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Development of Multiplex Real-Time RT-qPCR Assays for the Detection of SARS-CoV-2, Influenza A/B, and MERS-CoV
Published on: November 10, 2023
COVID-19, the disease that changed the world.
Ancuţa Petrovan1,2, Ligia Puiu3, Carmen Monica Pop4,5
1Doctoral School, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania.
The COVID-19 pandemic, caused by SARS-CoV-2, highlights the need for rapid genomic surveillance. This review synthesizes data on SARS-CoV-2, its host interactions, and severe disease mechanisms.
Area of Science:
- Virology
- Immunology
- Genomics
Background:
- The COVID-19 pandemic, caused by SARS-CoV-2, has led to significant global morbidity and mortality.
- Genomic surveillance has become crucial for tracking viral evolution and informing public health strategies.
- SARS-CoV-2 likely originated from wildlife, representing the third highly pathogenic human coronavirus.
Purpose of the Study:
- To synthesize current knowledge on SARS-CoV-2 etiology.
- To review the complex interactions between SARS-CoV-2 and the host immune system.
- To elucidate the mechanisms underlying severe COVID-19, including cytokine storm and endothelial dysfunction.
Main Methods:
- Literature review of scientific data on SARS-CoV-2.
- Analysis of viral etiology and host-pathogen interactions.
- Synthesis of information on molecular mechanisms and clinical manifestations.
Main Results:
- SARS-CoV-2's spike glycoprotein enhances viral attachment and contagiousness.
- Infection triggers oxidative stress, inflammation (cytokine storm), and endothelial dysfunction.
- These factors contribute to cellular damage, thrombosis, and organ failure in severe COVID-19.
Conclusions:
- Understanding SARS-CoV-2 pathogenesis is vital for combating the pandemic.
- The virus's interaction with the host leads to a damaging triad of oxidative stress, inflammation, and endothelial dysfunction.
- Multisystemic involvement, including pulmonary, cardiovascular, neurological, and renal systems, characterizes severe disease.
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