Publications by authors named "B Mazel-Sanchez"
Article Synopsis
- Influenza A virus primarily enters host cells through a process called clathrin-dependent receptor-mediated endocytosis, but the exact entry receptor has not been definitively identified.
- Researchers used a method involving proximity ligation and mass spectrometry to identify transferrin receptor 1 (TfR1) as a potential receptor that facilitates IAV entry.
- Experiments confirmed that TfR1's recycling is crucial for virus entry, and even modified forms of TfR1 can assist in IAV uptake, highlighting a unique mechanism by which the virus exploits the receptor.
Over the last century, the number of epidemics caused by RNA viruses has increased and the current SARS-CoV-2 pandemic has taught us about the compelling need for ready-to-use broad-spectrum antivirals. In this scenario, natural products stand out as a major historical source of drugs. We analyzed the antiviral effect of 4 stilbene dimers [1 (trans-δ-viniferin); 2 (11',13'-di-O-methyl-trans-δ-viniferin), 3 (11,13-di-O-methyl-trans-δ-viniferin); and 4 (11,13,11',13'-tetra-O-methyl-trans-δ-viniferin)] obtained from plant substrates using chemoenzymatic synthesis against a panel of enveloped viruses.
View Article and Find Full Text PDFTogether with inactivated influenza vaccines (IIV), live attenuated influenza vaccines (LAIV) are an important tool to prevent influenza A virus (IAV) illnesses in patients. LAIVs present the advantages to have a needle-free administration and to trigger a mucosal immune response. LAIV is approved for healthy 2- to 49-year old individuals.
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- * Early-life exposure to antibiotics or infections can lead to imbalances in microbiota development, potentially increasing the risk of metabolic disorders in adulthood.
- * A study on infant mice infected with a mild strain of influenza A virus showed lasting changes in microbiota and increased fat mass, suggesting that even minor viral infections during infancy can have significant long-term effects on health and physiology.
Influenza A viruses balance ER stress with host protein synthesis shutoff.
Proc Natl Acad Sci U S A
September 2021
Excessive production of viral glycoproteins during infections poses a tremendous stress potential on the endoplasmic reticulum (ER) protein folding machinery of the host cell. The host cell balances this by providing more ER resident chaperones and reducing translation. For viruses, this unfolded protein response (UPR) offers the potential to fold more glycoproteins.
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