Publications by authors named "A Bugatti"

Genomic surveillance based on sequencing the entire genetic code of SARS-CoV-2 involves monitoring and studying genetic changes and variations in disease-causing organisms such as viruses and bacteria. By tracing the virus, it is possible to prevent epidemic spread in the community, ensuring a 'precision public health' strategy. A peptide-based design was applied to provide an efficacious strategy that is able to counteract any emerging viral variant of concern dynamically and promptly to affect the outcomes of a pandemic at an early stage while waiting for the production of the anti-variant-specific vaccine, which require longer times.

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  • HIV-1 matrix protein p17 variants (vp17s) have amino acid insertions and exhibit stronger B cell growth and clonogenic activity than the wild-type version (refp17).
  • Higher prevalence of vp17s has been observed in people living with HIV-1 who have lymphoma, suggesting a possible link to lymphomagenesis.
  • The study explored the molecular mechanisms behind vp17s development, identifying mutation hot spots in the matrix protein region and demonstrating that these areas contribute to genetic recombination events that might lead to vp17s formation.
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  • During the COVID-19 pandemic, drug repurposing was used to quickly address medical challenges, focusing on methotrexate (MTX) and its anti-viral effects.
  • Research found that DHFR inhibitors significantly impacted virus-induced cell damage, showing both anti-metabolic and anti-viral properties.
  • Pralatrexate and trimetrexate were particularly effective against viral infections, suggesting that their broader effects could benefit patients already using similar treatments for SARS-CoV-2.
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  • Severe COVID-19 shows angiogenic characteristics due to direct infection of lung endothelial cells (ECs) by SARS-CoV-2, particularly through the Spike protein's Arg-Gly-Asp (RGD) motif.
  • * Recent findings indicate that SARS-CoV-2 can infect ACE2-negative human lung microvascular ECs, leading to a pro-inflammatory and pro-angiogenic response.
  • * The emergence of the D405N mutation in recent Omicron subvariants may reduce the virus's ability to infect these cells, potentially resulting in milder disease compared to earlier variants.*
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