Publications by authors named "F Jessop"
Article Synopsis
- The yellow fever virus 17D (YFV-17D) vaccine is highly effective at generating antiviral immunity, but the mechanisms behind its immune response remain unclear.
- Researchers discovered that YFV-17D infection triggers mitochondrial activity and metabolic changes that enhance the production of type I interferon (IFN), a key part of the immune response.
- The study found that reactive oxygen species (mROS) and peroxynitrite produced by mitochondrial hyperactivity play a crucial role in activating innate immunity, making the vaccine more effective against infection.
Article Synopsis
- The PINK1/Parkin pathway is linked to both Parkinson's disease and prion diseases, indicating its role in neurodegeneration.
- Mice lacking PINK1 or Parkin (PINK1KO and ParkinKO) showed faster disease progression when infected with prions, succumbing to the disease sooner than normal mice.
- Despite similar prion pathology across the groups, the increased activity of mitochondrial respiration Complex I in the KO mice suggests that PINK1/Parkin helps reduce reactive oxygen species (ROS), potentially slowing disease progression.
Streptococcus agalactiae (Group B Streptococcus; GBS) is a common cause of sepsis in neonates. Previous work detected GBS DNA in the placenta in ~5% of women before the onset of labour, but the clinical significance of this finding is unknown. Here we re-analysed this dataset as a case control study of neonatal unit (NNU) admission.
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- The study examines how the route of infection (intranasal vs. intradermal) with the bacterium Francisella tularensis affects disease progression and host metabolism in mice.
- Researchers found that metabolic changes varied depending on the infection route, with intradermal infections causing early metabolic shifts at the infection site, while intranasal infections did not show this response in the lungs.
- The findings suggest that understanding these specific metabolic responses could lead to new therapeutic strategies targeting unique metabolic features in different tissues during infections.
Dysregulation of host metabolism is a feature of lethal SARS-CoV-2 infection. Perturbations in α-ketoglutarate levels can elicit metabolic reprogramming through 2-oxoglutarate-dependent dioxygenases (2-ODDGs), leading to stabilization of the transcription factor HIF-1α. HIF1-α activation has been reported to promote antiviral mechanisms against SARS-CoV-2 through direct regulation of ACE2 expression (a receptor required for viral entry).
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