Human Coronavirus-229E, -OC43, -NL63, and -HKU1 (Coronaviridae)

Liu, Ding X.; Liang, Jia Qi; Fung, To Sing

doi:10.1016/b978-0-12-809633-8.21501-x

Cited by 342 publications

(340 citation statements)

References 10 publications

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“…Also, the 2002-4 epidemic due to severe acute respiratory syndrome coronavirus (SARS-CoV) and the 2012 epidemic due to Middle East respiratory syndrome coronavirus (MERS-CoV) were considered as members of the HCoVs with mild to severe consequences and death. In December 2019, the coronavirus disease-2019 (COVID-19) pandemic as a result of a novel virus outbreak, SARS-CoV2 from Wuhan, China (Liu et al 2020a). This virus is categorized as a beta-CoV subgroup which belongs to the Coronaviridae family (Sahu et al 2020a).…”

Section: Introductionmentioning

confidence: 99%

COVID-19 and multiorgan failure: A narrative review on potential mechanisms

et al. 2020

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The outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) in December 2019 form Wuhan, China leads to coronavirus disease 2019 (COVID-19) pandemic. While the common cold symptoms are observed in mild cases, COVID-19 is accompanied by multiorgan failure in severe patients. The involvement of different organs in severe patients results in lengthening the hospitalization duration and increasing the mortality rate. In this review, we aimed to investigate the involvement of different organs in COVID-19 patients, particularly in severe cases. Also, we tried to define the potential underlying mechanisms of SARS-CoV2 induced multiorgan failure. The multi-organ dysfunction is characterized by acute lung failure, acute liver failure, acute kidney injury, cardiovascular disease, and as well as a wide spectrum of hematological abnormalities and neurological disorders. The most important mechanisms are related to the direct and indirect pathogenic features of SARS-CoV2. Although the presence of angiotensin-converting enzyme 2, a receptor of SARS-CoV2 in the lung, heart, kidney, testis, liver, lymphocytes, and nervous system was confirmed, there are controversial findings to about the observation of SARS-CoV2 RNA in these organs. Moreover, the organ failure may be induced by the cytokine storm, a result of increased levels of inflammatory mediators, endothelial dysfunction, coagulation abnormalities, and infiltration of inflammatory cells into the organs. Therefore, further investigations are needed to detect the exact mechanisms of pathogenesis. Since the involvement of several organs in COVID-19 patients is important for clinicians, increasing their knowledge may help to improve the outcomes and decrease the rate of mortality and morbidity.

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Section: Introductionmentioning

confidence: 99%

COVID-19 and multiorgan failure: A narrative review on potential mechanisms

et al. 2020

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“…Seven human coronaviruses (HCoVs) have been identified so far, which likely all emerged as zoonosis from bats, mice or domestic animals (Ye et al, 2020). The four so-called 'common cold HCoVs' are the alphacoronaviruses 229E and NL63, and betacoronaviruses OC43 and HKU1, which only cause mild upper respiratory tract illnesses (Liu et al, 2020). In contrast, the betacoronaviruses SARS-CoV, MERS-CoV and the recently emerged SARS-CoV-2, are highly pathogenic and can cause severe, potentially lethal respiratory infections.…”

Section: Introductionmentioning

confidence: 99%

Identification of TMEM106B as proviral host factor for SARS-CoV-2

Baggen

Persoons

Jansen

et al. 2020

Preprint

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SUMMARYThe ongoing COVID-19 pandemic is responsible for worldwide economic damage and nearly one million deaths. Potent drugs for the treatment of severe SARS-CoV-2 infections are not yet available. To identify host factors that support coronavirus infection, we performed genome-wide functional genetic screens with SARS-CoV-2 and the common cold virus HCoV-229E in non-transgenic human cells. These screens identified PI3K type 3 as a potential drug target against multiple coronaviruses. We discovered that the lysosomal protein TMEM106B is an important host factor for SARS-CoV-2 infection. Furthermore, we show that TMEM106B is required for replication in multiple human cell lines derived from liver and lung and is expressed in relevant cell types in the human airways. Our results identify new coronavirus host factors that may potentially serve as drug targets against SARS-CoV-2 or to quickly combat future zoonotic coronavirus outbreaks.

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“…α-Coronaviruses (αCoVs, e.g., HCoV-229E and HCoV-NL63) and β-coronaviruses (βCoVs, e.g., HCoV-OC43 and HCoV-HKU1) are two of four Coronaviridae genres which commonly infect humans (Liu, Liang, & Fung, 2020). These HCoVs usually cause mild to moderate upper respiratory tract infections, for example, the common cold.…”

mentioning

confidence: 99%

Non‐steroidal anti‐inflammatory drugs, prostaglandins, and COVID‐19

Robb

Goepp

Rossi

et al. 2020

British J Pharmacology

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of the novel coronavirus disease 2019 (COVID-19), a highly pathogenic and sometimes fatal respiratory disease responsible for the current 2020 global pandemic. Presently, there remains no effective vaccine or efficient treatment strategies against COVID-19. Non-steroidal anti-inflammatory drugs (NSAIDs) are medicines very widely used to alleviate fever, pain, and inflammation (common symptoms of COVID-19 patients) through effectively blocking production of prostaglandins (PGs) via inhibition of cyclooxyganase enzymes. PGs can exert either proinflammatory or anti-inflammatory effects depending on the inflammatory scenario. In this review, we survey the potential roles that NSAIDs and PGs may play during SARS-CoV-2 infection and the development and progression of COVID-19.

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Human Coronavirus-229E, -OC43, -NL63, and -HKU1 (Coronaviridae)

Cited by 342 publications

References 10 publications

COVID-19 and multiorgan failure: A narrative review on potential mechanisms

COVID-19 and multiorgan failure: A narrative review on potential mechanisms

Identification of TMEM106B as proviral host factor for SARS-CoV-2

Non‐steroidal anti‐inflammatory drugs, prostaglandins, and COVID‐19

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