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May 28, 2013PLoS ONEOpen Access

Mechanisms of Foot-and-Mouth Disease Virus Tropism Inferred from Differential Tissue Gene Expression

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Key result

FMDV tissue tropism is driven by differential expression of the integrin aVb6 receptor, fibronectin, IL-1 cytokines, death receptors, and genes involved in extracellular matrix turnover and interferon signaling.

Population

5 Holstein steers weighing 225 to 300 kg

Comparison

Aerosol-inoculation with FMDV-A24-Cruzeiro vs Mock inoculation with sterile cell culture media

Design

Preclinical

Follow-up

72 hours

Authors

JZJames ZhuAgricultural Research ServiceJAJonathan ArztNational Agricultural Statistics ServiceMPMichael PucketteNational Agricultural Statistics Service

Discussion

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Implication

Hypothesis-generating for FMDV host specificity in cattle; leaves open validation and therapeutic translation in vivo.

Structured PICO

P
Population
5 Holstein steers weighing 225 to 300 kg, either infected with FMDV or mock-inoculated, evaluated for differential tissue gene expression at 72 hours.
E
Exposure
Aerosol-inoculation with FMDV-A24-Cruzeiro
C
Comparator
Mock inoculation with sterile cell culture media
O
Outcome
Differential gene expression between FMDV-targeted and non-targeted tissuessurrogate

Differential gene expression of integrin receptors, interferon signaling, and extracellular matrix turnover determines FMDV tissue tropism in cattle.

Limitations

  • Small sample size of 5 animals
  • Inferences based on mRNA expression levels rather than protein or functional assays
  • Evaluated at a single time point (72 hours post-infection)

Cite This Study

Zhu et al. (2013) studied Foot-and-Mouth Disease Virus (FMDV) infection (n=5). FMDV-targeted tissues vs. Non-targeted tissues was evaluated on Differential gene expression between FMDV-targeted and non-targeted tissues. FMDV tissue tropism is driven by differential expression of the integrin aVb6 receptor, fibronectin, IL-1 cytokines, death receptors, and genes involved in extracellular matrix turnover and interferon signaling.

synapsesocial.com/papers/6a6f58fb6ceb2bbd16dfa640https://doi.org/10.1371/journal.pone.0064119
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Antibodies to the vitronectin receptor (integrin alpha V beta 3) inhibit binding and infection of foot-and-mouth disease virus to cultured cells1995 · 301 citations
  2. 2Integrin αvβ8 Functions as a Receptor for Foot-and-Mouth Disease Virus: Role of the β-Chain Cytodomain in Integrin-Mediated Infection2004 · 144 citations
  3. 3The Epithelial Integrin αvβ6 Is a Receptor for Foot-and-Mouth Disease Virus2000 · 301 citations
  4. 4Interferon-Induced Protection against Foot-and-Mouth Disease Virus Infection Correlates with Enhanced Tissue-Specific Innate Immune Cell Infiltration and Interferon-Stimulated Gene Expression2009 · 68 citations
  5. 5Interleukin-1beta-induced expression of the urokinase-type plasminogen activator receptor and its co-localization with MMPs in human articular chondrocytes.2004 · 29 citations