J Bacteriol Virol.  2020 Jun;50(2):65-75. 10.4167/jbv.2020.50.2.065.

Strength and Weakness of Molecular Identification Strategies Against Causative Viral Agent from Emerging COVID-19

Affiliations
  • 1Department of Microbiology, Institute for Viral Diseases, College of Medicine, Korea University, 73, Goryeodae-ro, Seongbuk-gu, Seoul 02841,Republic of Korea

Abstract

A century ago, more exactly 102 years ago, there was a devastating pandemic of influenza in 1918 and thereafter, periodic recurrences of pandemic events have been reported in the human population. Unfortunately, whenever it happened, the outcome was concomitant with over millions of death tolls due to considerably higher case fatality rates, compared to other infectious diseases at that time. In this regard, pandemics, which continued at irregular time intervals, give a great significance to global public health responses. However, it is far from feasibility to predict when a next pandemic will begin and how much disease burden will be despite our efforts to utilize all kinds of available scientific information and knowledge. The one clear thing is that approximately 70% of the causative agents of emerging and/or re-emerging diseases including COVID-19 (coronavirus disease 2019), which has been started from Wuhan province, China in December 2019 and has resulted in more than 4 million human cases within a few months, are viruses. Therefore, it is very important to secure fast and accurate identification methods of a causative pathogen in order to provide scientific clues and to prepare in advance for the abrupt occurrence of unknown viral diseases in a timely manner. In this review, the current status and future perspectives of the molecular technology for identification of viral pathogens such as SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) with regard to rapid public health responses in the early stage of infectious diseases including COVID-19, will be discussed.

Keyword

COVID-19; Molecular diagnosis; Pandemic; qRT-PCR; SARS-CoV-2

Figure

  • Fig. 1 Schematic diagram of postulated SARS-CoV-2 cell entry through endocytosis and direct membrane fusion. The SARS-CoV-2 preferentially utilizes ACE2 (angiotensin converting enzyme 2) as a cellular receptor for recognition of susceptible cells. Once cellular receptor interacts with trimerized viral spike proteins, multifactorial entry machineries including conformational alteration of spike proteins at the cell membrane involving endocytic pathways (A) and/or unique trans-membranous protease activities (B) are processed.


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