• Journal of Veterinary Science
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• v.21 no.3
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• pp.51.1-51.5
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• 2020

A novel coronavirus emerged in human populations and spread rapidly to cause the global coronavirus disease 2019 pandemic. Although the origin of the associated virus (severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2]) remains unclear, genetic evidence suggests that bats are a reservoir host of the virus, and pangolins are a probable intermediate. SARS-CoV-2 has crossed the species barrier to infect humans and other animal species, and infected humans can facilitate reverse-zoonotic transmission to animals. Considering the rapidly changing interconnections among people, animals, and ecosystems, traditional roles of veterinarians should evolve to include transdisciplinary roles.

• Journal of Veterinary Science
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• v.23 no.6
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• pp.80.1-80.6
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• 2022

A 10-year-old male neutered Labrador Retriever presented with a history of acute-onset tachypnoea, lethargy and anorexia. The dog was pyrexic, tachypnoeic and dyspnoeic on examination. A rapid antigen test for severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) was performed on an oropharyngeal swab and yielded a positive result. SARS-CoV-2 infection was subsequently confirmed by reverse transcription polymerase chain reaction (RT-PCR) analysis. Both of the dog's owners had positive rapid antigen test and RT-PCR analysis results for SARS-CoV-2. Additional diagnostics included computed tomography. Resolution of the dog's clinical signs was achieved with symptomatic treatment.

• IMMUNE NETWORK
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• v.21 no.2
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• pp.12.1-12.17
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• 2021

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Since the emergence of SARS-CoV-2 in the human population in late 2019, it has spread on an unprecedented scale worldwide leading to the first coronavirus pandemic. SARS-CoV-2 infection results in a wide range of clinical manifestations from asymptomatic to fatal cases. Although intensive research has been undertaken to increase understanding of the complex biology of SARS-CoV-2 infection, the detailed mechanisms underpinning the severe pathogenesis and interactions between the virus and the host immune response are not well understood. Thus, the development of appropriate animal models that recapitulate human clinical manifestations and immune responses against SARS-CoV-2 is crucial. Although many animal models are currently available for the study of SARS-CoV-2 infection, each has distinct advantages and disadvantages, and some models show variable results between and within species. Thus, we aim to discuss the different animal models, including mice, hamsters, ferrets, and non-human primates, employed for SARS-CoV-2 infection studies and outline their individual strengths and limitations for use in studies aimed at increasing understanding of coronavirus pathogenesis. Moreover, a significant advantage of these animal models is that they can be tailored, providing unique options specific to the scientific goals of each researcher.

• Clinical and Experimental Pediatrics
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• v.65 no.4
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• pp.153-166
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• 2022

During the coronavirus disease 2019 (COVID-19) pandemic, a novel multisystem inflammatory syndrome in children (MIS-C) has been reported worldwide since the first cases were reported in Europe in April 2020. MIS-C is temporally associated with severe acute respiratory syndrome coronavirus 2 infection and shows Kawasaki disease (KD)-like features. The epidemiological and clinical characteristics in COVID-19, KD, and MIS-C differ, but severe cases of each disease share similar clinical and laboratory findings such as a protracted clinical course, multiorgan involvement, and similar activated biomarkers. These findings suggest that a common control system of the host may act against severe disease insult. To solve the enigmas, we proposed the protein-homeostasis-system hypothesis in that every disease involves etiological substances and the host's immune system controls them by their size and biochemical properties. Also, it is proposed that the etiological agents of KD and MIS-C might be certain strains in the microbiota of human species and etiological substances in severe COVID-19, KD, and MIS-C originate from pathogen-infected cells. Since disease severity depends on the amounts of inflammation-inducing substances and corresponding immune activation in the early stage of the disease, an early proper dose of corticosteroids and/or intravenous immunoglobulin (IVIG) may help reduce morbidity and possibly mortality among patients with these diseases. Corticosteroids are low cost and an analogue of host-origin cortisol among immune modulators. This study's findings will help clinicians treating severe COVID-19, KD, and MIS-C, especially in developing countries, where IVIG and biologics supplies are insufficient.

• International Journal of Advanced Culture Technology
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• v.10 no.4
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• pp.316-321
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• 2022

Since 2019, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread rapidly, infecting millions of people worldwide. On March 11, 2020, the World Health Organization declared coronavirus disease (COVID-19) a pandemic owing to the worldwide spread of SARS-CoV-2, which created an unprecedented burden on the global healthcare system. In this context, there are increasing concerns regarding co-infections with other respiratory viruses, such as the influenza virus. In this study, clinical data of patients infected with SARS-CoV-2 and other respiratory viruses were compared with patients infected with SARS-CoV-2 alone. The hematology and blood biochemistry results of 178 patients infected with SARS-CoV-2 , who were tested on admission, were retrospectively reviewed. In patients with SARS-CoV-2 and adenovirus co-infection, C-reactive protein levels were elevated on admission, whereas lactate dehydrogenase (LDH), prothrombin time, international normalized ratio, activated partial thromboplastin clotting time, and bilirubin values were all within the normal range. Moreover, patients with SARS-CoV-2 and human bocavirus co-infection had low LDH and high bilirubin levels on admission. These findings reveal the clinical features of respiratory virus and SARS-CoV-2 co-infections and support the development of appropriate approaches for treating patients with SARS-CoV-2 and other respiratory virus co-infections.

• Journal of Ginseng Research
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• v.46 no.6
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• pp.722-730
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• 2022

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the pathogenic virus that causes coronavirus disease 2019 (COVID-19), with major symptoms including hyper-inflammation and cytokine storm, which consequently impairs the respiratory system and multiple organs, or even cause death. SARS-CoV-2 activates inflammasomes and inflammasome-mediated inflammatory signaling pathways, which are key determinants of hyperinflammation and cytokine storm in COVID-19 patients. Additionally, SARS-CoV-2 inhibits inflammasome activation to evade the host's antiviral immunity. Therefore, regulating inflammasome initiation has received increasing attention as a preventive measure in COVID-19 patients. Ginseng and its major active constituents, ginsenosides and saponins, improve the immune system and exert anti-inflammatory effects by targeting inflammasome stimulation. Therefore, this review discussed the potential preventive and therapeutic roles of ginseng in COVID-19 based on its regulatory role in inflammasome initiation and the host's antiviral immunity.

• IMMUNE NETWORK
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• v.21 no.1
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• pp.3.1-3.16
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• 2021

Coronavirus disease 2019 caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been spreading worldwide since its outbreak in December 2019, and World Health Organization declared it as a pandemic on March 11, 2020. SARS-CoV-2 is highly contagious and is transmitted through airway epithelial cells as the first gateway. SARS-CoV-2 is detected by nasopharyngeal or oropharyngeal swab samples, and the viral load is significantly high in the upper respiratory tract. The host cellular receptors in airway epithelial cells, including angiotensin-converting enzyme 2 and transmembrane serine protease 2, have been identified by single-cell RNA sequencing or immunostaining. The expression levels of these molecules vary by type, function, and location of airway epithelial cells, such as ciliated cells, secretory cells, olfactory epithelial cells, and alveolar epithelial cells, as well as differ from host to host depending on age, sex, or comorbid diseases. Infected airway epithelial cells by SARS-CoV-2 in ex vivo experiments produce chemokines and cytokines to recruit inflammatory cells to target organs. Same as other viral infections, IFN signaling is a critical pathway for host defense. Various studies are underway to confirm the pathophysiological mechanisms of SARS-CoV-2 infection. Herein, we review cellular entry, host-viral interactions, immune responses to SARS-CoV-2 in airway epithelial cells. We also discuss therapeutic options related to epithelial immune reactions to SARS-CoV-2.

• Clinical and Experimental Pediatrics
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• v.64 no.12
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• pp.652-660
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• 2021

Background: Viral load and shedding duration are highly associated with the transmission of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection. However, limited studies have reported on viral load or shedding in children and adolescents infected with sudden acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Purpose: This study aimed to investigate the natural course of viral load in asymptomatic or mild pediatric cases. Methods: Thirty-one children (<18 years) with confirmed SARS-CoV-2 infection were hospitalized and enrolled in this study. Viral loads were evaluated in nasopharyngeal swab samples using real-time reverse transcription polymerase chain reaction (E, RdRp, N genes). cycle threshold (Ct) values were measured when patients met the clinical criteria to be released from quarantine. Results: The mean age of the patients was 9.8 years, 18 (58%) had mild disease, and 13 (42%) were asymptomatic. Most children were infected by adult family members, most commonly by their mothers. The most common symptoms were fever and sputum (26%), followed by cough and runny nose. Nine patients (29%) had a high or intermediate viral load (Ct value≤30) when they had no clinical symptoms. Viral load showed no difference between symptomatic and asymptomatic patients. Viral rebounds were found in 15 cases (48%), which contributed to prolonged viral detection. The mean duration of viral detection was 25.6 days. Viral loads were significantly lower in patients with viral rebounds than in those with no rebound (E, P=0.003; RdRp, P=0.01; N, P=0.02). Conclusion: Our study showed that many pediatric patients with coronavirus disease 2019 (COVID-19) experienced viral rebound and showed viral detection for more than 3 weeks. Further studies are needed to investigate the relationship between viral rebound and infectiousness in COVID-19.

• Pediatric Infection and Vaccine
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• v.29 no.3
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• pp.155-160
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• 2022

Children and adolescents with coronavirus disease 2019 (COVID-19) generally have mild symptoms. Severe infection due to severe acute respiratory syndrome coronavirus 2 (SARSCoV-2) involving multiorgan dysfunction is rare in this population. Herein, we present an unusual case of severe SARS-CoV-2 infection with multiorgan involvement followed by multisystem inflammatory syndrome in children (MIS-C) in a vaccinated 16-year-old boy. The patient was unconscious on initial presentation, and had severe paralytic ileus. On laboratory examination, there was severe metabolic acidosis, lymphocytopenia, thrombocytopenia, elevated inflammatory markers, elevated liver enzymes, and evidence of acute kidney injury with proteinuria and hematuria. His symptoms improved with the administration of remdesivir and dexamethasone. The patient briefly experienced MIS-C 2 weeks after the diagnosis of COVID-19, but the patient was discharged without any complications.

• Clinical and Experimental Pediatrics
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• v.64 no.7
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• pp.322-327
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• 2021

School closures during the coronavirus disease 2019 (COVID-19) pandemic have been outlined in studies from different disciplines, including economics, sociology, mathematical modeling, epidemiology, and public health. In this review, we discuss the implications of school closures in the context of the current COVID-19 pandemic. Modeling studies of the effects of school closures, largely derived from the pandemic influenza model, on severe acute respiratory syndrome coronavirus 2 produced conflicting results. Earlier studies assessed the risk of school reopening by modeling transmission across schools and communities; however, it remains unclear whether the risk is due to increased transmission in adults or children. The empirical findings of the impact of school closures on COVID-19 outbreaks suggest no clear effect, likely because of heterogeneity in community infection pressure, differences in school closure strategies, or the use of multiple interventions. The benefits of school closings are unclear and not readily quantifiable; however, they must be weighed against the potential high social costs, which can also negatively affect the health of this generation.