Natural selection
Can leaky vaccines favor nastier viruses?
Open access · cc by · source: Europe PMC
Imperfect Marek’s disease vaccination keeps infected chickens alive longer, boosting transmission of strains too lethal to persist without vaccines.
Study at a glance
- Design
- Animal / in-vitro — Experimental MDV infection of vaccinated vs unvaccinated chicks with shedding and sentinel transmission assays
- N
- Multiple experiments (e.g., n=200, 120, 60 vaccinated + 60 maternal-Ab groups) — no single primary N
- Population
- One-day-old chicks infected with Marek's disease virus strains
- Outcome
- Infectious period, shedding, and sentinel infection under imperfect vaccination
Structured fields used in claim comparison tables when every cited study has a complete layer.
Key findings
Vaccination prolongs infectious periods (~2 weeks), speeds sentinel infection (~9 days earlier), and can maintain hyperpathogenic strains that kill unvaccinated birds at up to 100%.
Methodology
Authors experimentally infected vaccinated and unvaccinated chickens with MDV strains of different virulence and measured shedding, sentinel infection, and infectious periods.
Limitations
Experiments show vaccination can maintain hypervirulent strains, not that vaccines alone historically caused MDV evolution.
How this study connects
Role on claims
Each row is a claim on a concept or method page where this paper supports, challenges, or qualifies the statement. Roles are hand-checked — not a model guess.
Multiple empirical papers in this library examine natural selection with mechanistic biological findings.
Evidence for the claim as stated.
Vaccination prolongs infectious periods (~2 weeks), speeds sentinel infection (~9 days earlier), and can maintain hyperpathogenic strains that kill unvaccinated birds at up to 100%.
Evidence for the claim as stated.
Systems and scales differ across natural selection studies (species, tissues, methods), so mechanisms should not be over-generalised.
Evidence for the claim as stated.
Leaky Marek's disease vaccines in chickens prolonged infectious periods by about 2 weeks, sped sentinel infection by about 9 days, and allowed hyperpathogenic strains that kill unvaccinated birds at up to 100% to be maintained. Shedding and sentinel infection are the endpoints; plate immunoassays, if used for virus or antibody, are not described as the intellectual core, and the experiment shows vaccines can maintain hypervirulent strains rather than that vaccines historically caused MDV evolution by themselves.
Evidence for the claim as stated.
The three tagged studies disagree about what an 'ELISA paper' would even be measuring. MC4R work is cellular receptor trafficking and cAMP/ERK; MDV work is shedding, infectious period (~2 weeks) and sentinel timing (~9 days earlier) in chickens; E. coli OMV work is NOD1/NOD2 ligands and epithelial barrier signalling. They share an immunoassay-shaped supporting assay at most, not a common antigen.
Evidence for the claim as stated.
Implications also conflict if someone treats every plate assay as the same. A normal cAMP well for an MC4R variant can hide a trafficking defect relevant to obesity genetics; a high viral titre after leaky vaccination can hide increased transmission of hyperpathogenic MDV; an epithelial cytokine bump after OMVs is not probiotic efficacy in patients.
Evidence for the claim as stated.
Open questions
Tensions this paper is part of
From concept pages' “where studies disagree.” Disagreement means the same question; scope means different assays, populations, or outcomes.
Systems and scales differ across natural selection studies (species, tissues, methods), so mechanisms should not be over-generalised.
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The three tagged studies disagree about what an 'ELISA paper' would even be measuring. MC4R work is cellular receptor trafficking and cAMP/ERK; MDV work is shedding, infectious period (~2 weeks) and sentinel timing (~9 days earlier) in chickens; E. coli OMV work is NOD1/NOD2 ligands and epithelial barrier signalling. They share an immunoassay-shaped supporting assay at most, not a common antigen.
Implications also conflict if someone treats every plate assay as the same. A normal cAMP well for an MC4R variant can hide a trafficking defect relevant to obesity genetics; a high viral titre after leaky vaccination can hide increased transmission of hyperpathogenic MDV; an epithelial cytokine bump after OMVs is not probiotic efficacy in patients.
Related papers in this topic
Same topic cluster — not a recommendation engine.