Question: You are an expert researcher providing comprehensive, well-cited information.

Provide detailed information focusing on: 1. Key concepts and definitions with current understanding 2. Recent developments and latest research (prioritize 2023-2024 sources) 3. Current applications and real-world implementations 4. Expert opinions and analysis from authoritative sources 5. Relevant statistics and data from recent studies

Format as a comprehensive research report with proper citations. Include URLs and publication dates where available. Always prioritize recent, authoritative sources and provide specific citations for all major claims.

Disease Pathophysiology Research Template

Target Disease

• Disease Name: Influenza
• MONDO ID: (if available)
• Category: Infectious Disease

Research Objectives

Please provide a comprehensive research report on the pathophysiology of Influenza. Focus on the molecular and cellular mechanisms underlying disease progression.

Required Information

1. Core Pathophysiology

• What are the primary pathophysiological mechanisms?
• What molecular pathways are dysregulated?
• What cellular processes are affected?

2. Key Molecular Players

• Genes/Proteins: Which genes are causally involved or implicated?
• Chemical Entities: What metabolites, drugs, or small molecules are relevant?
• Cell Types: Which cell types are primarily affected?
• Anatomical Locations: Which tissues/organs are involved?

3. Biological Processes (for GO annotation)

• What biological processes (GO terms) are disrupted?
• Consider: signaling pathways, metabolic processes, cellular responses, transport, etc.

4. Cellular Components

• Where in the cell do key processes occur?
• Consider: organelles, membrane compartments, extracellular space, etc.

5. Disease Progression

• What is the sequence of events from initial trigger to clinical manifestation?
• Are there distinct stages or phases?

6. Phenotypic Manifestations

• What are the key clinical phenotypes?
• How do they relate to the underlying mechanisms?

Citation Requirements

• Cite primary literature (PMID preferred) for all mechanistic claims
• Prioritize recent reviews and landmark papers
• Include direct quotes where possible to support key statements

Output Format

Structure your response as a narrative that could be used to populate a disease knowledge base entry with: - Pathophysiology description - Gene/protein annotations with ontology terms (HGNC, GO) - Phenotype associations (HP terms) - Cell type involvement (CL terms) - Anatomical locations (UBERON terms) - Chemical entities (CHEBI terms) - Evidence items with PMIDs

Influenza pathophysiology (molecular & cellular mechanisms) — research report (2023–2024 emphasis)

Disease & scope

Disease: Influenza (primarily influenza A virus (IAV), but mechanisms generalize to influenza B in many host-response pathways).
Category: Infectious disease (acute respiratory viral infection).
MONDO ID: Not retrieved in current tool context.

Executive summary

Influenza pathophysiology reflects the coupled dynamics of (i) viral infection/replication in respiratory epithelial cells, (ii) host innate recognition (notably TLR3/7/8 and other PRRs) that drives interferon and inflammatory programs, (iii) inflammasome-driven IL‑1 family cytokine release and inflammatory cell death (pyroptosis/necroptosis/PANoptosis), and (iv) downstream tissue injury including endothelial barrier dysfunction, vascular leakage, and thromboinflammatory complications in severe disease. Recent 2023–2024 human and translational studies sharpen this model by defining cell-type-resolved early lung signatures (e.g., a core 6-gene interferon/ISG module) and by quantifying real-world treatment effects (baloxavir vs oseltamivir) and severe-complication rates (e.g., thrombosis incidence in critically ill cohorts). (an2024hostinnateantiviral pages 1-2, an2024hostinnateantiviral pages 4-5, sohail2024differentialtranscriptomichost pages 10-12, qiu2024thrombosisincritically pages 1-2)

Table: A structured summary of key influenza pathophysiological mechanisms, molecular players, affected cells/tissues, and recent clinical findings extracted from 2023–2024 literature.

1) Core pathophysiology: key concepts and definitions (current understanding)

1.1 Viral tropism and replication

IAV is an enveloped, segmented negative-sense ssRNA virus whose genome is packaged as eight vRNPs with NP and polymerase subunits PA/PB1/PB2; the virion surface contains HA, NA, and M2. HA binds sialic-acid receptors, enabling endocytic entry; vRNPs traffic to the nucleus for transcription/replication; progeny virions bud from the plasma membrane. (an2024hostinnateantiviral pages 1-2)

Mechanistic implication: the need for nuclear replication and the requirement for HA/NA/M2 at distinct lifecycle stages creates multiple intervention points (PA cap-dependent endonuclease inhibition; NA inhibition; host-directed blockade of entry/trafficking). (an2024hostinnateantiviral pages 1-2)

1.2 Innate sensing as a “double-edged sword”

A central concept in modern influenza pathophysiology is that early innate sensing is necessary for viral control but can also drive immunopathology. The innate response can become “hyperactive” and damage host tissues if not properly regulated. (an2024hostinnateantiviral pages 1-2)

2) Primary molecular pathways dysregulated in influenza

2.1 TLR-driven sensing → IRF/NF‑κB programs

Recent 2024 reviews consolidate evidence that endosomal TLRs are major influenza sensors and define canonical signaling routes.

Key mechanistic statement (signal flow): * TLR7/TLR8 signal via MYD88 to activate IRF5/IRF7, AP‑1, and NF‑κB. * TLR3 signals via TRIF (TICAM1) to activate IRF3 (via TBK1/IKKε) and NF‑κB-associated programs. * The consequence is transcription of interferons, cytokines, and pro-inflammatory mediators. (an2024hostinnateantiviral pages 4-5)

Definitions/notes: Kayesh et al. (2024) emphasize that multiple TLRs participate (TLR2/3/4/7/8/9/10) and that TLRs can be “a double-edged sword,” motivating interest in balanced modulation and use of TLR agonists as adjuvants. (kayesh2024recentinsightsinto pages 2-4, kayesh2024recentinsightsinto pages 8-10)

2.2 Interferon and ISG responses as early tissue-scale signatures

A key 2024 human lung explant study (bulk + scRNA-seq) provides direct evidence of early (first 24h) lung antiviral transcriptional programs.

Predominant infected cell types: airway epithelial cells and macrophages. (sohail2024differentialtranscriptomichost pages 1-2)

Core ISG module (6 mRNAs): IFI6, IFI44L, IRF7, ISG15, MX1, MX2. (sohail2024differentialtranscriptomichost pages 1-2)

Additional inflammatory/chemokine signal: infection induced “brisk interferon responses,” with CCL8 described as the most strongly upregulated mRNA. (sohail2024differentialtranscriptomichost pages 1-2)

Pathway-level dysregulation: Gene set enrichment showed induction of IFNα/IFNγ response programs, IL6–JAK–STAT3 signaling, and TNFα signaling via NF‑κB, with suppression of cell-cycle programs (E2F targets). (sohail2024differentialtranscriptomichost pages 8-10)

2.3 Inflammasomes and IL‑1 family cytokines

Inflammasome signaling is increasingly framed as central to severe influenza immunopathology, linking PRR activation, cell death, and IL‑1 family cytokines.

AIM2 inflammasome in influenza

A major 2024 review focuses on AIM2 (Absent in Melanoma 2), canonically a cytosolic dsDNA sensor, but “unexpectedly” implicated in IAV (an RNA virus). (xu2024takingaimat pages 2-4)

Mechanism: IAV-associated host DNA (especially mitochondrial DNA released after mitochondrial damage; also DNA from NETs or phagocytosed material) can activate AIM2, recruiting ASC and caspase-1, leading to IL‑1β/IL‑18 processing and gasdermin-mediated pyroptosis. (xu2024takingaimat pages 7-9, xu2024takingaimat pages 2-4)

Clinical/pathology linkage: excessive IL‑1β/IL‑18 correlates with severity in multiple influenza subtypes; and gasdermin D deficiency is cited as protective in mouse influenza hyperinflammation/lung damage contexts. (xu2024takingaimat pages 2-4)

Important nuance (expert synthesis): AIM2’s role is context-dependent, with “AIM2 deficiency… linked to both enhanced and reduced vulnerability to IAV infection,” suggesting timing/strain/dose and redundancy with other sensors (e.g., cGAS-STING, NLRP3) influence phenotype. (xu2024takingaimat pages 1-2, xu2024takingaimat pages 5-7)

2.4 Programmed cell death and PANoptosis (tissue injury vs viral control)

A 2024 mechanistic review synthesizes how influenza engages apoptosis, necroptosis, pyroptosis, and integrated PANoptosis.

Key sensor: ZBP1 recognizes viral Z-RNA and coordinates apoptosis/necroptosis/pyroptosis via RHIM-dependent interactions with RIPK3/RIPK1. (sun2024mechanisticinsightsinto pages 4-6, sun2024mechanisticinsightsinto pages 6-8)

Necroptosis arm: RIPK1/RIPK3 → MLKL phosphorylation → MLKL oligomerization and pore formation; MLKL-driven membrane rupture can drive potassium efflux that activates NLRP3 inflammasome. (sun2024mechanisticinsightsinto pages 4-6, sun2024mechanisticinsightsinto pages 8-10)

Pyroptosis arm: Inflammasome-activated caspase-1 cleaves GSDMD; caspase-3 can cleave GSDME (linking apoptosis to pyroptosis). (sun2024mechanisticinsightsinto pages 8-10)

Integrated PANoptosis: PANoptosis can “ensure[] the efficient elimination of infected cells while triggering a robust inflammatory response,” illustrating the mechanistic tradeoff between clearance and immunopathology. (sun2024mechanisticinsightsinto pages 11-13)

3) Key molecular players (knowledge-base style)

3.1 Host genes/proteins (examples supported by 2024 sources)

Innate sensing & signaling: TLR3, TLR7, TLR8, MYD88, TICAM1/TRIF, IRF3, IRF7, NFKB1 (an2024hostinnateantiviral pages 4-5, kayesh2024recentinsightsinto pages 2-4)
ISG module / antiviral state: IFI6, IFI44L, IRF7, ISG15, MX1, MX2 (sohail2024differentialtranscriptomichost pages 1-2)
Inflammasome & cytokines: AIM2, NLRP3, PYCARD/ASC, CASP1, IL1B, IL18, GSDMD (xu2024takingaimat pages 2-4, sun2024mechanisticinsightsinto pages 10-11)
Cell death (PANoptosis): ZBP1, RIPK1, RIPK3, MLKL, CASP8, CASP3, GSDME (sun2024mechanisticinsightsinto pages 10-11, sun2024mechanisticinsightsinto pages 4-6)
Endothelial/thromboinflammation: VWF (von Willebrand factor), ICAM1, VCAM1; tissue factor pathway is discussed in thrombosis context (marchenko2024endothelialactivationand pages 12-13, qiu2024thrombosisincritically pages 1-2)

3.2 Viral proteins implicated

HA (entry), NA (release), M2 (ion channel; implicated in inflammasome/mitochondrial perturbation in reviews), polymerase components PA/PB1/PB2 and accessory proteins including NS1 (immune antagonism), PB1-F2 (mitochondrial damage; inflammasome-related context), PA-X (host shutoff context). (an2024hostinnateantiviral pages 1-2, xu2024takingaimat pages 7-9)

3.3 Chemical entities / drugs (real-world and translational)

• Baloxavir marboxil (targets viral polymerase acidic (PA) cap-dependent endonuclease). (cai2024realworldeffectivenessand pages 1-2)
• Oseltamivir (neuraminidase inhibitor targeting NA). (cai2024realworldeffectivenessand pages 1-2)

4) Key cell types and anatomical locations

4.1 Cell types (with evidence)

Airway epithelial cells and macrophages are identified as predominant IAV host cells early after infection in human lung tissue explants (24h). (sohail2024differentialtranscriptomichost pages 1-2)

Inflammatory responses can occur in bystander cell types with few/no detectable viral transcripts, indicating paracrine cytokine signaling and tissue-level propagation of innate programs. (sohail2024differentialtranscriptomichost pages 1-2)

4.2 Anatomical sites

• Nasal mucosa / upper airway: critical for mucosal vaccination responses; LAIV provokes early IL‑33 and subsequent IFN-associated mucosal programs. (thwaites2023earlymucosalevents pages 1-2, thwaites2023earlymucosalevents pages 2-2)
• Lower airway / lung parenchyma: key site of viral pneumonia, ISG responses, inflammatory cell recruitment, and cell death-mediated injury. (sohail2024differentialtranscriptomichost pages 1-2, sun2024mechanisticinsightsinto pages 11-13)
• Pulmonary microvasculature / endothelium: endothelial infection/activation contributes to leakage and thromboinflammatory complications in severe disease. (marchenko2024endothelialactivationand pages 12-13)

5) Disease progression: sequence of events (stage model)

1. Exposure & entry: HA binds sialic acid receptors; endocytosis and fusion release vRNPs. (an2024hostinnateantiviral pages 1-2)
2. Early replication (hours–day 1): nuclear replication/transcription; early innate sensing begins. (an2024hostinnateantiviral pages 1-2)
3. Innate immune amplification: TLR3/7/8 signaling activates IRFs and NF‑κB, inducing interferons/cytokines and ISGs. (an2024hostinnateantiviral pages 4-5)
4. Tissue-scale antiviral state: core ISG module (IFI6/IFI44L/IRF7/ISG15/MX1/MX2) emerges as an early hallmark in human lung tissue, with chemokines such as CCL8 prominent. (sohail2024differentialtranscriptomichost pages 1-2)
5. Inflammasome and inflammatory cell death: AIM2 and NLRP3 pathways process IL‑1β/IL‑18; ZBP1-coordinated PANoptosis links viral nucleic acid sensing to apoptosis/necroptosis/pyroptosis; the combined effect can clear infection but also intensify inflammation. (xu2024takingaimat pages 2-4, sun2024mechanisticinsightsinto pages 11-13)
6. Barrier dysfunction and systemic complications in severe disease: endothelial activation/dysfunction promotes vascular leakage and supports thrombosis risk; critically ill cohorts show measurable VTE incidence. (marchenko2024endothelialactivationand pages 12-13, qiu2024thrombosisincritically pages 1-2)

6) Phenotypic manifestations (mechanism → phenotype links)

6.1 Respiratory phenotypes

• Viral pneumonia / ARDS-like lung injury: driven by cytokine and inflammasome activation and inflammatory cell death; PANoptosis is explicitly linked to “robust inflammatory response” that can contribute to tissue damage. (sun2024mechanisticinsightsinto pages 11-13, xu2024takingaimat pages 1-2)

6.2 Thromboinflammatory phenotypes

A cohort of 854 adults with severe influenza reported VTE incidence 9.37% (80/854); thrombosis was associated with greater requirement for advanced respiratory support (mechanical ventilation, ECMO) and higher co-infection incidence. (qiu2024thrombosisincritically pages 1-2)

Mechanistically, reviews link influenza to endothelial activation and dysfunction, including pulmonary microvascular endothelial infection, leakage, cytokine release, adhesion molecule upregulation (ICAM‑1/VCAM‑1), and NET-associated damage. (marchenko2024endothelialactivationand pages 12-13)

7) Recent developments and real-world implementations (2023–2024)

7.1 Real-world antiviral effectiveness: baloxavir vs oseltamivir

A multicenter real-world ambispective cohort study in outpatient fever clinics in East China (study period 2022.06–2023.06; published 23 July 2024, DOI: https://doi.org/10.3389/fmicb.2024.1428095) enrolled 509 influenza A outpatients.

Key findings: * Median time to alleviation of all influenza symptoms (TTAIS): 28.0 h (baloxavir) vs 48.0 h (oseltamivir). (cai2024realworldeffectivenessand pages 1-2) * Median time to alleviation of fever (TTAF): 18 h vs 30 h. (cai2024realworldeffectivenessand pages 1-2) * Multivariable Cox model: baloxavir associated with faster symptom alleviation (HR ~1.36) and fever resolution (HR ~1.93) compared to oseltamivir. (cai2024realworldeffectivenessand pages 1-2)

The main Kaplan–Meier and adjusted hazard ratio results are visualized in the extracted Figure/Table crops. (cai2024realworldeffectivenessand media 252c64e8, cai2024realworldeffectivenessand media b5b8ace7)

7.2 Antiviral resistance surveillance: baloxavir PA substitutions

A 2024 surveillance analysis of PA sequences in the Americas (published Sep 2024; DOI: https://doi.org/10.2147/DHPS.S470868) analyzed 58,816 IAV and 14,684 IBV PA sequences (up to May 31, 2023).

Key statistics: * IAV: 55/58,816 (0.1%) with resistance markers (~1 in 1000). (acocaljuarez2024baloxavirresistancemarkers pages 2-4) * Most frequent IAV markers: I38V (21), I38M (7), E199G (9). (acocaljuarez2024baloxavirresistancemarkers pages 2-4) * IBV: 8/14,684 (0.05%) with markers; M34I (5) and I38V (3). (acocaljuarez2024baloxavirresistancemarkers pages 4-7)

Clinical relevance emphasized: I38M is described as causing about a tenfold reduction in susceptibility, motivating ongoing molecular surveillance (with noted geographic sequencing gaps). (acocaljuarez2024baloxavirresistancemarkers pages 4-7, acocaljuarez2024baloxavirresistancemarkers pages 7-9)

7.3 Vaccine technology trends and mucosal vaccination rationale

A 2024 Clinical Microbiology Reviews overview emphasizes that limitations of current seasonal vaccines (e.g., egg adaptation, moderate effectiveness) motivate new technologies (cell-based, recombinant, adjuvanted/high-dose, LAIV, nucleic-acid vaccines including mRNA). (clark2024recentadvancesin pages 12-14, clark2024recentadvancesin pages 25-27)

The review notes that LAIV requires intranasal delivery and can elicit mucosal responses (including mucosal IgA), which may better prevent infection at the point of entry; it also summarizes effectiveness/effect size examples (e.g., LAIV reducing ILI by 31% in cited data; cell-based QIIV reducing lab-confirmed influenza by 54.6% in children). (clark2024recentadvancesin pages 19-22)

7.4 Mechanistic immunology of intranasal LAIV in humans (2023)

A Nature Communications 2023 study (Received 18 May 2023; Accepted 22 Nov 2023; DOI: https://doi.org/10.1038/s41467-023-43842-7) reports that LAIV induces “distinct, compartmentalized, antibody responses in the mucosa and blood,” and identifies early mucosal IL‑33 release within the first 8 hours as associated with these response patterns. The study is registered as NCT04110366. (thwaites2023earlymucosalevents pages 1-2)

8) GO/Cellular component and ontology-oriented curation snippets

Below are curation-ready suggestions (labels; IDs not computed here) aligned with evidence above:

8.1 GO Biological Process candidates (examples)

• Toll-like receptor signaling pathway (TLR3/TLR7/TLR8; MYD88/TRIF) (an2024hostinnateantiviral pages 4-5, kayesh2024recentinsightsinto pages 2-4)
• Response to type I interferon; interferon-stimulated gene expression (IFI6/IFI44L/IRF7/ISG15/MX1/MX2) (sohail2024differentialtranscriptomichost pages 1-2)
• Cytokine-mediated signaling pathway; TNFα signaling via NF‑κB; IL6–JAK–STAT3 signaling (sohail2024differentialtranscriptomichost pages 8-10)
• Inflammasome complex assembly; IL‑1β and IL‑18 production (AIM2/NLRP3/ASC/CASP1) (xu2024takingaimat pages 2-4, sun2024mechanisticinsightsinto pages 10-11)
• Pyroptosis; necroptosis; apoptosis; PANoptosis (ZBP1/RIPK1/RIPK3/MLKL; caspases; gasdermins) (sun2024mechanisticinsightsinto pages 11-13, sun2024mechanisticinsightsinto pages 8-10)
• Blood coagulation / immunothrombosis-like processes; endothelial activation (marchenko2024endothelialactivationand pages 12-13, qiu2024thrombosisincritically pages 1-2)

8.2 GO Cellular Component candidates

• Endosome; nucleus (viral entry/nuclear replication) (an2024hostinnateantiviral pages 1-2)
• Inflammasome complex; cytosol (AIM2/ASC/CASP1) (xu2024takingaimat pages 2-4)
• Plasma membrane pore complex (MLKL, gasdermins) (sun2024mechanisticinsightsinto pages 4-6, sun2024mechanisticinsightsinto pages 8-10)
• Endothelial glycocalyx / junctional complexes (barrier dysfunction context) (marchenko2024endothelialactivationand pages 12-13)

8.3 Phenotype (HP) candidates (labels)

• Fever; cough; influenza-like illness; viral pneumonia; acute respiratory distress syndrome (ARDS) (inferred linkage to described mechanisms of lung injury and severe respiratory disease) (an2024hostinnateantiviral pages 1-2, xu2024takingaimat pages 1-2)
• Venous thromboembolism (VTE) (qiu2024thrombosisincritically pages 1-2)

9) Evidence highlights (direct-quote style snippets)

• TLR signaling architecture (MYD88 vs TRIF; IRF3/7/NF‑κB activation) is explicitly summarized in the Pathogens 2024 review excerpt describing Myddosome formation and TRIF→TRAF3→TBK1/IKKε→IRF3 phosphorylation. (an2024hostinnateantiviral pages 4-5)
• Human lung early response: the Respiratory Research 2024 paper identifies a 6‑mRNA “core transcriptomic response” (IFI6, IFI44L, IRF7, ISG15, MX1, MX2) and states airway epithelial cells and macrophages are predominant host cells. (sohail2024differentialtranscriptomichost pages 1-2)
• AIM2 paradox: “AIM2 deficiency has been linked to both enhanced and reduced vulnerability to IAV infection.” (xu2024takingaimat pages 1-2)
• PANoptosis tradeoff: PANoptosis “ensures the efficient elimination of infected cells while triggering a robust inflammatory response.” (sun2024mechanisticinsightsinto pages 11-13)

10) Limitations of this tool-based synthesis (PMID requirement)

Several included sources are clearly peer-reviewed and provide DOIs and journal metadata. However, PMIDs/PMCIDs were not consistently extractable from the provided text snippets within this tool run (e.g., Qiu et al. and Cai et al. excerpts did not contain PubMed identifiers). Where PMIDs are required for curation, the DOIs provided should be used to resolve the PubMed records.

Key recent references (URLs; publication dates from retrieved text)

• Cai et al. “Real-world effectiveness and safety of Baloxavir Marboxil or Oseltamivir…” Published 23 Jul 2024. https://doi.org/10.3389/fmicb.2024.1428095 (cai2024realworldeffectivenessand pages 1-2)
• Sohail et al. “Differential transcriptomic host responses…” 2024. https://doi.org/10.1186/s12931-024-02988-8 (sohail2024differentialtranscriptomichost pages 1-2)
• Kayesh et al. “Recent Insights… TLR response…” Published 29 May 2024. https://doi.org/10.3390/ijms25115909 (kayesh2024recentinsightsinto pages 1-2)
• An et al. “Host innate antiviral response…” Published 3 Jul 2024. https://doi.org/10.3390/pathogens13070561 (an2024hostinnateantiviral pages 1-2)
• Xu & Tate. “Taking AIM at Influenza…” Sep 2024. https://doi.org/10.3390/v16101535 (xu2024takingaimat pages 1-2)
• Sun & Liu. “Mechanistic insights into influenza A virus-induced cell death…” Nov 2024. https://doi.org/10.3390/vetsci11110555 (sun2024mechanisticinsightsinto pages 1-2)
• Thwaites et al. “Early mucosal events…” 2023. https://doi.org/10.1038/s41467-023-43842-7 (thwaites2023earlymucosalevents pages 1-2)
• Acocal-Juárez et al. “Baloxavir resistance markers…” Sep 2024. https://doi.org/10.2147/DHPS.S470868 (acocaljuarez2024baloxavirresistancemarkers pages 2-4)
• Qiu et al. “Thrombosis in Critically Ill Influenza Patients…” 2024. https://doi.org/10.1177/10760296241278615 (qiu2024thrombosisincritically pages 1-2)

References

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2. (an2024hostinnateantiviral pages 4-5): Wenlong An, Simran Lakhina, Jessica Leong, Kartik Rawat, and Matloob Husain. Host innate antiviral response to influenza a virus infection: from viral sensing to antagonism and escape. Pathogens, 13:561, Jul 2024. URL: https://doi.org/10.3390/pathogens13070561, doi:10.3390/pathogens13070561. This article has 18 citations.

3. (sohail2024differentialtranscriptomichost pages 10-12): Aaqib Sohail, Fakhar H. Waqas, Peter Braubach, Laurien Czichon, Mohamed Samir, Azeem Iqbal, Leonardo de Araujo, Stephan Pleschka, Michael Steinert, Robert Geffers, and Frank Pessler. Differential transcriptomic host responses in the early phase of viral and bacterial infections in human lung tissue explants ex vivo. Respiratory Research, Oct 2024. URL: https://doi.org/10.1186/s12931-024-02988-8, doi:10.1186/s12931-024-02988-8. This article has 9 citations and is from a domain leading peer-reviewed journal.

4. (qiu2024thrombosisincritically pages 1-2): Xianming Qiu, Mingjie Liu, Quanzhen Wang, Yuke Zhang, Li Kong, and Lei Zhou. Thrombosis in critically ill influenza patients: incidence and risk factors. Clinical and Applied Thrombosis/Hemostasis, Jan 2024. URL: https://doi.org/10.1177/10760296241278615, doi:10.1177/10760296241278615. This article has 3 citations.

5. (kayesh2024recentinsightsinto pages 4-5): Mohammad Enamul Hoque Kayesh, Michinori Kohara, and Kyoko Tsukiyama-Kohara. Recent insights into the molecular mechanisms of the toll-like receptor response to influenza virus infection. International Journal of Molecular Sciences, 25:5909, May 2024. URL: https://doi.org/10.3390/ijms25115909, doi:10.3390/ijms25115909. This article has 15 citations.

6. (kayesh2024recentinsightsinto pages 2-4): Mohammad Enamul Hoque Kayesh, Michinori Kohara, and Kyoko Tsukiyama-Kohara. Recent insights into the molecular mechanisms of the toll-like receptor response to influenza virus infection. International Journal of Molecular Sciences, 25:5909, May 2024. URL: https://doi.org/10.3390/ijms25115909, doi:10.3390/ijms25115909. This article has 15 citations.

7. (kayesh2024recentinsightsinto pages 1-2): Mohammad Enamul Hoque Kayesh, Michinori Kohara, and Kyoko Tsukiyama-Kohara. Recent insights into the molecular mechanisms of the toll-like receptor response to influenza virus infection. International Journal of Molecular Sciences, 25:5909, May 2024. URL: https://doi.org/10.3390/ijms25115909, doi:10.3390/ijms25115909. This article has 15 citations.

8. (sohail2024differentialtranscriptomichost pages 1-2): Aaqib Sohail, Fakhar H. Waqas, Peter Braubach, Laurien Czichon, Mohamed Samir, Azeem Iqbal, Leonardo de Araujo, Stephan Pleschka, Michael Steinert, Robert Geffers, and Frank Pessler. Differential transcriptomic host responses in the early phase of viral and bacterial infections in human lung tissue explants ex vivo. Respiratory Research, Oct 2024. URL: https://doi.org/10.1186/s12931-024-02988-8, doi:10.1186/s12931-024-02988-8. This article has 9 citations and is from a domain leading peer-reviewed journal.

9. (xu2024takingaimat pages 7-9): Dianne W. Xu and Michelle D. Tate. Taking aim at influenza: the role of the aim2 inflammasome. Viruses, 16:1535, Sep 2024. URL: https://doi.org/10.3390/v16101535, doi:10.3390/v16101535. This article has 6 citations.

10. (sun2024mechanisticinsightsinto pages 10-11): Yuling Sun and Kaituo Liu. Mechanistic insights into influenza a virus-induced cell death and emerging treatment strategies. Veterinary Sciences, 11:555, Nov 2024. URL: https://doi.org/10.3390/vetsci11110555, doi:10.3390/vetsci11110555. This article has 14 citations.

11. (sun2024mechanisticinsightsinto pages 11-13): Yuling Sun and Kaituo Liu. Mechanistic insights into influenza a virus-induced cell death and emerging treatment strategies. Veterinary Sciences, 11:555, Nov 2024. URL: https://doi.org/10.3390/vetsci11110555, doi:10.3390/vetsci11110555. This article has 14 citations.

12. (qiu2024thrombosisincritically pages 2-3): Xianming Qiu, Mingjie Liu, Quanzhen Wang, Yuke Zhang, Li Kong, and Lei Zhou. Thrombosis in critically ill influenza patients: incidence and risk factors. Clinical and Applied Thrombosis/Hemostasis, Jan 2024. URL: https://doi.org/10.1177/10760296241278615, doi:10.1177/10760296241278615. This article has 3 citations.

13. (thwaites2023earlymucosalevents pages 9-10): Ryan S. Thwaites, Ashley S. S. Uruchurtu, Victor Augusti Negri, Megan E. Cole, Nehmat Singh, Nelisa Poshai, David Jackson, Katja Hoschler, Tina Baker, Ian C. Scott, Xavier Romero Ros, Emma Suzanne Cohen, Maria Zambon, Katrina M. Pollock, Trevor T. Hansel, and Peter J. M. Openshaw. Early mucosal events promote distinct mucosal and systemic antibody responses to live attenuated influenza vaccine. Nature Communications, Dec 2023. URL: https://doi.org/10.1038/s41467-023-43842-7, doi:10.1038/s41467-023-43842-7. This article has 56 citations and is from a highest quality peer-reviewed journal.

14. (thwaites2023earlymucosalevents pages 2-2): Ryan S. Thwaites, Ashley S. S. Uruchurtu, Victor Augusti Negri, Megan E. Cole, Nehmat Singh, Nelisa Poshai, David Jackson, Katja Hoschler, Tina Baker, Ian C. Scott, Xavier Romero Ros, Emma Suzanne Cohen, Maria Zambon, Katrina M. Pollock, Trevor T. Hansel, and Peter J. M. Openshaw. Early mucosal events promote distinct mucosal and systemic antibody responses to live attenuated influenza vaccine. Nature Communications, Dec 2023. URL: https://doi.org/10.1038/s41467-023-43842-7, doi:10.1038/s41467-023-43842-7. This article has 56 citations and is from a highest quality peer-reviewed journal.

15. (thwaites2023earlymucosalevents pages 1-2): Ryan S. Thwaites, Ashley S. S. Uruchurtu, Victor Augusti Negri, Megan E. Cole, Nehmat Singh, Nelisa Poshai, David Jackson, Katja Hoschler, Tina Baker, Ian C. Scott, Xavier Romero Ros, Emma Suzanne Cohen, Maria Zambon, Katrina M. Pollock, Trevor T. Hansel, and Peter J. M. Openshaw. Early mucosal events promote distinct mucosal and systemic antibody responses to live attenuated influenza vaccine. Nature Communications, Dec 2023. URL: https://doi.org/10.1038/s41467-023-43842-7, doi:10.1038/s41467-023-43842-7. This article has 56 citations and is from a highest quality peer-reviewed journal.

16. (cai2024realworldeffectivenessand pages 1-2): Jianpeng Cai, Hongyu Wang, Xiaoting Ye, Shengjia Lu, Zhili Tan, Zhonghua Li, Dan Lin, Jiancheng Qian, Xiaoxian Lu, Jiaolong Wan, Jie Wang, Jingwen Ai, Yonglan Pu, Lihong Qu, and Sen Wang. Real-world effectiveness and safety of baloxavir marboxil or oseltamivir in outpatients with uncomplicated influenza a: an ambispective, observational, multi-center study. Frontiers in Microbiology, Jul 2024. URL: https://doi.org/10.3389/fmicb.2024.1428095, doi:10.3389/fmicb.2024.1428095. This article has 11 citations and is from a peer-reviewed journal.

17. (cai2024realworldeffectivenessand media 252c64e8): Jianpeng Cai, Hongyu Wang, Xiaoting Ye, Shengjia Lu, Zhili Tan, Zhonghua Li, Dan Lin, Jiancheng Qian, Xiaoxian Lu, Jiaolong Wan, Jie Wang, Jingwen Ai, Yonglan Pu, Lihong Qu, and Sen Wang. Real-world effectiveness and safety of baloxavir marboxil or oseltamivir in outpatients with uncomplicated influenza a: an ambispective, observational, multi-center study. Frontiers in Microbiology, Jul 2024. URL: https://doi.org/10.3389/fmicb.2024.1428095, doi:10.3389/fmicb.2024.1428095. This article has 11 citations and is from a peer-reviewed journal.

18. (kayesh2024recentinsightsinto pages 8-10): Mohammad Enamul Hoque Kayesh, Michinori Kohara, and Kyoko Tsukiyama-Kohara. Recent insights into the molecular mechanisms of the toll-like receptor response to influenza virus infection. International Journal of Molecular Sciences, 25:5909, May 2024. URL: https://doi.org/10.3390/ijms25115909, doi:10.3390/ijms25115909. This article has 15 citations.

19. (sohail2024differentialtranscriptomichost pages 8-10): Aaqib Sohail, Fakhar H. Waqas, Peter Braubach, Laurien Czichon, Mohamed Samir, Azeem Iqbal, Leonardo de Araujo, Stephan Pleschka, Michael Steinert, Robert Geffers, and Frank Pessler. Differential transcriptomic host responses in the early phase of viral and bacterial infections in human lung tissue explants ex vivo. Respiratory Research, Oct 2024. URL: https://doi.org/10.1186/s12931-024-02988-8, doi:10.1186/s12931-024-02988-8. This article has 9 citations and is from a domain leading peer-reviewed journal.

20. (xu2024takingaimat pages 2-4): Dianne W. Xu and Michelle D. Tate. Taking aim at influenza: the role of the aim2 inflammasome. Viruses, 16:1535, Sep 2024. URL: https://doi.org/10.3390/v16101535, doi:10.3390/v16101535. This article has 6 citations.

21. (xu2024takingaimat pages 1-2): Dianne W. Xu and Michelle D. Tate. Taking aim at influenza: the role of the aim2 inflammasome. Viruses, 16:1535, Sep 2024. URL: https://doi.org/10.3390/v16101535, doi:10.3390/v16101535. This article has 6 citations.

22. (xu2024takingaimat pages 5-7): Dianne W. Xu and Michelle D. Tate. Taking aim at influenza: the role of the aim2 inflammasome. Viruses, 16:1535, Sep 2024. URL: https://doi.org/10.3390/v16101535, doi:10.3390/v16101535. This article has 6 citations.

23. (sun2024mechanisticinsightsinto pages 4-6): Yuling Sun and Kaituo Liu. Mechanistic insights into influenza a virus-induced cell death and emerging treatment strategies. Veterinary Sciences, 11:555, Nov 2024. URL: https://doi.org/10.3390/vetsci11110555, doi:10.3390/vetsci11110555. This article has 14 citations.

24. (sun2024mechanisticinsightsinto pages 6-8): Yuling Sun and Kaituo Liu. Mechanistic insights into influenza a virus-induced cell death and emerging treatment strategies. Veterinary Sciences, 11:555, Nov 2024. URL: https://doi.org/10.3390/vetsci11110555, doi:10.3390/vetsci11110555. This article has 14 citations.

25. (sun2024mechanisticinsightsinto pages 8-10): Yuling Sun and Kaituo Liu. Mechanistic insights into influenza a virus-induced cell death and emerging treatment strategies. Veterinary Sciences, 11:555, Nov 2024. URL: https://doi.org/10.3390/vetsci11110555, doi:10.3390/vetsci11110555. This article has 14 citations.

26. (marchenko2024endothelialactivationand pages 12-13): Vladimir A. Marchenko and Irina N. Zhilinskaya. Endothelial activation and dysfunction caused by influenza a virus (alphainfluenzavirus influenzae). Voprosy virusologii, 69 6:465-478, Dec 2024. URL: https://doi.org/10.36233/0507-4088-264, doi:10.36233/0507-4088-264. This article has 9 citations.

27. (cai2024realworldeffectivenessand media b5b8ace7): Jianpeng Cai, Hongyu Wang, Xiaoting Ye, Shengjia Lu, Zhili Tan, Zhonghua Li, Dan Lin, Jiancheng Qian, Xiaoxian Lu, Jiaolong Wan, Jie Wang, Jingwen Ai, Yonglan Pu, Lihong Qu, and Sen Wang. Real-world effectiveness and safety of baloxavir marboxil or oseltamivir in outpatients with uncomplicated influenza a: an ambispective, observational, multi-center study. Frontiers in Microbiology, Jul 2024. URL: https://doi.org/10.3389/fmicb.2024.1428095, doi:10.3389/fmicb.2024.1428095. This article has 11 citations and is from a peer-reviewed journal.

28. (acocaljuarez2024baloxavirresistancemarkers pages 2-4): Erick Acocal-Juárez, Luis Márquez-Domínguez, Verónica Vallejo-Ruíz, Lilia Cedillo, and Gerardo Santos-López. Baloxavir resistance markers in influenza a and b viruses in the americas. Drug, Healthcare and Patient Safety, 16:105-113, Sep 2024. URL: https://doi.org/10.2147/dhps.s470868, doi:10.2147/dhps.s470868. This article has 2 citations and is from a peer-reviewed journal.

29. (acocaljuarez2024baloxavirresistancemarkers pages 4-7): Erick Acocal-Juárez, Luis Márquez-Domínguez, Verónica Vallejo-Ruíz, Lilia Cedillo, and Gerardo Santos-López. Baloxavir resistance markers in influenza a and b viruses in the americas. Drug, Healthcare and Patient Safety, 16:105-113, Sep 2024. URL: https://doi.org/10.2147/dhps.s470868, doi:10.2147/dhps.s470868. This article has 2 citations and is from a peer-reviewed journal.

30. (acocaljuarez2024baloxavirresistancemarkers pages 7-9): Erick Acocal-Juárez, Luis Márquez-Domínguez, Verónica Vallejo-Ruíz, Lilia Cedillo, and Gerardo Santos-López. Baloxavir resistance markers in influenza a and b viruses in the americas. Drug, Healthcare and Patient Safety, 16:105-113, Sep 2024. URL: https://doi.org/10.2147/dhps.s470868, doi:10.2147/dhps.s470868. This article has 2 citations and is from a peer-reviewed journal.

31. (clark2024recentadvancesin pages 12-14): Tristan W. Clark, John S. Tregoning, Helen Lister, Tiziano Poletti, Femy Amin, and Jonathan S. Nguyen-Van-Tam. Recent advances in the influenza virus vaccine landscape: a comprehensive overview of technologies and trials. Clinical Microbiology Reviews, Dec 2024. URL: https://doi.org/10.1128/cmr.00025-24, doi:10.1128/cmr.00025-24. This article has 12 citations and is from a highest quality peer-reviewed journal.

32. (clark2024recentadvancesin pages 25-27): Tristan W. Clark, John S. Tregoning, Helen Lister, Tiziano Poletti, Femy Amin, and Jonathan S. Nguyen-Van-Tam. Recent advances in the influenza virus vaccine landscape: a comprehensive overview of technologies and trials. Clinical Microbiology Reviews, Dec 2024. URL: https://doi.org/10.1128/cmr.00025-24, doi:10.1128/cmr.00025-24. This article has 12 citations and is from a highest quality peer-reviewed journal.

33. (clark2024recentadvancesin pages 19-22): Tristan W. Clark, John S. Tregoning, Helen Lister, Tiziano Poletti, Femy Amin, and Jonathan S. Nguyen-Van-Tam. Recent advances in the influenza virus vaccine landscape: a comprehensive overview of technologies and trials. Clinical Microbiology Reviews, Dec 2024. URL: https://doi.org/10.1128/cmr.00025-24, doi:10.1128/cmr.00025-24. This article has 12 citations and is from a highest quality peer-reviewed journal.

34. (sun2024mechanisticinsightsinto pages 1-2): Yuling Sun and Kaituo Liu. Mechanistic insights into influenza a virus-induced cell death and emerging treatment strategies. Veterinary Sciences, 11:555, Nov 2024. URL: https://doi.org/10.3390/vetsci11110555, doi:10.3390/vetsci11110555. This article has 14 citations.