specific GSDME inhibitor, rescued EV-A71-induced T-cell loss, and significantly improved the survival rate (80%) of EV-A71-infected newborn mice. Furthermore, the combined treatment with MeCbl and AGS-A (a T cell-dependent therapeutic agent) exerted a synergistic protective effect, achieving 90% survival rate in wild-type mice, which was abrogated in T cell-deficient BALB/c-nu-/- mice. Collectively, our findings identify GSDME-dependent T-cell pyroptosis as a key pathogenic mechanism of EV-A71 infection and highlight MeCbl as a promising targeted agent for HFMD treatment, either used alone or in combination with AGS-A.
2026, 41(3): 662-675.
doi: 10.1016/j.virs.2026.06.002
Received: 07 December 2025
Accepted: 01 June 2026
Published: 03 June 2026
Saponin C (also known as DT-13) is the dominant ingredient extracted from the tuber of Liriope muscari (Decne.) L. H. Bailey, which exhibits multiple pharmacological activities, including anti-tumor, anti-thrombotic, cardioprotective and anti-inflammatory effects. However, its antiviral potential remains unexplored. This study aimed to investigate the inhibitory activity and underlying mechanisms of Saponin C against both influenza A virus (IAV) and SARS-CoV-2. In vitro experiments demonstrated that Saponin C dose-dependently inhibited IAV replication in MDCK and A549 cells. Time-of-addition assay revealed that Saponin C targeted the post-entry stages of IAV replication by impairing viral ribonucleoprotein (vRNP) function. This was evidenced by the suppression of viral polymerase activity, reduction of viral RNA synthesis, and delayed nuclear export of vRNP. The in vivo efficacy was further validated in a lethal H1N1 mouse model, where both prophylactic and therapeutic administration of Saponin C significantly improved the survival rate of infected mice, reduced viral loads in lung tissues, and attenuated virus-induced pulmonary inflammation in a dose-dependent manner. Beyond IAV, Saponin C also effectively inhibited SARS-CoV-2 infection by blocking viral entry, specifically through interfering with the binding of viral spike protein to the human ACE2 receptor and suppressing spike-mediated membrane fusion. Collectively, these findings demonstrate that Saponin C possesses antiviral potential against IAV and SARS-CoV-2, and may thus serve as a promising therapeutic agent for the treatment of respiratory viral infections.
2026, 41(3): 676-687.
doi: 10.1016/j.virs.2026.06.003
Received: 18 January 2026
Accepted: 01 June 2026
Published: 04 June 2026
Klebsiella pneumoniae is an important opportunistic pathogen in both humans and animals. Controlling it has become increasingly difficult due to the rapid spread of antimicrobial resistance. In this study, we isolated and characterized a novel lytic bacteriophage, vB_Kp_Z1, and evaluated its therapeutic efficacy against K1-serotype K. pneumoniae. Host range analysis showed that vB_Kp_Z1 was strictly specific to K1 strains, as confirmed across multiple prevalent capsular types. The in vivo efficacy of vB_Kp_Z1 was assessed using intraperitoneal infection models in mice. Two hypervirulent K1 strains were used: a pigeon-derived strain (KP1897) and a human clinical strain (KP177). Phage treatment significantly improved survival compared with phosphate-buffered saline-treated controls. It provided complete protection in KP1897-infected mice and achieved an 87.5% survival rate in KP177-infected mice. In addition, phage administration markedly reduced bacterial loads in the blood, liver, and lungs, indicating effective control of systemic dissemination. These findings demonstrate that vB_Kp_Z1 is a K1-specific bacteriophage with therapeutic potential against hypervirulent K. pneumoniae, including strains from different host species.
A C-type single-domain antibody with protective efficacy against H1N1 via respiratory administration
2026, 41(3): 688-699.
doi: 10.1016/j.virs.2026.05.007
Received: 03 March 2026
Accepted: 25 May 2026
Published: 28 May 2026
Influenza A viruses, particularly H1N1, pose a significant public health threat, highlighting the continued need for novel prophylactics and therapeutics. Monoclonal antibodies are promising, but conventional IgGs face challenges in respiratory delivery due to their large size. This study presents A1-B7, a C-type single-domain antibody (C-sdAb) based on a scaffold derived from a human IgG1 CH2 domain, targeting the hemagglutinin (HA) of H1N1 influenza virus. A1-B7 potently neutralizes multiple H1N1 subtypes in vitro. Both prophylactic intranasal administration and therapeutic aerosol inhalation of A1-B7 confer complete protection and reduce live virus in the lungs to undetectable levels. Structural prediction and epitope mapping reveal that A1-B7 binds a conserved stem-region epitope, engaging the HA2 A-helix and a hydrophobic groove. A1-B7 can block low-pH induced conformational change of HA. These findings establish A1-B7 as a promising candidate for further development as a convenient, respiratory tract delivered countermeasure against influenza.
2026, 41(3): 700-710.
doi: 10.1016/j.virs.2026.06.011
Received: 10 December 2025
Accepted: 16 June 2026
Published: 19 June 2026
The recent global outbreak of mpox virus (MPXV) infections underscores the urgent need for antiviral therapies against orthopoxviruses. In this study, using a high-content screening (HCS) platform based on a modified vaccinia virus Tiantan strain with GFP insertion (MVTT-GFP) under BSL-2 conditions, we screened 1513 kinase inhibitors for antiviral activity. Among these, Bruton's tyrosine kinase inhibitor BTKi-2 emerged as a potent candidate, exhibiting IC50 of 0.535 μM against vaccinia virus (VACV) and 0.260 μM against MPXV in vitro, while maintaining low cytotoxicity. In a murine model of VACV-induced pneumonia, BTKi-2 treatment reduced lung viral loads by 90% and a significantly improved survival compared to vehicle-treated controls. Notably, mechanistic studies indicate that BTKi-2's antiviral effects cannot be completely attributed to the inhibition of BTK or EGFR/ErbB2 signaling. These findings highlight BTKi-2 as a promising antiviral agent in vitro and in vivo, suggesting that BTKi-2 may offer a potential avenue for future therapeutic development against orthopoxvirus infections.
2026, 41(3): 711-715.
doi: 10.1016/j.virs.2026.05.005
Received: 09 February 2026
Accepted: 21 May 2026
Published: 27 May 2026
Highlights
1 First report of HPgV genotype 3 strains in Heilongjiang, China, revealing its genetic diversity in East Asia.
2 Phylogeographic analysis demonstrated spatial clustering in the distribution of human pegivirus genotypes 1-6.
3 Identified an anomalous evolutionary branch in the NS4A region and ten specific amino acid mutation sites.
4 Subgenomic alignments yield different lineage calls, necessitating full-length genomes for accurate genotyping.
1 First report of HPgV genotype 3 strains in Heilongjiang, China, revealing its genetic diversity in East Asia.
2 Phylogeographic analysis demonstrated spatial clustering in the distribution of human pegivirus genotypes 1-6.
3 Identified an anomalous evolutionary branch in the NS4A region and ten specific amino acid mutation sites.
4 Subgenomic alignments yield different lineage calls, necessitating full-length genomes for accurate genotyping.
2026, 41(3): 716-719.
doi: 10.1016/j.virs.2026.05.010
Received: 14 March 2026
Accepted: 29 May 2026
Published: 03 June 2026
Highlights
1 The nucleotide analog bemnifosbuvir (AT-527) inhibits hepatitis E virus (HEV) infection in cell and organoid models.
2 Supplementation with guanosine largely reversed the anti-HEV activity of AT-527.
3 Combining AT-527 with ribavirin or interferon-α resulted in synergistic antiviral effects.
1 The nucleotide analog bemnifosbuvir (AT-527) inhibits hepatitis E virus (HEV) infection in cell and organoid models.
2 Supplementation with guanosine largely reversed the anti-HEV activity of AT-527.
3 Combining AT-527 with ribavirin or interferon-α resulted in synergistic antiviral effects.
2026, 41(3): 720-723.
doi: 10.1016/j.virs.2026.06.009
Received: 03 April 2026
Accepted: 08 June 2026
Published: 13 June 2026
Highlights
1 A novel iELISA utilizing ferritin-nanoparticle-displayed PDCoV S protein was established.
2 Excellent diagnostic performance with high sensitivity, specificity, and correlation with NAb titers.
3 Revealed widespread PDCoV circulation (48.64%) in the surveyed provinces of China, supporting field epidemiological studies.
1 A novel iELISA utilizing ferritin-nanoparticle-displayed PDCoV S protein was established.
2 Excellent diagnostic performance with high sensitivity, specificity, and correlation with NAb titers.
3 Revealed widespread PDCoV circulation (48.64%) in the surveyed provinces of China, supporting field epidemiological studies.
2026, 41(3): 724-727.
doi: 10.1016/j.virs.2026.06.012
Received: 14 May 2026
Accepted: 17 June 2026
Published: 19 June 2026
Highlights
1 Construction of a MAYV replicon expressing both PAC and Rluc genes.
2 A stable BHK-21 cell line containing MAYV-Rep with puromycin selection was obtained.
3 A robust replicon cell-based HTS assay based was established.
1 Construction of a MAYV replicon expressing both PAC and Rluc genes.
2 A stable BHK-21 cell line containing MAYV-Rep with puromycin selection was obtained.
3 A robust replicon cell-based HTS assay based was established.
2026, 41(3): 728-731.
doi: 10.1016/j.virs.2026.06.010
Received: 05 June 2025
Accepted: 15 June 2026
Published: 17 June 2026
Highlights
1 First set of three complete genomic sequences of RABV strains was obtained from Sierra Leone.
2 Phylogenetic analysis identified the endemic Africa 2H subclade with high homology to those from neighboring countries.
3 Low dog vaccination coverage underscores urgent need for coordinated vaccination and surveillance.
1 First set of three complete genomic sequences of RABV strains was obtained from Sierra Leone.
2 Phylogenetic analysis identified the endemic Africa 2H subclade with high homology to those from neighboring countries.
3 Low dog vaccination coverage underscores urgent need for coordinated vaccination and surveillance.

