Two Years into the COVID-19 Pandemic: Lessons Learned

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a highly transmissible and virulent human-infecting coronavirus that emerged in late December 2019 in Wuhan, China, causing a respiratory disease called coronavirus disease 2019 (COVID-19), which has massively impacted global public health and caused widespread disruption to daily life. The crisis caused by COVID-19 has mobilized scientists and public health authorities across the world to rapidly improve our knowledge about this devastating disease, shedding light on its management and control, and spawned the development of new countermeasures. Here we provide an overview of the state of the art of knowledge gained in the last 2 years about the virus and COVID-19, including its origin and natural reservoir hosts, viral etiology, epidemiology, modes of transmission, clinical manifestations, pathophysiology, diagnosis, treatment, prevention, emerging variants, and vaccines, highlighting important differences from previously known highly pathogenic coronaviruses. We also discuss selected key discoveries from each topic and underline the gaps of knowledge for future investigations.

The emergence of new SARS-CoV-2 omicron subvariants introduces uncertainty about the end of the COVID-19 pandemic

“…The emergence of SARS-CoV-2 has been characterized by the identification of several variants of concern (VOCs) during the pandemic course: alpha (B.1.1.7), beta (B.1.351), gamma (P.1), and delta (B.1.617.2) ( 4 , 5 ). Over the last 2 years these emerging variants have been associated with an abrupt increase in the number of COVID-19 cases, catalyzing several waves of the pandemic in many countries around the globe ( 6 ). More recently, the omicron (B.1.1.529) variant was first reported in Botswana and South Africa at the end of November 2021.…”

Use of traditional and complementary medicine for COVID 19 prophylaxis among healthcare professionals and students in Jordan: A cross-sectional study

“…The median incubation period of the infection is approximately 4−5 days, up to 14 days. Most of COVID-19 patients present with mild to moderate symptoms (81%) [ 3 ] including cough, fever, weariness, myalgia, and diarrhea; in severe cases (approximately 14% of infected patients) the disease may cause lung damage [ 4 ] and may require ventilation in an intensive care unit (ICU), and 5% eventually develop more critical manifestations such as acute respiratory distress syndrome (ARDS), septic shock, and multiple organ dysfunction or failure [ 3 ]. COVID 19 has an impact on many elements of a patient’s life and can be particularly harmful to people with pre-existing health problems [ 4 ].…”

“…The SARS-CoV-2 virus’ main determinant of viral entry in host cells is the spike (S) glycoprotein, which forms trimers on the surface of virions [ 6 ]. To promote viral entry, proteases, including TMPRSS2, furin, and CatB/L, cleave the S protein, with subsequent entry of SARS-CoV-2 and fusion of the viral envelope and endosome, followed by release of the viral ribonucleoprotein complex into the cell [ 3 , 6 ]. The main cells infected by SARS-CoV-2 are nasopharyneal or tracheal mucosal cells.…”

“…CCL2, CCL3, CCL7 and CXCL10 are potent chemokines for monocytes found at high concentrations in patients with severe COVID 19. Increased levels of several cytokines (interleukin (IL)-1β, IL-2, IL-6, IL-7, IL-8, IL-10, IL-17, IFN-γ, IFN-γ-inducible protein 10, MCP-1, G-CSF, MIP-1α, and TNF-α) that leads to systemic inflammatory response (cytokine storm) have been reported in patients with severe COVID-19 [ 3 ]. Severe COVID-19 may also lead to extrapulmonary disease, including gastrointestinal symptoms and acute cardiac, kidney and liver injury, in addition to cardiac arrhythmias, rhabdomyolysis, coagulopathy and shock; in extreme cases manifested as multiorgan injury [ 3 , 6 ].…”

“…Increased levels of several cytokines (interleukin (IL)-1β, IL-2, IL-6, IL-7, IL-8, IL-10, IL-17, IFN-γ, IFN-γ-inducible protein 10, MCP-1, G-CSF, MIP-1α, and TNF-α) that leads to systemic inflammatory response (cytokine storm) have been reported in patients with severe COVID-19 [ 3 ]. Severe COVID-19 may also lead to extrapulmonary disease, including gastrointestinal symptoms and acute cardiac, kidney and liver injury, in addition to cardiac arrhythmias, rhabdomyolysis, coagulopathy and shock; in extreme cases manifested as multiorgan injury [ 3 , 6 ]. The mechanisms of multiorgan injury include endothelial cell damage, thromboinflammation, dysregulation of the renin−angiotensin−aldosterone system (RAAS) and of the immune response, and direct viral toxicity [ 3 ].…”