Remdesivir: A Closer Look at Its Effect in COVID-19 Pandemic.

BACKGROUND: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiology of COVID-19 pandemic, resulted in significant harm to the affected countries in every aspect of life. The virus infected over 139 million patients and resulted in over 2.9 million deaths until April 16, 2021. New variants of this virus were identified that spread rapidly worldwide. SUMMARY: Remdesivir, a prodrug of adenosine nucleotide analog, is an antiviral with a broad spectrum of activity that was tested on SARS and Middle East respiratory syndrome infections. In vitro studies conducted on SARS-CoV-2 revealed that remdesivir inhibited viral replication with high selectivity index in cell cultures. In vivo studies showed that remdesivir reduced viral load in bronchoalveolar lavage fluid and attenuated pulmonary infiltrates in infected animals. Further, remdesivir showed promising results in terms of clinical improvement, shortening the recovery time, mortality rate, and the duration of oxygen need, despite that some clinical trials did not reveal significant effect on remdesivir use. Several studies showed positive results of remdesivir against the new variants. Key Messages: Remdesivir showed a promising beneficial effect against new variants of SARS-CoV-2, but more clinical evidence is needed to confirm this effect.

Effect of E-Cigarette aerosol exposure on airway inflammation in a murine model of asthma.

OBJECTIVE: The popularity of electronic cigarettes (E-Cigs) smoking is increasing worldwide including patients with asthma. In this study, the effects of E-Cigs aerosol exposure on airway inflammation in an allergen-driven murine model of asthma were investigated. MATERIALS AND METHODS: Balb/c mice were randomly assigned to; control group (received fresh air, Ovalbumin (Ova) sensitization and saline challenge), E-Cig group (received E-Cig aerosol, Ova sensitization, and saline challenge), Ova S/C group (received fresh air, Ova sensitization and Ova challenge) and E-Cig + Ova S/C group. Bronchoalveolar lavage fluid (BALF) and lung tissue were evaluated for inflammatory cells and inflammatory mediators, respectively. RESULTS: Exposure to E-Cig aerosol significantly increased the number of all types of inflammatory cells in BALF (p < 0.05). Further, E-Cig aerosol reduced levels of transforming growth factor (TGF)-ß1 and matrix metalloproteinase (MMP)-2 in lung tissue homogenate (p < 0.05). Combined E-Cig aerosol and Ova S/C increased the airway recruitment of inflammatory cells, especially neutrophils, eosinophils, and lymphocytes (p < 0.05), increased the level of interleukin (IL)-13, and reduced the level of TGF-ß1 (p < 0.05). CONCLUSIONS: E-Cig aerosol exposure induced airway inflammation in both control mice and allergen-driven murine model of asthma. The inflammatory response induced by E-Cig was slightly higher in allergen-driven murine model of asthma than in healthy animals.