Статья

Why covid-19 transmission is more efficient and aggressive than viral transmission in previous coronavirus epidemics?

F. Elrashdy, E. Redwan, V. Uversky,
2021

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. © 2020 by the authors. Licensee MDPI, Basel, Switzerland.

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  • 1. Version of Record от 2021-04-27

Метаданные

Об авторах
  • F. Elrashdy
    Department of Endemic Medicine and Hepatogastroenterology, Kasr Alainy School of Medicine, Cairo University, Cairo, 11562, Egypt
  • E. Redwan
    Biological Science Department, Faculty of Science, King Abdulaziz University, P.O. Box 80203, Jeddah, 21589, Saudi Arabia
  • V. Uversky
    Department of Molecular Medicine and USF Health Byrd Alzheimer’s Research Institute, Morsani College of Medicine, University of South Florida, Tampa, FL 33612, United States
Название журнала
  • Biomolecules
Том
  • 10
Выпуск
  • 9
Страницы
  • 1-33
Ключевые слова
  • angiotensin converting enzyme 2; chloroquine; dipeptidyl peptidase IV; epithelial sodium channel; glutamyl aminopeptidase; hemagglutinin; hydroxychloroquine; membrane protein; microsomal aminopeptidase; nucleocapsid protein; plasmin; tumor necrosis factor; virus envelope protein; virus spike protein; angiotensin converting enzyme 2; dipeptidyl carboxypeptidase; peptide hydrolase; viral protein; virus receptor; coronavirus disease 2019; DNA polymorphism; Editorial; endocytosis; environmental factor; epidemic; human; innate immunity; Middle East respiratory syndrome coronavirus; nonhuman; SARS coronavirus; Severe acute respiratory syndrome coronavirus 2; signal transduction; single cell RNA seq; smoking; virus entry; virus load; virus morphology; virus pathogenesis; virus replication; virus transmission; virus virulence; age; animal; antibody specificity; Betacoronavirus; comparative study; complication; Coronavirinae; Coronavirus infection; cytokine release syndrome; disease carrier; epidemic; female; genetics; global health; host pathogen interaction; host range; male; pandemic; pathogenicity; pathophysiology; physiology; risk factor; severe acute respiratory syndrome; veterinary medicine; viral tropism; virology; virulence; virus pneumonia; Age Factors; Animals; Betacoronavirus; Coronavirus; Coronavirus Infections; Cytokine Release Syndrome; Disease Outbreaks; Disease Reservoirs; Female; Global Health; Host Specificity; Host-Pathogen Interactions; Humans; Male; Middle East Respiratory Syndrome Coronavirus; Organ Specificity; Pandemics; Peptide Hydrolases; Peptidyl-Dipeptidase A; Pneumonia, Viral; Receptors, Virus; Risk Factors; SARS Virus; Severe Acute Respiratory Syndrome; Viral Proteins; Viral Tropism; Virulence; Virus Internalization
Издатель
  • MDPI AG
Тип документа
  • Editorial
Тип лицензии Creative Commons
  • CC
Правовой статус документа
  • Свободная лицензия
Источник
  • scopus