Fighting the War Against COVID-19 via Cell-Based Regenerative Medicine: Lessons Learned from 1918 Spanish Flu and Other Previous Pandemics

Abstract

The human population is in the midst of battling a rapidly-spreading virus- Severe Acute Respiratory Syndrome Coronavirus 2, responsible for Coronavirus disease 2019 or COVID-19. Despite the resurgences in positive cases after reopening businesses in May, the country is seeing a shift in mindset surrounding the pandemic as people have been eagerly trickling out from federally-mandated quarantine into restaurants, bars, and gyms across America. History can teach us about the past, and today's pandemic is no exception. Without a vaccine available, three lessons from the 1918 Spanish flu pandemic may arm us in our fight against COVID-19. First, those who survived the first wave developed immunity to the second wave, highlighting the potential of passive immunity-based treatments like convalescent plasma and cell-based therapy. Second, the long-term consequences of COVID-19 are unknown. Slow-progressive cases of the Spanish flu have been linked to bacterial pneumonia and neurological disorders later in life, emphasizing the need to reduce COVID-19 transmission. Third, the Spanish flu killed approximately 17 to 50 million people, and the lack of human response, overcrowding, and poor hygiene were key in promoting the spread and high mortality. Human behavior is the most important strategy for preventing the virus spread and we must adhere to proper precautions. This review will cover our current understanding of the pathology and treatment for COVID-19 and highlight similarities between past pandemics. By revisiting history, we hope to emphasize the importance of human behavior and innovative therapies as we wait for the development of a vaccine. Graphical Abstract.

Keywords: 1918 Influenza Pandemic; Antiviral Drugs; COVID-19; Coronavirus; Pandemics; SARS Virus; Stem Cells; Vaccines.

Graphical Abstract

Fig. 1

The trimeric spike protein of SARS-Cov-2 mediates the entry of the virus into host cells via the ACE2 receptor. The ACE2 receptor is present in various organs throughout the body making multi-organ infection possible

Fig. 2

The coexpression of ACE2 receptors and TMPRSS2 transmembrane proteases by type 2 pneumocytes explains the susceptibility of the lungs to SP-mediated SARS-Cov-2 infection. Infection activates the immune cascade resulting in extensive tracheobronchial inflammation, diffuse alveolar damage, alveolar edema, pneumocyte desquamation, fibrin deposition, pneumocyte hyperplasia, and recruitment of alveolar macrophages