scholarly journals The Features of Pathobiology and Clinical translation of Approved treatments for Coronavirus Disease 2019 (COVID-19)

Intervirology ◽  
2021 ◽  
Author(s):  
Hamidreza Abbasi ◽  
Hadi Razavi Nikoo ◽  
Ali Fallah ◽  
Azadeh Mohammad-Hasani ◽  
Abasalt Hosseinzadeh Colagar ◽  
...  

Background: The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is currently the most important etiological agent of acute respiratory distress syndrome (ARDS) with millions of infections and deaths in the last two years worldwide. Several reasons and parameters are responsible for the difficult management of coronavirus disease-2019 (COVID-19) patients; the first is virus behavioral factors such as high transmission rate, and the different molecular and cellular mechanisms of pathogenesis remain a matter of controversy, is another factor. Summary: In the present review, we attempted to explain about features of SARS-COV-2, particularly focusing on the various aspects of pathogenesis and treatment strategies. Key Messages: We note evidence for the understanding of the precise molecular and cellular mechanisms of SARS-CoV-2 pathogenesis, which can help design the appropriate drug or vaccine. Additionally, and importantly, we reported the updated issues associated with the history and development of treatment strategies such as, drugs, vaccines, and other medications that have been approved or under consideration in clinics and markets worldwide.

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Braira Wahid ◽  
Noshaba Rani ◽  
Muhammad Idrees

Abstract After wreaking havoc on a global level with a total of 5,488,825 confirmed cases and 349,095 deaths as of May 2020, severe acute respiratory syndrome coronavirus 2 is truly living up to the expectations of a 21st-century pandemic. Since the major cause of mortality is a respiratory failure from acute respiratory distress syndrome, the only present-day management option is supportive as the transmission relies solely on human-to-human contact. Patients suffering from coronavirus disease 2019 (COVID-19) should be tested for hyper inflammation to screen those for whom immunosuppression can increases chances of survival. As more and more clinical data surfaces, it suggests patients with mild or severe cytokine storms are at greater risk of failing fatally and hence these cytokine storms should be targets for treatment in salvaging COVID-19 patients.


Author(s):  
Subhashis Debnath ◽  
Runa Chakravorty ◽  
Donita Devi

In December 2019, severe acute respiratory syndrome-coronavirus-2, a novel coronavirus, initiated an outbreak of pneumonia from Wuhan in China, which rapidly spread worldwide. The outbreak was declared as “a public health emergency of international concern” by the WHO on January 30, 2020, and as a pandemic on March 11, 2020. The disease is transmitted by inhalation or contact with infected droplets and the incubation period ranges from 2 to 14 d. The symptoms are usually fever, cough, sore throat, breathlessness, fatigue, malaise among others. The disease is mild in most people; in some (usually the elderly and those with comorbidities), it may progress to pneumonia, acute respiratory distress syndrome (ARDS) and multi organ dysfunction. Many people are asymptomatic. The virus spreads faster than its two ancestors the SARS-CoV and Middle East respiratory syndrome coronavirus (MERS-CoV), but has lower fatality.


2019 ◽  
Vol 35 (8) ◽  
pp. 723-737 ◽  
Author(s):  
Shawn Kaku ◽  
Christopher D. Nguyen ◽  
Natalie N. Htet ◽  
Dominic Tutera ◽  
Juliana Barr ◽  
...  

The acute respiratory distress syndrome (ARDS) has multiple causes and is characterized by acute lung inflammation and increased pulmonary vascular permeability, leading to hypoxemic respiratory failure and bilateral pulmonary radiographic opacities. The acute respiratory distress syndrome is associated with substantial morbidity and mortality, and effective treatment strategies are limited. This review presents the current state of the literature regarding the etiology, pathogenesis, and management strategies for ARDS.


2009 ◽  
Vol 83 (14) ◽  
pp. 7062-7074 ◽  
Author(s):  
Barry Rockx ◽  
Tracey Baas ◽  
Gregory A. Zornetzer ◽  
Bart Haagmans ◽  
Timothy Sheahan ◽  
...  

ABSTRACT Several respiratory viruses, including influenza virus and severe acute respiratory syndrome coronavirus (SARS-CoV), produce more severe disease in the elderly, yet the molecular mechanisms governing age-related susceptibility remain poorly studied. Advanced age was significantly associated with increased SARS-related deaths, primarily due to the onset of early- and late-stage acute respiratory distress syndrome (ARDS) and pulmonary fibrosis. Infection of aged, but not young, mice with recombinant viruses bearing spike glycoproteins derived from early human or palm civet isolates resulted in death accompanied by pathological changes associated with ARDS. In aged mice, a greater number of differentially expressed genes were observed than in young mice, whose responses were significantly delayed. Differences between lethal and nonlethal virus phenotypes in aged mice could be attributed to differences in host response kinetics rather than virus kinetics. SARS-CoV infection induced a range of interferon, cytokine, and pulmonary wound-healing genes, as well as several genes associated with the onset of ARDS. Mice that died also showed unique transcriptional profiles of immune response, apoptosis, cell cycle control, and stress. Cytokines associated with ARDS were significantly upregulated in animals experiencing lung pathology and lethal disease, while the same animals experienced downregulation of the ACE2 receptor. These data suggest that the magnitude and kinetics of a disproportionately strong host innate immune response contributed to severe respiratory stress and lethality. Although the molecular mechanisms governing ARDS pathophysiology remain unknown in aged animals, these studies reveal a strategy for dissecting the genetic pathways by which SARS-CoV infection induces changes in the host response, leading to death.


2022 ◽  
Vol 71 (6) ◽  
pp. 2254-55
Author(s):  
Seema Shafiq ◽  
Asim Riaz

Dear Editor, It is indeed an honour for us to contribute towards the ongoing research regarding the latest contagion, Coronavirus disease (COVID-19) as caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) leading to global pandemic with variable clinical outcomes. COVID-19 positive individuals present with a variety of signs and symptoms as sore throat, cough, fever, dyspnoea, headache, myalgia, nausea, and vomiting whereas, some develop severe acute respiratory distress syndrome with a fatality rate of about 10%.1 Possible oral findings include xerostomia, hypogeusia, and chemosensory alterations. Common routes of transmission being person-to-person via direct sneeze, cough, and droplet inhalation or by contact through mucosa of eyes, nose and saliva.


2022 ◽  
Vol 12 ◽  
Author(s):  
Jing Liu ◽  
David A. Dean

Acute respiratory distress syndrome (ARDS) is a devastating clinical syndrome that leads to acute respiratory failure and accounts for over 70,000 deaths per year in the United States alone, even prior to the COVID-19 pandemic. While its molecular details have been teased apart and its pathophysiology largely established over the past 30 years, relatively few pharmacological advances in treatment have been made based on this knowledge. Indeed, mortality remains very close to what it was 30 years ago. As an alternative to traditional pharmacological approaches, gene therapy offers a highly controlled and targeted strategy to treat the disease at the molecular level. Although there is no single gene or combination of genes responsible for ARDS, there are a number of genes that can be targeted for upregulation or downregulation that could alleviate many of the symptoms and address the underlying mechanisms of this syndrome. This review will focus on the pathophysiology of ARDS and how gene therapy has been used for prevention and treatment. Strategies for gene delivery to the lung, such as barriers encountered during gene transfer, specific classes of genes that have been targeted, and the outcomes of these approaches on ARDS pathogenesis and resolution will be discussed.


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