Differences in TGF-β1 Signaling in SIV Infections
Author Information
Author(s): Mickaël J-Y Ploquin, Jean-François Desoutter, Patricia R Santos, Ivona Pandrea, Ousmane M Diop, Anne Hosmalin, Cécile Butor, Françoise Barre-Sinoussi, Michaela C Müller-Trutwin
Primary Institution: Institut Pasteur, Paris, France
Hypothesis
Macaques are unable to respond to TGF-β1 and thus cannot resorb virus-driven inflammation.
Conclusion
The inability to control inflammation during pathogenic SIV infections is linked to unresponsiveness to TGF-β1.
Supporting Evidence
- SIVmac infection leads to stronger inflammatory responses compared to SIVagm.
- AGMs show a longer-lasting up-regulation of smad4, enhancing TGF-β1 signaling.
- SIV-infected MACs exhibit up-regulation of smad7, inhibiting TGF-β1 signaling.
Takeaway
This study shows that some monkeys can handle a virus better than others because their bodies respond differently to a signaling molecule that helps control inflammation.
Methodology
Real-time PCR was used to measure the expression of inflammatory markers and TGF-β1 signaling mediators in blood samples from 6 AGMs and 6 MACs.
Participant Demographics
6 African Green Monkeys and 6 Rhesus Macaques
Statistical Information
P-Value
p ≤ 0.046
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
Want to read the original?
Access the complete publication on the publisher's website