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influenza vaccine (Ultravac / Ultravak)

✓ Approved

Microgen · Vaccine · Vaccine

What is influenza vaccine?

influenza vaccine is a vaccine developed by Microgen. It is approved for therapeutic indications via inhaled.

Drug Profile

Brand NamesUltravac, Ultravak
CompanyMicrogen
Drug ClassVaccine, Large Molecules
RouteInhaled
StatusApproved
Sources: ClinicalTrials.gov, Microgen

Related Research Articles

PubMedThe Journal of infectious diseases2026-07-17

Influenza Antibody Levels Associated with Laboratory-Confirmed Influenza in a Test-Negative Study Design, US Flu VE Network, November 2018-May 2019.

Flannery Brendan B, Chung Jessie R JR, Holiday Crystal C, Jefferson Stacie S et al.

We assessed associations between antibody concentrations within 7 days of symptom onset and testing positive for influenza virus infection among outpatients enrolled in a test-negative study. From November 2018─May 2019, study sites in five states obtained serum and respiratory specimens from outpatients aged ≥18 years presenting with acute respiratory illness. Respiratory specimens were tested for influenza virus, and viral clades were identified by genomic sequencing. We measured influenza antibody titers against vaccine and circulating viruses by hemagglutination inhibition (HI), microneutralization (MN) and neuraminidase inhibition (NAI) assays. Reduction in odds of influenza-associated illness at increasing HI, MN and NAI antibody titers was estimated using logistic regression adjusting for influenza vaccination status and time since beginning of influenza season. Among 175 patients with confirmed influenza virus infection, including 112 with influenza A(H1N1)pdm09 and 63 with A(H3N2) (44 clade 3C.3a), and 130 test-negative control patients, higher HI, MN and NAI antibody titers against circulating influenza viruses were associated with lower odds of confirmed influenza. Odds of A(H1N1)pdm09 infection were 44% and 54% lower for each two-fold increase in A(H1N1)pdm09 HI or NAI titer, respectively. Odds of A(H3N2) infection were 49% and 28% lower, respectively, for each two-fold increase in MN or NAI titer against circulating A(H3N2) virus clade. NAI titers were independently associated with lower odds of influenza A(H1N1)pdm09 and A(H3N2) after controlling for HI titer. Higher influenza antibody titers against circulating viruses were associated with lower likelihood of influenza virus infection among adult patients with acute respiratory illness.

PMID 42463137
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PubMedIndian journal of medical microbiology2026-07-17

The Resurgence of Respiratory Viruses After COVID-19: Molecular Insights from Pediatric SARI in Kashmir.

Wani Sanam Rasool SR, Fomda Bashir Ahmad BA, Bhat Mushtaq Ahmad MA, Bashir Gulnaz G et al.

Respiratory viruses are major contributors to severe acute respiratory infections (SARI) in children. Data on their molecular epidemiology in northern India remains limited, particularly in the post-COVID-19 period. This study aimed to determine the prevalence and distribution of respiratory viral pathogens among hospitalized pediatric SARI patients in Kashmir. A prospective study was conducted from October 2023 to April 2025 at Sher-i-Kashmir Institute of Medical Sciences, Srinagar. Children aged ≤15 years meeting the World Health Organization SARI case definition were enrolled. Nasopharyngeal and/or oropharyngeal samples were collected and tested using real-time polymerase chain reaction assays for SARS-CoV-2, Influenza A and B, Respiratory Syncytial virus (RSV) A and B, Adenovirus, Human metapneumovirus, Rhinovirus, and Para-influenza viruses. A total of 326 pediatric SARI cases were included. At least one respiratory virus was detected in 200 patients (61.3%). RSV was the most frequently detected virus, with RSV-B identified in 111 cases (34.0%) and RSV-A in 26 cases (7.9%). Influenza viruses accounted for a smaller proportion, including influenza A(H1N1) in 12 cases (3.6%), influenza A(H3N2) in 6 cases (1.8%), and influenza B (Victoria lineage) in 21 cases (6.4%). Other viruses detected included Adenovirus, Para-influenza virus, Rhinovirus, and Human metapneumovirus. Most infections occurred during winter months and predominantly affected infants. Respiratory viruses account for a substantial proportion of pediatric SARI cases in Kashmir, with RSV emerging as the predominant pathogen in the post-pandemic period. Strengthening molecular surveillance may improve diagnostic stewardship and guide targeted prevention strategies.

PMID 42462876
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PubMedVirologica Sinica2026-07-17

Pygenic Acid A, a Small-Molecule PD-1/SHP-2 Inhibitor, Enhances Efficacy of Therapeutic Melanoma Vaccines and Prophylactic Influenza Vaccines.

Yan Yan Y, Li Yitong Y, Mei Wenyi W, Li Yixin Y et al.

Overcoming immunosuppressive tumor microenvironments remains a critical challenge in advanced vaccine development. Here, we evaluated Pygenic acid A (PA), an intracellular small-molecule inhibitor targeting the PD-1/SHP-2 axis, as a novel vaccine adjuvant. The adjuvant efficacy of PA was systematically assessed in two murine models: a therapeutic B16-F10 melanoma lung metastasis model and a prophylactic lethal H1N1 influenza virus challenge model. In the melanoma metastasis model, PA potentiated the anti-tumor effect of the mTRP2 vaccine, markedly inhibiting pulmonary metastatic lesions and prolonging the survival of tumor-bearing mice. Mechanistically, PA robustly boosted the intratumoral infiltration of functional T cells, thereby reversing local tumor immunosuppression. In the influenza vaccination model, consistent immunostimulatory effects were observed: the PA-adjuvanted hemagglutinin (HA) vaccine effectively elicited broad-spectrum cross-neutralizing antibody responses and provided complete protection against lethal heterologous influenza virus challenge. Further mechanistic investigations demonstrated that PA specifically promoted the differentiation of T follicular helper (Tfh) cells and the expansion of germinal center (GC) B cells in draining lymph nodes, while triggering a robust Th1-type cellular immune response dominated by IFN-γ secretion. Furthermore, in vivo safety assessments verified that PA intervention induced no obvious systemic inflammation, hematological abnormalities, or visceral organ injury, indicating a favorable safety profile. Collectively, these results demonstrate that PA serves as a potent and safe intracellular checkpoint-targeting adjuvant capable of potentiating both cellular immunity and cross-protective humoral immunity, holding great translational promise for the development of advanced cancer vaccines and broad-spectrum influenza vaccines.

PMID 42462877
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PubMedmedRxiv : the preprint server for health sciences2026-07-17

Post-vaccination expansion of extrafollicular Th10 and regulatory Tfr cells distinguishes strong from weak influenza vaccine responses in older adults.

Mahajan Avinash S AS, Ravichandran Sathyabaarathi S, Marches Radu R, Yazici Yilmaz Yucehan YY et al.

Despite the superior efficacy of high-dose influenza vaccines, over one-third of older adults fail to respond. Yet, the mechanisms underlying this impaired vaccine responsiveness remain poorly understood. Here, we performed longitudinal profiling of older adults (n=60) receiving high-dose influenza vaccination to identify immune programs associated with vaccine responsiveness. Strong responders exhibited a primed baseline immune state characterized by elevated plasma cytokines and chemokines, followed by enhanced IFN-γ responses and coordinated transcriptional and epigenetic activation of cDC2 cells at day 1. By day 7, CD4⁺ T-cell trajectories diverged: strong responders preferentially expanded influenza-specific activated cTfh1 ( CXCR5 + CXCR3 + ICOS + CD38 + ) and influenza-specific Th10 ( CXCR5⁻ CXCR3 + PD1 + IL10⁺ ) cells, whereas weak responders expanded regulatory cTfr ( CXCR5⁺ FOXP3⁺ ) cells. Th10 expansion correlated with plasmablast and antibody responses and was independently validated in a larger influenza vaccination cohort, including younger adults. Functionally, Th10 cells promoted memory B-cell differentiation into plasmablasts and production of influenza-specific IgGs. TCR analyses revealed minimal clonal overlap between Th10 and cTfh1 cells. Together, these findings identify divergent helper and regulatory CD4⁺ T cell programs associated with vaccine responsiveness and establish Th10 cells as a previously unrecognized component of vaccine-induced humoral immunity.

PMID 42465941
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PubMedbioRxiv : the preprint server for biology2026-07-17

Molecular-level analysis of serum IgG repertoires in COVID-19-vaccinated people with cystic fibrosis identifies abundant convergent antibodies.

Ionov Steven S, Connor Ruth I RI, Curtis Nicholas C NC, Shin Seungmin S et al.

People with cystic fibrosis (pwCF) are at increased risk of severe disease following respiratory viral infections including influenza and respiratory syncytial virus, and were therefore given priority for COVID-19 vaccination. Retrospective epidemiological data have revealed a lower incidence of SARS-CoV-2 infection and a reduced fatality rate among pwCF than in the general population, possibly from the stringent infection control measures and early adoption of protective behaviors. Despite several reports of adequate binding and neutralizing titers after vaccination, the molecular features of vaccine-elicited serum antibody repertoires in pwCF remain unknown. We performed high-resolution proteomic analysis of serum IgG, combined with next-generation sequencing of B cells, to quantitatively profile Spike (S)-reactive serological repertoires from nine infection-naïve pwCF after two doses of COVID-19 mRNA vaccine. We recombinantly expressed 20 IgG clonotypes from 6 pwCF as monoclonal antibodies (mAbs) and measured their binding and neutralization against vaccine-strain and variant viruses. All donors mounted strong binding and neutralizing titers to vaccine-strain virus. Ig-Seq revealed diverse serum repertoires in all vaccinees, with antibodies targeting the receptor-binding domain (RBD) comprising 64% of each circulating repertoire by abundance. Several serum IgG clonotypes identified across our cohort shared identical or similar IGHV and CDRH3 amino acid sequences with serum IgG from other pwCF or S-reactive mAbs isolated from non-CF individuals. These 'convergent' antibodies made up 14.6% of the anti-S repertoires in our cohort, reaching 24.8% in one pwCF. Convergent antibodies tended to be RBD-reactive and enriched in specific IGHV ; surprisingly, a higher abundance of convergent antibodies in serum correlated with a lower breadth of serum neutralization. All 20 mAbs bound Wuhan S with high affinity (EC 50 < 10 nM), and only RBD-reactive mAbs conferred neutralization to vaccine or variant pseudovirus. While most mAbs bound both the B.1.617.2 (Delta, 17/20) and B.1.1.529 (Omicron, 12/20) strains, convergent mAbs were less likely to bind either variant. Post-vaccine serum IgG repertoires in pwCF are dominated by RBD-focused, high-affinity antibodies and include a substantial convergent component shared with non-CF vaccinees. These findings demonstrate that pwCF mount antibody responses comparable to the general population, and a large group of convergent antibodies may contribute to strain-specific rather than cross-variant immunity.

PMID 42465256
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PubMedVeterinary research2026-07-17

In vitro and in vivo studies of GAPLINC identify it as a critical host factor involved in the regulation of influenza A virus infection.

Wang Lulu L, Xu Haiyan H, Li Jiajie J, Zhang Qianxi Q et al.

Although previous studies have suggested a role for GAPLINC in regulating influenza A virus (IAV) infection, the functional involvement of GAPLINC in IAV infection in vitro and in vivo remains largely unknown. Here, we found that expression of lncRNA GAPLINC is significantly downregulated by infections with several strains of IAV, including PR8, WSN, H3N2, and H9N2. Interestingly, infections with several other viruses, such as pseudorabies virus (PRV), Sendai virus (SeV), and Herpes simplex virus (HSV), also result in a significant reduction in GAPLINC expression. During IAV infection, activation of NF-κB and the downstream IL-6/STAT3 signaling pathway contribute, at least in part, to the downregulation of GAPLINC expression. Knockdown of GAPLINC in host cells impairs the viral replication, whereas overexpression of GAPLINC increases the viral titers. Both heterozygous GAPLINC knockout (KO) mice (GAPLINC+/-) and homozygous GAPLINC KO mice (GAPLINC⁻/⁻) were further employed to determine its function in vivo. GAPLINC knockout renders mice more resistant to IAV infection than wild-type counterparts, as evidenced by lower viral load and lung injury, slower body weight loss, and improved survival. We confirmed that GAPLINC obviously suppresses the IRF3 activation in IAV-infected cells. Moreover, we noticed that inhibition of ATG7-involved autophagy weakens the pro-viral activity of GAPLINC. Together, the results support the conclusion that GAPLINC plays a critical role in enhancing the pathogenesis of IAV, at least by targeting the IRF3 and ATG7-mediated autophagy pathway.

PMID 42464369
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