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Record W4406736953 · doi:10.1128/jvi.01804-24

Mitochondrial injury and complement dysregulation are drivers of pathological inflammation in viral myocarditis

2025· article· en· W4406736953 on OpenAlexafffund
Yasir Mohamud, Amirhossein Bahreyni, Sinwoo Wendy Hwang, Jingfei Carly Lin, Zhihan Claire Wang, Jingchun Zhang, Honglin Luo

Bibliographic record

VenueJournal of Virology · 2025
Typearticle
Languageen
FieldMedicine
TopicViral Infections and Immunology Research
Canadian institutionsSt. Paul's HospitalUniversity of British Columbia
FundersNatural Sciences and Engineering Research Council of CanadaCanadian Institutes of Health Research
KeywordsBiologyInflammationCoxsackievirusImmunologyMyocarditisComplement systemImmune systemInnate immune systemMacrophagePathogenesisVirusVirologyEnterovirusMedicineIn vitro

Abstract

fetched live from OpenAlex

ABSTRACT Enteroviruses cause nearly 1 billion global infections annually and are associated with a diverse array of human illnesses. Among these, myocarditis and the resulting chronic inflammation have been recognized as major contributing factors to virus-induced heart failure. Despite our growing understanding, very limited therapeutic strategies have been developed to address the pathological consequences of virus-induced chronic innate immune activation. Coxsackievirus B3 (CVB3) was used as a model cardiotropic enterovirus. We leveraged in vitro cell-based studies to investigate cardiomyocyte and macrophage interaction during CVB3 infection, as well as animal studies and unique human cardio specimens to evaluate mechanisms of viral heart injury. We present evidence that viral myocarditis is in part exacerbated by pathological activation of the complement pathway in cells, mice, and human cardiac tissues. We demonstrate unique cell type-specific responses to viral infection that are exacerbated by mitochondrial injury in cardiomyocytes and NFκB-dependent pro-inflammatory response in macrophages. Macrophages are robustly activated by damage-associated mitochondrial components, including mitochondrial proteins and lipid extracts. Mechanistically, we identify complement protective factors CD59/protectin and CD55/DAF as novel targets of viral proteinase that acts to release the brakes on complement-mediated autoinjury. Collectively, our study highlights a novel mechanism that can act as a potential contributor to CVB3 pathogenesis through mitochondrial injury-mediated autoimmunity. IMPORTANCE This study sheds light on how enteroviruses, specifically coxsackievirus B3, may contribute to heart failure by triggering harmful immune responses in the heart. We discovered that viral infections in heart cells cause mitochondrial damage, which in turn activates a destructive immune response involving the complement system. This immune activation is one of the significant contributors that lead to further injury of heart tissues, worsening the damage caused by the virus. Additionally, we identified key protective molecules that are targeted and disrupted by the virus, allowing the immune system to attack the heart even more aggressively. Understanding these mechanisms may provide additional insights into how viral infections can lead to chronic heart conditions and suggests potential therapeutic targets to prevent or reduce heart damage in patients affected by viral myocarditis.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.001
Threshold uncertainty score0.004

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.001
Insufficient payload (model declined to judge)0.0010.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.012
GPT teacher head0.323
Teacher spread0.311 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations7
Published2025
Admission routes2
Has abstractyes

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