Why COVID-19 Transmission Is More Efficient and Aggressive Than Viral Transmission in Previous Coronavirus Epidemics?

Biomolecules. 2020 Sep 11;10(9):1312. doi: 10.3390/biom10091312.

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is causing a pandemic of coronavirus disease 2019 (COVID-19). The worldwide transmission of COVID-19 from human to human is spreading like wildfire, affecting almost every country in the world. In the past 100 years, the globe did not face a microbial pandemic similar in scale to COVID-19. Taken together, both previous outbreaks of other members of the coronavirus family (severe acute respiratory syndrome (SARS-CoV) and middle east respiratory syndrome (MERS-CoV)) did not produce even 1% of the global harm already inflicted by COVID-19. There are also four other CoVs capable of infecting humans (HCoVs), which circulate continuously in the human population, but their phenotypes are generally mild, and these HCoVs received relatively little attention. These dramatic differences between infection with HCoVs, SARS-CoV, MERS-CoV, and SARS-CoV-2 raise many questions, such as: Why is COVID-19 transmitted so quickly? Is it due to some specific features of the viral structure? Are there some specific human (host) factors? Are there some environmental factors? The aim of this review is to collect and concisely summarize the possible and logical answers to these questions.

Keywords: COVID-19; SARS-CoV-2; coronavirus disease 2019; severe acute respiratory syndrome coronavirus 2; viral infection; virus-host interaction.

Publication types

  • Comparative Study
  • Editorial
  • Review

MeSH terms

  • Age Factors
  • Angiotensin-Converting Enzyme 2
  • Animals
  • Betacoronavirus / genetics
  • Betacoronavirus / pathogenicity*
  • COVID-19
  • Coronavirus / pathogenicity*
  • Coronavirus Infections / complications
  • Coronavirus Infections / epidemiology
  • Coronavirus Infections / transmission*
  • Coronavirus Infections / veterinary
  • Coronavirus Infections / virology
  • Cytokine Release Syndrome / etiology
  • Cytokine Release Syndrome / physiopathology
  • Disease Outbreaks
  • Disease Reservoirs / virology
  • Female
  • Global Health
  • Host Specificity
  • Host-Pathogen Interactions
  • Humans
  • Male
  • Middle East Respiratory Syndrome Coronavirus / pathogenicity
  • Organ Specificity
  • Pandemics*
  • Peptide Hydrolases / physiology
  • Peptidyl-Dipeptidase A / physiology
  • Pneumonia, Viral / complications
  • Pneumonia, Viral / epidemiology
  • Pneumonia, Viral / transmission*
  • Pneumonia, Viral / virology
  • Receptors, Virus / physiology
  • Risk Factors
  • SARS-CoV-2
  • Severe Acute Respiratory Syndrome / epidemiology
  • Severe acute respiratory syndrome-related coronavirus / pathogenicity
  • Viral Proteins / physiology
  • Viral Tropism
  • Virulence
  • Virus Internalization

Substances

  • Receptors, Virus
  • Viral Proteins
  • Peptide Hydrolases
  • Peptidyl-Dipeptidase A
  • ACE2 protein, human
  • Angiotensin-Converting Enzyme 2