A critical analysis of SARS-CoV-2 (COVID-19) complexities, emerging variants, and therapeutic interventions and vaccination strategies.

Coronavirus is a family of viruses that can cause diseases such as the common cold, severe acute respiratory syndrome (SARS), and Middle East respiratory syndrome (MERS). The universal outbreak of coronavirus disease 2019 (COVID-19) caused by SARS coronaviruses 2 (SARS-CoV-2) has become a global pandemic. The ß-Coronaviruses, which caused SARS-CoV-2 (COVID-19), have spread in more than 213 countries, infected over 81 million people, and caused more than 1.79 million deaths. COVID-19 symptoms vary from mild fever, flu to severe pneumonia in severely ill patients. Difficult breathing, acute respiratory distress syndrome (ARDS), acute kidney disease, liver damage, and multi-organ failure ultimately lead to death. Researchers are working on different pre-clinical and clinical trials to prevent this deadly pandemic by developing new vaccines. Along with vaccines, therapeutic intervention is an integral part of healthcare response to address the ongoing threat posed by COVID-19. Despite the global efforts to understand and fight against COVID-19, many challenges need to be addressed. This article summarizes the current pandemic, different strains of SARS-CoV-2, etiology, complexities, surviving medications of COVID-19, and so far, vaccination for the treatment of COVID-19.

Anti-Inflammatory Effects of Famotidine

The COVID-19 pandemic in the U.S. currently exceeds 21.1 million cases and 350,000 deaths. Consumption of famotidine, a histamine H2 receptor antagonist widely used to treat acid reflux and gastritis, is associated with improved survival and attenuated COVID-19 disease severity (Mather JF et al. Am J Gastroenterol. 115:1617,2020;Freedberg DE, et al. Gastroenterology 159: 1129, 2020;Janowitz T et al. Gut, 69:1592, 2020). However, the mode of action for these beneficial effects is unknown. Here we studied famotidine in mice exposed to bacterial endotoxin (lipopolysaccharide, LPS). LPS (6 mg/kg) was administered intraperitoneally in male C57BL/6 mice followed by intraperitoneal injection of famotidine (100 µg/mouse) or vehicle (PBS) twice daily for 3 days. Two-week survival was 100% in the famotidine-treated group vs. 70% in the PBS-control group (n=30/group, p < 0.05). Furthermore, famotidine administration significantly reduced serum and splenic TNF levels and serum IL-6 levels in the endotoxemic mice (p<0.05, famotidine vs. PBS). Human peripheral blood mononuclear cells co-cultured with famotidine and LPS also express significantly reduced amounts of pro-inflammatory cytokines (TNF, IL-6, HMGB1, IP-10, GM-CSF). Together these results indicate famotidine inhibits endotoxin induced cytokine storm and attenuates lethality in mice exposed to lethal endotoxemia.