Publications by authors named "Shawna Benjamin"

The gut microbiota metabolizes drugs and alters their efficacy and toxicity. Diet alters drugs, the metabolism of the microbiota, and the host. However, whether diet-triggered metabolic changes in the microbiota can alter drug responses in the host has been largely unexplored.

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Influenza virus causes infected cells to generate large numbers of lipid droplets. Because the virus envelope contains substantial cholesterol, we applied atorvastatin (ATV) to Madin-Darby Canine Kidney cells before infecting them. Five micromolars ATV, within physiologic range, strongly (>95%) inhibits reproduction of influenza A as measured by PCR of viral RNA, plaque assay for viable virus, and production of virus nucleoprotein (NP).

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Lysosomes are highly acidic cellular organelles traditionally viewed as sacs of enzymes involved in digesting extracellular or intracellular macromolecules for the regeneration of basic building blocks, cellular housekeeping, or pathogen degradation. Bound by a single lipid bilayer, lysosomes receive their substrates by fusing with endosomes or autophagosomes, or through specialized translocation mechanisms such as chaperone-mediated autophagy or microautophagy. Lysosomes degrade their substrates using up to 60 different soluble hydrolases and release their products either to the cytosol through poorly defined exporting and efflux mechanisms or to the extracellular space by fusing with the plasma membrane.

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Article Synopsis
  • Autophagy is a cellular response activated during influenza A virus infection that helps infected cells avoid programmed cell death (apoptosis).
  • Infected cells can experience increased autophagy, leading to cell death even when apoptosis is blocked, indicating the presence of different control mechanisms for protective and lethal autophagy.
  • The activation of autophagy involves specific signaling pathways, with a distinction between the conditions that promote survival versus those leading to cell death, suggesting that inhibiting certain autophagy pathways can reduce virus replication.
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