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influenza vaccine (MonoGrippol Neo)

✓ Approved

Npo Petrovax Pharm · 疫苗 · 疫苗

什么是 influenza vaccine?

influenza vaccine 是一种疫苗,由Npo Petrovax Pharm研发。该药已获批,用于治疗相关适应症,给药途径:Injectable (Others)、Intramuscular (IM) Injection、Subcutaneous Injection。

药物档案

商品名MonoGrippol Neo
公司Npo Petrovax Pharm
药物类别疫苗, 大分子
给药途径Injectable (Others), Intramuscular (IM) Injection, Subcutaneous Injection
状态Approved

相关研究文献

PubMedmBio2026-09-10

Sex and age differences in antibody responses to seasonal influenza vaccination are mediated by estrogenic upregulation of NF-κB and TNF signaling in B cells.

Park Han-Sol H-S, Yin Anna A, Zhou Weiqiang W, Wenstedt Eliane F E EFE et al.

Sex differences in the humoral immune responses to the seasonal quadrivalent influenza vaccine (QIV) in young adults (YA; 18-49 years old) or high-dose QIV in old adults (OA; 75+ years old) were analyzed to determine how age-related changes, including in steroids, impact sex differences in B cells. Among YAs, females had greater H3N2, but not H1N1, neutralizing antibody titers, and greater proportions of hemagglutinin (HA)+ CD19+ B cells and HA+ memory B cells than males through 28 days post-vaccination (DPV), that was not observed among OAs. Machine learning algorithms illustrated that baseline (0 DPV) steroids, including 17-hydroxyprogesterone, estrogens, and testosterone, as well as HA+ CD19+ B cells and HA+ antibody-secreting B cells (ASCs), were major predictors of seroconversion at 28 DPV, particularly in YA. Single-cell RNA sequencing demonstrated that CD19+ B cells from YA females had greater transcriptional activity at 7 DPV than YA males, with upregulation of genes with estrogen-response elements (EREs) along NF-κB-mediated TNF signaling pathways in B-cell subsets, which was mitigated in OA. Estradiol treatment of ASCs from YA females, but not males, increased the number and size of HA+ IgG+ cells and expression of ERE genes along the NF-κB-mediated TNF signaling pathway,that was inhibited by an estrogen receptor antagonist. Pharmacological inhibition of either NF-κB or TNF signaling blocked the ability of E2 to upregulate antibody secretion in cells from YA females. This study provides mechanistic insights into estrogen-mediated increases in influenza vaccine-induced antibody responses among reproductive-aged females and suggests a role for estrogen signaling in the reduction of sex differences in vaccine-induced immunity with old age. Sex differences in influenza vaccine-induced immune responses become less pronounced with old age, which we hypothesize could be related to changes in circulating gonadal steroids. Our study shows that after receipt of the seasonal influenza vaccine, young adult females, who have elevated estrogenic activity, have more B cells that recognize influenza hemagglutinin; their B cells have greater activity along estrogen signaling and inflammatory pathways, and mount stronger antibody responses than young adult males, with these sex differences being mitigated in old adults. We identify estrogen as a key driver of sex differences in influenza immunity by showing that ex vivo estradiol increases antibody production by B cells through the estrogen receptor and engagement with NF-κB. These findings help explain the biological basis for sex differences in vaccine immunity and suggest that the hormonal environment, not just chronological age, shapes how well a person responds to vaccination.

PMID 42720319
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PubMedJournal of medicinal chemistry2026-09-10

Structure-Based Design and Optimization of Onradivir-Derived PB2 Inhibitors for the Treatment of Influenza A.

Yang Yujian Y, Rong Binhao B, Zhou Xingyu X, Liu Yongqing Y et al.

Influenza A remains a major seasonal public health burden. With the approval of onradivir, PB2 has emerged as an attractive antiviral target due to its unique and conserved structural features. Herein, using onradivir as the lead, we employed bioisosteric replacement strategies to design a series of derivatives for SAR studies. Compound 5B, bearing a cyano carboxamide moiety, exhibited strong antiviral activity with a superior safety index relative to onradivir, along with broad-spectrum inhibition against H1N1 and H3N2 strains. In an H1N1-infected mouse model, oral administration of 5B reduced lung viral load and ameliorated virus-induced pulmonary pathology and inflammatory responses. Remarkably, oral administration of 5B significantly improved survival (85.7% across all dose groups), outperforming onradivir at equivalent doses. Consistently, 5B exhibited favorable oral bioavailability, supporting sufficient plasma exposure. Molecular dynamics simulations revealed a highly stable complex with the PB2 cap-binding domain. These findings establish 5B as a promising preclinical candidate for influenza A.

PMID 42720457
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PubMedBiotechnology and bioengineering2026-09-10

Engineering the Vero Cell Lineage: Toward a Programmable Vaccine Manufacturing Platform.

Zhang Hanfu H, Wang Zihao Z, Yang Zhaoqing Z

Vero cells remain an indispensable continuous substrate for human viral vaccine manufacturing. Despite decades of empirical process optimization, intrinsic genomic instability, including segmental aneuploidy and dynamic chromatin rearrangements, continues to limit the durability of engineered phenotypes under sustained viral burden and bioreactor stress. Here, we review the expanding engineering toolkit for the Vero lineage across a three-layered functional framework: the membrane interface, cytoplasmic foundry, and nuclear blueprint, evaluating translational prospects at each level. Receptor transplantation and morphological reprogramming have broadened viral entry range and enabled suspension-adapted culture formats, while metabolic flux management and temporally controlled apoptosis modulation have addressed intracellular production bottlenecks, albeit often with trade-offs between productivity, biosafety, and long-term population stability. At the genomic level, targeted perturbations of transcriptional regulators and emerging epigenetic interventions offer more durable gains, yet expression drift, clonal heterogeneity, and karyotypic instability during extended passaging highlight the need for locus-level precision rather than constitutive trait installation. Looking forward, infection-responsive dynamic logic circuits and the systematic identification of Vero-specific genomic safe harbors could shift the paradigm toward a conditionally responsive manufacturing architecture. Collectively, these advances suggest a pathway for transitioning the Vero lineage from a passive, empirically optimized biological substrate into a conditionally responsive, genomically stable, and programmable platform for modern vaccine preparedness.

PMID 42717571
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PubMedJournal of virology2026-09-10

Spike protein derived from an apathogenic IBV strain confers attenuated phenotype to a nephropathogenic IBV strain.

Kirk James J, Sives Samantha S, Rayment Adam A, Tappin Amber A et al.

Infectious bronchitis virus (IBV), a Gammacoronavirus, causes the economically damaging disease of poultry, infectious bronchitis. Development of IBV live attenuated vaccines (LAVs) is dependent on the supply of embryonated hens' eggs and attenuation through serial passaging, upwards of 80 times. Vaccine development needs to keep pace with IBV evolution; an issue compounded as cross protection between individual IBV serotypes is unpredictable and often limited. Rational attenuation alongside the ability to propagate LAVs in cell culture offers significant advantages in terms of adaptability, cost, and speed. Most field IBV strains exhibit restricted in vitro tropism, being unable to replicate in primary or continuous cells without serial passage and adaptation. Beaudette, an attenuated IBV strain, is capable of replication in Vero cells, an ability conferred by the spike (S) glycoprotein. In this study, utilizing a recombinant IBV based on the nephropathogenic IBV strain D388, in which the S sequence is replaced with the equivalent sequence derived from Beaudette, we determine that the Beaudette spike can confer the ability to replicate in Vero cells and Beaudette's associated attenuated in vivo phenotype to a distantly related IBV strain. Assessment of infectious progeny and viral RNA in vivo suggests that attenuation was conferred by a tissue tropism-independent molecular mechanism. Analysis of innate immune responses revealed a lower intensity and less inflammatory profile. Our findings support the use of the Beaudette S protein as an avenue for the development of rationally attenuated, cell culture-propagated rIBV vaccines and identify the S protein as a contributor to nephropathogenicity.IMPORTANCEInfectious bronchitis virus (IBV), a Gammacoronavirus of chickens, causes significant economic losses worldwide. Current live attenuated vaccines (LAVs) are generated through extensive serial passage of virulent IBV strains in specific-pathogen-free (SPF) embryonated hen's eggs, upwards of 80 passages. This process is slow, dependent on the availability of SPF embryonated eggs, and the molecular basis of attenuation remains poorly understood. Development of rationally attenuated, cell-culture-based IBV vaccines would enable more rapid responses to emerging viral variants/strains. Using a recombinant IBV, we demonstrated the spike glycoprotein from the attenuated IBV strain Beaudette can confer attenuation and the ability to replicate in Vero cells to a distantly related virulent IBV strain. Attenuation was not linked to changes in tissue tropism but was associated with altered host responses. Our research provides new insights into IBV pathogenesis and presents an avenue for rational attenuation that can be exploited for future development of cell-based IBV vaccines.

PMID 42720295
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PubMedCritical pathways in cardiology2026-09-10

Effect of Influenza Vaccination on Major Cardiovascular Events and Mortality: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.

Shahid Muhammad Waqar MW, Hameed Abdullah A, Naseem Ayesha A, Sajjad Fatima F et al.

Cardiovascular disease remains the leading global cause of mortality despite advances in preventive therapies. Influenza infection is increasingly recognized as a trigger for acute cardiovascular events, prompting interest in influenza vaccination as a potential cardioprotective intervention in high-risk patients. We aimed to conduct a systematic review and meta-analysis to evaluate the effect of influenza vaccination on cardiovascular outcomes in adults with established cardiovascular disease. PubMed, Embase, and Cochrane databases were systematically searched using relevant keywords from inception until October 2025. Seven studies were included after the final screening. Outcomes were reported as all cause mortality, myocardial infarction, major adverse cardiovascular events and heart failure related hospitalization. Interstudy heterogeneity was assessed using I² and X² statistics. Statistical calculations were performed using Review Manager 5.4.1, with a p-value of < 0.05 indicating statistical significance. Seven randomized controlled trials including 12,224 participants were analyzed. Influenza vaccination significantly reduced major adverse cardiovascular events and cardiovascular mortality. A borderline reduction was observed for myocardial infarction and all-cause mortality. No significant differences were found for stroke, coronary revascularization, or heart failure-related hospitalization. Heterogeneity was low for most primary outcomes. The routine use of influenza vaccination as an effective adjunctive strategy in secondary cardiovascular prevention is supported by the fact that it significantly lowers cardiovascular mortality and major cardiovascular events in patients with established heart disease.

PMID 42720234
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PubMedBiotechnology and bioengineering2026-09-10

Autonomous Control of Gene Expression Using Endogenous Transcription Signals.

Subsoontorn Pakpoom P, Endy Drew D, Borkowski Olivier O

Autonomous cell-based control of heterologous gene expression can simplify batch-culture bioprocessing by eliminating external monitoring and extrinsic control of culture conditions. Existing approaches use auto-induction media, synthetic cell-cell communication systems, or application-specific biosensors. A simpler, resource-efficient, and general-purpose expression control system responsive to common changes during batch culture would be highly valuable. We used native E. coli promoters, including PhdeA, PdpS, PfumA, PrpoA, PrpoS, PgadA, and PyiaG, and recombinase-based switches to repurpose endogenous transcription signals for control of heterologous gene expression. Specifically, natural changes, covering 1-2 orders of magnitude across growth phases, in transcription from endogenous promoters result in recombinase expression at the exponential-to-stationary phase transition. So-expressed recombinases invert a constitutive promoter regulating expression of arbitrary heterologous genes amplifying the endogenous transcriptional input signal by more than 10-fold. We realized reversible and single-use switching with reduced static and dynamic cell-to-cell variation and overall expression amplification. We used "off-the-shelf" genetic parts and abstraction-based composition frameworks to realize reliable forward engineering of our synthetic genetic systems. We engineered autonomous control systems for regulating heterologous gene expression. Our system uses generic endogenous promoters to sense and control heterologous expression during growth-phase transitions. Our system does not require specialized auto-induction media, production or activation of quorum sensing, or the development of application-specific biosensors. Cells programmed to control themselves could simplify existing bioprocess operations and enable the development of more powerful synthetic genetic systems. Modern biotechnology uses engineered microbes to manufacture molecules that are incorporated into medicines, flavors, fuels, and other materials. Making molecules inside cells requires enzymes, whose expression levels and timing need to be optimized to maximize final product yields. Many engineered microbes use enzymes that should only be expressed during the later stages of cell growth to avoid overconsumption of resources or accumulation of toxic intermediates. Here, we develop simple genetic devices that enable engineered cells to control themselves, automatically switching on or off enzyme expression during batch cell culture. Unlike existing approaches, our devices do not require specialized growth media or wasteful synthesis of cell-cell signaling molecule.

PMID 42717550
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