Abstract Background Mpox, caused by monkeypox virus (MPXV), remains a public health priority. Standard qPCR detects viral DNA but cannot distinguish infectious virions from residual genetic material of inactivated virus, complicating transmission risk assessment. This study aimed to develop a rapid assay for quantifying infectious MPXV across clinical and environmental matrices in Guangdong Province, China. Methods We developed a propidium monoazide-assisted qPCR (PMA-qPCR) assay that selectively amplifies DNA from intact virions, and embedded it within the Guangdong provincial Center for Disease Control and Prevention surveillance network. We examined 23 clinical fluid specimens from 15 mpox patients, 337 surface swabs and 53 domestic wastewater samples from patient living environments, and 498 terminal wastewater samples from flights and sewage treatment plants collected between June 2023 and August 2024. Decay kinetics were evaluated at 25 °C and 30 °C under varying pH, with initial viral loads of 10 3 and 10 4 PFU/mL. Results PMA-qPCR discriminated infectious from non-infectious virus. Co-incubation with 50 μM PMA and 0.005% SDS effectively blocked amplification of non-infectious DNA, and the assay showed quantitative concordance with the standard plaque assay. Infectious MPXV loads were highest in skin lesions and anal swabs, exceeding throat swabs by more than 100-fold. Among surface samples, 41.54% (140/337) tested positive for MPXV DNA by qPCR, but only 25.71% (36/140) of these contained infectious virus at low loads (126.79 ± 93.57 PFU/mL). For wastewater, 11.32% (6/53) of domestic samples from patient living environments tested positive by qPCR, yet no infectious MPXV was detected. No MPXV DNA was detected in 498 terminal wastewater samples from flights or sewage treatment plants. Decay experiments demonstrated that when the initial concentration was 10 3 to 10 4 PFU/mL, infectious MPXV decreased by more than 99% within 48 h, with accelerated decay under acidic pH and elevated temperature, particularly at lower initial concentrations. Conclusions PMA-qPCR provides a practical tool for rapid cross-matrix quantification of infectious MPXV. Direct contact with skin lesions or anal secretions likely dominates transmission, whereas environmental persistence is limited. Testing for infectious virus within 48 h of collection is recommended, as infectious MPXV decays by over 99% within this window.

Zika virus (ZIKV) is a key member of the Flavivirus genus that has emerged as a major global public health concern. The fusion loop region (residues 98-110), located within domain II of the envelope protein, is highly conserved among flaviviruses, including ZIKV and Japanese encephalitis virus (JEV). However, the functional consequences of such conservation for cross-reactive immunity remains unclear. Here, we integrated bioinformatic analyses, functional assays in vitro and mouse models in vivo to systematically determine the effects of antibodies directed against the JEV fusion loop (FL) region on ZIKV infection. Sequence alignment and structural analysis revealed complete amino acid identity and almost identical three-dimensional conformations between the FL regions of the two viruses, providing a molecular basis for cross-reactivity. Antisera generated against the JEV FL region recognized ZIKV particles and displayed concentration-dependent bidirectional effects. Increased and decreased antibody levels respectively neutralized viral entry and replication, and facilitated infection via antibody-dependent enhancement (ADE). These effects were confirmed in vivo, in which high and low antibody doses reduced tissue pathology and improved survival, and increased viremia and exacerbated inflammatory responses, respectively. These findings highlight the importance of antibody concentration in determining whether cross-reactive responses to conserved structural elements engender neutralization or enhancement response. Our findings provide experimental evidence for assessing ZIKV susceptibility in JEV-vaccinated populations and offer structural insights for designing flavivirus vaccines that maximize protection while minimizing ADE risk. These findings further highlight potential pathogenic and clinical considerations for optimizing vaccine formulations to reduce cross-reactive enhancement risks.

The membrane fusion process, mediated by the entry fusion complex (EFC) of the monkeypox virus (MPXV), is crucial for host cell invasion. Apolipoprotein B mRNA Editing Catalytic Polypeptide-like 3 (APOBEC3)-driven mutation bias is a key factor in MPXV’s adaptive evolution during its global spread. However, how these mutations affect the structure and function of EFC proteins remains poorly understood. To address this, we performed genomic mutation analysis on globally circulating MPXV clades Ib and IIb, combined with protein monomer, binary, and quaternary complex structure modeling based on AlphaFold 3 and experimental validation by ELISA. We first delineated the mutational spectra of all 11 EFC proteins, revealing that although EFC proteins in clade Ib are highly conserved, lineage IIb B exhibits extensive APOBEC3-driven mutations and the G9 M142I mutation is identified as a lineage-associated APOBEC3-type mutation of lineage IIb B. Structural predictions revealed that while the M142I mutation does not alter G9 monomer folding, it induces a conformational shift in the G9/A16 subcomplex. Furthermore, within the predicted G9/A16/A56/K2 quaternary complex, this mutation enlarges the interfacial gap and reduces docking stability between the G9/A16 subcomplex and A56/K2. Experimental validation demonstrated that the M142I mutation significantly reduces the binding affinity of G9 for A16 and impairs the recruitment of A56/K2 to the quaternary complex, confirming the computationally predicted mechanism of interface destabilization. These findings highlight a dynamic interplay between APOBEC3-driven evolution and EFC protein structure, demonstrating that the M142I mutation alters EFC complex assembly dynamics and may shift the regulatory balance of the membrane fusion system. These structural changes provide molecular insights into MPXV lineage differentiation, though direct functional assays are required to determine the net effect on viral entry efficiency.

IntroductionDefective viral genomes (DVGs) have been detected in clinical samples, and their antiviral effects have been verified. However, due to the limitations of traditional methods, all the reported DENV DVGs to date are Deletion DVGs, and it has not been proven that these DVGs can be stabilized across different hosts.MethodsWe used the bioinformatics software DVGfinder with various dengue virus NGS data, including samples from patients, Aedes albopictus, C6/36 cells, and Vero cells, to identify DVGs. We compared the distribution of DVGs across different hosts and analyzed the dynamics of DENV-1 DVGs during serial passaging, identifying DVGs that are stably maintained across hosts.ResultsFirst of all, we found copyback type DVGs in different datasets, with the dominant DVGs in patient sera being 3’ copyback. Secondly, we observed that in C6/36 cells and Aedes albopictus, the DVGs did not change significantly with DENV-1 passages, while in Vero cells, the number of specific Deletion DVGs continuously increased with DENV-1 passage. Finally, using clustering algorithms, we identified a set of candidate deletion DVGs predicted to stably exist across different hosts. One of these candidates, designated DeletionA6 (BP 1320, RI 7700), was experimentally validated by nested PCR in sera from patients infected with DENV-1 to DENV-4.DiscussionThis study describes the distribution patterns of DVGs across different samples and provides preliminary bioinformatic evidence for a subset of deletion DVGs.

Marine algal polysaccharides have been widely investigated as antiviral candidates, yet nearly all anti-dengue studies have focused on sulfated species. Whether algal polysaccharides lacking prominent sulfation can inhibit dengue virus (DENV) remains unexplored. Here, we profiled the stage-specific antiviral activity of a heteropolysaccharide (GLHP) from Gracilaria lemaneiformis, whose Fourier-transform infrared (FT-IR) spectrum lacks characteristic sulfate ester absorption bands, against DENV serotype 2 (DENV-2) in Huh7 and BHK-21 cells. GLHP exhibited low cytotoxicity (CC50 exceeding 1000 μg/mL in Huh7 cells and approximately 950 μg/mL in BHK-21 cells). Time-of-addition analysis revealed that co-inoculation GLHP treatment (Co-inoc.) produced the strongest and most consistent inhibition of intracellular viral RNA, whereas pre-inoculation GLHP treatment (Pre-inoc.) was ineffective, indicating that the antiviral activity is predominantly associated with the virus–cell contact and entry stage. GLHP additionally reduced extracellular progeny virus output under post-inoculation GLHP treatment (Post-inoc.) conditions, and this reduction exceeded the corresponding change in intracellular viral RNA levels, suggesting an additional effect that may involve either a late replication step or secondary entry blockade of progeny virions. Attenuation of virus-induced cytopathic effects under Co-inoc. conditions further supported the antiviral activity. To our knowledge, these findings identify GLHP as the first non-sulfated marine polysaccharide shown to exhibit stage-defined antiviral activity against DENV-2 and support further investigation of its antiviral potential and structural determinants.

IntroductionDengue virus (DENV) neurological complications are increasingly reported, yet the viral genetic determinants of neurotropism remain poorly characterized.MethodsWe screened 25 DENV1 clinical isolates from the 2014 outbreak in Guangdong, China, for neurotropism in suckling mice, and integrated comparative genomics, pre-expression functional assays, population-scale sequence analysis, and OpenFold3 structural modeling to identify mutations associated with enhanced neuroinvasion.ResultsWe found that only strain P1253 induced neurological symptoms and mortality via subcutaneous inoculation, producing cortical-selective lesions distinct from the diffuse encephalitic damage observed after intracranial inoculation, and P1253 replicated preferentially in human brain microvascular endothelial cells (HBMEC) compared to contemporaneous strains. Comparative genomics identified three unique mutations in P1253 (NS1 175Y→H, NS2A 89V→F, NS4A 2V→I), and pre-expression assays demonstrated that only NS2A 89V→F significantly enhanced viral replication and cytopathic effect in HBMEC. Analysis of 1,990 complete DENV1 genomes revealed five natural mutant types in the NS2A 89 -96 residue region, with P1253 representing the FIPI quadruple-mutant type, and OpenFold3 structural prediction showed that 89V→F introduced on the VIPI background induced the most significant distal domain reorientation (RMSD 1.605 Å), increasing the centroid-to-centroid distance between residues 89 -96 and 185 -218 from 18.221 Å to 27.462 Å.DiscussionThese findings identify NS2A 89V→F as a candidate adaptive mutation associated with enhanced neurotropism in DENV1 and provide a framework for monitoring neurovirulent variants.

Enterohemorrhagic Escherichia coli (EHEC) O157:H7 is a foodborne pathogen that causes a variety of diseases, ranging from self-limiting gastroenteritis to life-threatening extra-intestinal diseases such as hemolytic uremic syndrome. EspF, an effector protein secreted by the type III secretion system of EHEC, is primarily responsible for the development of inflammatory colitis. Our previous study revealed that EspF interacts with the host Annexin A6 (ANXA6) protein and targets the endoplasmic reticulum (ER). Given the critical effects of ER stress on the host responses of gastroenteritis, we explored the role of EspF–ANXA6 interaction in ER stress. Caco-2 cells were infected with different strains of EHEC and transfected with modified plasmids to establish in vitro research models. Our results revealed that infection with espF-deletion EHEC strains significantly exacerbated ER stress. Specifically, the phosphorylation of eIF2α was elevated, and the expression levels of BiP, ATF4, and CHOP were increased by more than 15% compared to those in cells infected with wild-type EHEC strains. Further experiments showed that EspF co-localizes with BiP and down-regulates the PERK pathway. Meanwhile, the EspF–ANXA6 interaction could aggravate the inhibition of the PERK pathway and stimulate calcium influx to disturb ER homeostasis, eventually leading to apoptosis. Our findings suggest that the EspF–ANXA6 interaction could inhibit ER stress through the PERK pathway, which may limit cell-to-cell communication and block the clearance of bacteria in host cells.

Autophagy is a critical host defense mechanism against pathogens; however, enterohemorrhagic Escherichia coli (EHEC) O157:H7 exploits it to establish infection. Here, we revealed how EHEC's effector EspF collaborates with host Annexin A6 (ANXA6) to suppress autophagy and drive inflammation. Our results showed that CRISPR/Cas9-mediated anxa6 knockout in intestinal epithelial cells reversed EHEC-induced autophagic inhibition, as evidenced by elevated LC3B-II levels and reduced p62 accumulation. Mechanistically, EspF stabilizes ANXA6 to disrupt PI3K/mTOR signaling and impair autophagosome formation, whereas ANXA6 suppresses the expression of ATG16L1, a key autophagy regulator. In this study, EHEC infection triggered IL-1β hypersecretion in macrophages, which was coupled with NF-κB pathway hyperactivation via IκBα/p65 phosphorylation. In vivo, EHEC infection regulated intestinal ANXA6 expression, correlating with mucosal inflammation and barrier dysfunction. Crucially, ANXA6/ATG16L1 axis disruption created a self-reinforcing cycle of impaired autophagy, bacterial persistence, and inflammatory escalation. Our findings identified ANXA6 as a context-dependent autophagy modulator and ATG16L1 as a novel EHEC target, providing mechanistic insights into EHEC pathogenesis.

Effective mouse models for testing antiviral medications should be both cost-effective and require minimal labor. Immunodeficient mouse models, such as AG129, are commonly used in dengue virus (DENV) research; however, their high import and maintenance costs make them relatively expensive. Moreover, the absence of IFN-γ signaling limits the capacity of the AG129 model. To date, wild-type mouse models of DENV infection have only exhibited mild symptoms without lethality, limiting their research applicability. In this study, we developed a lethal C57BL/6 wild-type mouse model infected with DENV-2 365 strain. By blocking the type I interferon receptor before the virus challenge, we allowed the immune response to be restored at a later stage of infection. Following infection, the mice exhibited severe symptoms, including weight loss, high viremia levels, elevated inflammatory cytokines, significant vascular leakage, and pathological changes in the brain, kidney, liver and spleen. The model also displayed severe central nervous symptoms and 100

Defective viral genomes (DVGs) are fragments derived from defective interfering particles (DIPs) that form during viral replication. They play important roles by interfering with complete virus replication and regulating host immune responses. Advances in high-throughput sequencing (HTS) and bioinformatic technology have significantly improved the ability to identify DIPs and DVGs. Their heterogeneity and dynamic formation mechanisms have been analyzed using long-read sequencing technologies. Both DIPs and DVGs inhibit wild-type viral proliferation by competing for viral replication resources and activating innate immune pathways such as those of retinoic acid-inducible gene 1 and mitochondrial antiviral signaling protein. This might influence infection outcomes by regulating inflammatory cytokine storms. The clinical application of DIPs and DVGs in their natural attenuated virus forms has been investigated in terms of novel vaccine design and antiviral therapy. This report systematically reviews cutting-edge detection techniques, molecular mechanisms, and translational medicine advances of DIPs and DVGs and provides a theoretical basis for developing broad-spectrum antiviral strategies based on DIPs.

Chlamydia trachomatis, the most prevalent bacterial agent of sexually transmitted infections, poses a significant threat to reproductive health. The release of progeny through the orchestrated lysis of host cells plays a crucial role for the development of new infections, though the underlying molecular mechanisms remaining largely unexplored. In this study, we identified a novel mechanism by which Chlamydia induces host cell ferroptosis to facilitate its progeny release. This process involves the degradation of the host protein SLC7A11 by the chlamydial protease-like activity factor (CPAF), resulting in glutathione depletion and subsequent cell death characterized by lipid peroxidation. Infection with a CPAF-deficient strain fails to induce host cell ferroptosis. Notably, inhibiting ferroptosis by vitamin E reduces the Chlamydia burden in low genital tract of mice and trends toward attenuation of pathology. These findings provide new insights into the conserved survival strategies of Chlamydia and understanding of its pathogenesis.

Recently, exopolysaccharides (EPS) were found to alleviate cadmium (Cd) toxicity to crops by regulating the antioxidant system, but the mechanism remains unclear. Herein, by quantitative and transcriptomic approaches, a systematical map of the changes in the antioxidant system was drawn to dissected the underlying mechanism. The results demonstrated that the ascorbate-glutathione cycle (ASA-GSH cycle) is a major contributor. Specifically, compared to the control, the rice exposed to Cd exhibited a significant increase in the GSH pool (about 9-fold at 7 d), but a continuous decrease in the ASA pool (only 15.42% remained at 15 d) and an excessive accumulation of reactive oxygen species (ROS). Interestingly, with the addition of EPS, the increase of the GSH pool significantly slowed down (decreased by 180.18% at 7 d, compared to the Cd-stressed treatment), and the ASA pool remained high (consistently above 70.00% of the control group). ROS also maintained at a good level. Moreover, the activities of enzymatic antioxidants showed the similar trend. By RNA-Seq analysis, multiple genes enriched in ASA-GSH related pathway were screened (such as OsRBOHB, OsGST, OsPOD) for further study. This study provides a foundation for EPS application in agriculture, which also establishes a better way for analyzing antioxidant system.

Microbial remediation of cadmium-contaminated soil offers advantages like environmental friendliness, cost-effectiveness, and simple operation. However, the efficacy of this remediation process relies on obtaining dominant strains and a comprehensive understanding of their Cd adsorption mechanisms. This study identified two Cd-resistant bacteria, Burkholderia sp. 1-22 and Bacillus sp. 6-6, with significant growth-promoting effects from rice rhizosphere soil. The strains showed remarkable Cd resistance up to ∼200mg/L and alleviated Cd toxicity by regulating pH and facilitating bacterial adsorption of Cd. FTIR analysis showed crucial surface functional groups, like carboxyl and amino groups, on bacteria played significant roles in Cd adsorption. The strains could induce CdCO3 formation via a microbially induced calcium precipitation (MICP) mechanism, confirmed by SEM-EDS, X-ray analysis, and elemental mapping. Pot experiments showed these strains significantly increased organic matter and enzyme activity (e.g., urease, sucrase, peroxidase) in the rhizosphere soil versus the control group. These changes are crucial for restricting Cd mobility. Furthermore, strains 6-6 and 1-22 significantly enhance plant root detoxification of Cd, alleviating toxicity. Notably, increased pH likely plays a vital role in enhancing Cd precipitation and adsorption by strains, converting free Cd into non-bioavailable forms.

ABSTRACT Attaching/effacing (A/E) pathogens induce DNA damage and colorectal cancer by injecting effector proteins into host cells via the type III secretion system (T3SS). EspF is one of the T3SS-dependent effector proteins exclusive to A/E pathogens, which include enterohemorrhagic Escherichia coli . The role of EspF in the induction of double-strand breaks (DSBs) and the phosphorylation of the repair protein SMC1 has been demonstrated previously. However, the process of damage accumulation and DSB formation has remained enigmatic, and the damage response is not well understood. Here, we first showed a compensatory increase in the mismatch repair proteins MutS homolog 2 (MSH2) and MSH6, as well as poly(ADP-ribose) polymerase 1, followed by a dramatic decrease, threatening cell survival in the presence of EspF. Flow cytometry revealed that EspF arrested the cell cycle at the G2/M phase to facilitate DNA repair. Subsequently, 8-oxoguanine (8-oxoG) lesions, a marker of oxidative damage, were assayed by ELISA and immunofluorescence, which revealed the accumulation of 8-oxoG from the cytosol to the nucleus. Furthermore, the status of single-stranded DNA (ssDNA) and DSBs was confirmed. We observed that EspF accelerated the course of DNA lesions, including 8-oxoG and unrepaired ssDNA, which were converted into DSBs; this was accompanied by the phosphorylation of replication protein A 32 in repair-defective cells. Collectively, these findings reveal that EspF triggers various types of oxidative DNA lesions with impairment of the DNA damage response and may result in genomic instability and cell death, offering novel insight into the tumorigenic potential of EspF. IMPORTANCE Oxidative DNA lesions play causative roles in colitis-associated colon cancer. Accumulating evidence shows strong links between attaching/effacing (A/E) pathogens and colorectal cancer (CRC). EspF is one of many effector proteins exclusive to A/E pathogens with defined roles in the induction of oxidative stress, double-strand breaks (DSBs), and repair dysregulation. Here, we found that EspF promotes reactive oxygen species generation and 8-oxoguanine (8-oxoG) lesions when the repair system is activated, contributing to sustained cell survival. However, infected cells exposed to EspF presented 8-oxoG, which results in DSBs and ssDNA accumulation when the cell cycle is arrested at the G2/M phase and the repair system is defective or saturated by DNA lesions. In addition, we found that EspF could intensify the accumulation of nuclear DNA lesions through oxidative and replication stress. Overall, our work highlights the involvement of EspF in DNA lesions and DNA damage response, providing a novel avenue by which A/E pathogens may contribute to CRC.

This study presents a comparison between two hydrolysis systems (MnO 2 /H 2 O 2 and ascorbic acid (VC)/H 2 O 2 ) for the depolymerization of exopolysaccharide (EPS) from Lactobacillus plantarum LPC-1. Response surface methodology (RSM) was used to optimize these two degradation systems, resulting in two H 2 O 2 -free degradation products, MEPS (MnO 2 /H 2 O 2 -treated EPS) and VEPS (VC/H 2 O 2 -treated EPS), where H 2 O 2 residues in the final products and their antioxidant activity were considered vital points. The relationship between the structural variations of two degraded polysaccharides and their antioxidant activity was characterized. Physicochemical tests showed that H 2 O 2 had a notable impact on determining the total and reducing sugars in the polysaccharides, and both degradation systems efficiently eliminated this effect. After optimization, the average molecular weight of EPS was reduced from 265.75 kDa to 135.41 kDa (MEPS) and 113.11 kDa (VEPS), improving its antioxidant properties. Characterization results showed that the two hydrolysis products had similar major functional groups and monosaccharide composition as EPS. The crystal structure, main chain length, and branched chain number were crucial factors affecting the biological activity of polysaccharides. In pot testing, two degraded polysaccharides improved spinach quality more than EPS due to their lower molecular weights, suggesting the advantages of low-molecular-weight polysaccharides. In summary, these two degradation techniques offer valuable insights for further expanding the utilization of microbial resources.

Objectives: The aim of this study was to prepare monoclonal antibodies (mAbs) that broadly target Acinetobacter baumannii and protect against infection by multi-drug-resistant (MDR) A. baumannii from different sources. Methods: mAb 8E6 and mAb 1B5 were prepared by sequentially immunizing mice with a sublethal inoculation of three heterogeneous serotypes of pan-drug-resistant (PDR) A. baumannii, ST-208, ST-195, and ST-229. Results: The cross-recognition of heterogeneous bacteria (n = 13) by two mAbs and potential targets was verified, and the in vitro antibacterial efficacy of mAbs was assessed. The median killing rate of mAb 8E6 against A. baumannii in the presence of complement and dHL-60 cells was found to be 61.51%, while that of mAb 1B5 was 41.96%. When only dHL-60 cells were present, the killing rate of mAb 8E6 was 65.73%, while that of mAb 1B5 was 69.93%. We found that mAb 8E6 and mAb 1B5 broadly targeted MDR A. baumannii on the ATP synthase complex and were equipped with an antibacterial killing ability by enhancing the innate immune bacteriolytic effect of ST-208 and ST-195 strains. Both monoclonal antibodies were validated to protect against respiratory infection at 4 and 24 h via enhancing the release of innate immune substances and inflammatory cytokines, effectively shortening the disease period in mice. Conclusions: mAb 8E6 and mAb 1B5 significantly enhanced the opsonization process of phagocytosis against A. baumannii strains prevalent in southern China by targeting ATP synthase antigens thereof, resulting in protective effects in mice.

ABSTRACTHuman adenovirus (HAdV) infects the respiratory system, thus posing a threat to health. However, immunodiagnostic reagents for human adenovirus are limited. This study aimed to develop efficient diagnostic reagents based on monoclonal antibodies for diagnosing various human adenovirus infections. Evolutionary and homology analyses of various human adenoviral antigen genes revealed highly conserved antigenic fragments. The prokaryotic expression system was applied to recombinant penton, hexon, and IVa2 conserved fragments of adenovirus, which were injected into BALB/c mice to prepare human adenovirus-specific monoclonal antibodies. Enzyme-linked immunosorbent assay (ELISA), indirect immunofluorescence assay (IFA), and Western blotting were used to determine the immune specificity of the monoclonal antibodies. Indirect ELISA showed that monoclonal antibodies 1F10, 8D3, 4A1, and 9B2 were specifically bound to HAdV-3 and HAdV-55 and revealed high sensitivity and low detection limits for various human adenoviruses. Western blotting showed that 1F10 and 8D3 specifically recognized various human adenovirus types, including HAdV-1, HAdV-2, HAdV-3, HAdV-4, HAdV-5, HAdV-7, HAdV-21, and HAdV-55, and 4A1 specifically recognized HAdV-1, HAdV-2, HAdV-3, HAdV-5, HAdV-7, HAdV-21, and HAdV-55. IFAs showed that 1F10, 8D3, and 4A1 exhibited highly selective localization to A549 cells infected with HAdV-3 and HAdV-55. Finally, two antibody pairs that could detect hexon antigens HAdV-3 and HAdV-55 at low concentrations were developed. The monoclonal antibodies developed in this study show potential for detecting human adenoviruses.IMPORTANCEIn this study, we selected the three most conserved antigenic fragments of human adenovirus to prepare a murine monoclonal antibody for the first time, and human adenovirus antigenic fragments with heretofore unheard of degrees of conservatism were isolated. The three monoclonal antibodies with the ability to recognize human respiratory adenovirus over a broad spectrum were screened by hybridoma and monoclonal antibody preparation. Human adenovirus infections are serious; however, therapeutic drugs and diagnostic reagents are scarce. Thus, to reduce the serious consequences of human viral infections and adenovirus pneumonitis, early diagnosis of infection is required. The present study provides three monoclonal antibodies capable of recognizing a wide range of human adenoviruses, thereby offering guidance for subsequent research and development.

This study compared the humoral immune characteristics of children, elderly people, pregnant women, and adults infected with BA.5 and XBB strains in Guangzhou, China. It was found that binding and neutralizing antibodies the titers against distinct SARS-CoV-2 strains were low in the acute-phase sera of BA.5 infected patients, while the corresponding titers were significantly increased in the convalescent phase, the antibody titers against the Wuhan strain were the highest. Regardless of whether they were vaccinated, BA.5 infection did not induce high neutralizing antibodies against XBB. During the recovery phase, the titers of antiviral antibodies in the vaccinated population are more robust than those in the unvaccinated population. For BA.5 infections, the specific binding and neutralizing antibody titers in the children group were lower compared to other population groups. In the convalescence period of the disease, the titers of neutralizing antibodies against Wuhan, BA.5 and XBB strains induced by BA.5 infections are significantly correlated in pairs. XBB can induce a broader and balanced antiviral humoral immune response than BA.5 as a first-time infected strain. This finding can provide a reference for the judgment of the future epidemic law of SARS-CoV-2, and provide a scientific basis for developing novel COVID-19 vaccines, especially for discovering customized vaccines and immune strategies for different populations.