SARS-CoV-2 (previously 2019-nCoV or Wuhan coronavirus) caused an unprecedented fast-spreading worldwide pandemic. Although currently with a rather low mortality rate, the virus spread rapidly over the world using the modern world's traffic highways. The coronavirus (CoV) family members were responsible for several deadly outbreaks and epidemics during the last decade. Not only governments but also the scientific community reacted promptly to the outbreak, and information is shared quickly. For example, the genetic fingerprint was shared, and the 3D structure of key proteins was rapidly solved, which can be used for the discovery of potential treatments. An overview is given on the current knowledge of the spread, disease course, and molecular biology of SARS-CoV-2. We discuss potential treatment developments in the context of recent outbreaks, drug repurposing, and development timelines. SARS-CoV-2 OUTBREAK IN WUHANIn December 2019, an outbreak of pneumonia of an unknown cause was reported in Wuhan, in Hubei province, China. It was speculated that the first patient caught the infection from a seafood market that also traded wild animals. The causing agent was quickly identified as a novel coronavirus (CoV). The CoV responsible for the outbreak is now called SARS-CoV-2. The respiratory illness caused by SARS-CoV-2 is called COVID-19. The symptoms of the SARS-CoV-2 infection range from asymptomatic to mild to severe to death. 1 It soon became clear that personto-person transmission was also occurring, as was the case with the previous human CoV. In an unprecedented documented speed, the SARS-CoV-2 travels around the globe, and as of May 15 th led to >4.5 million infections and 300,000 fatalities. Based on the previous experience with the SARS-CoV outbreak at the beginning of this century, very stringent measures were taken by the Chinese government, and several multimillion-inhabitant cities were isolated and put under quarantine in order to slow the pandemic spread. Different hosts of the SARS-CoV-2 are proposed, including snails, bats, and pangolins. 2 CoVs are a large family of zoonotic viruses and their outbreaks are common to humans, although major outbreaks have been experienced in animals, especially in cattle. Under the electron microscope, they exhibit formations that are reminiscent of the solar corona. The common cold is often caused by human CoVs. They are single-stranded enveloped positive RNA viruses and stand out because of their rather large genome. As with viruses in general, the structure is rather simple. SARS-CoV-2 is generally less pathogenic than SARS-CoV, much less pathogenic than the Middle East respiratory syndrome MERS-CoV, but more pathogenic than practically harmless HCoV-OC43, HCoV-HKU1, HCoV-229E, and HCoV-NL63. The reported case-fatality rate of COVID-19 is %3% and is thus rather low as compared with SARS (30%, Table 1). However, the transmission rate (TR) (number of newly infected people per infected person) of 2.5 to 3 is high and accounts

Aim To investigate the factors associated with the duration of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) RNA shedding in patients with coronavirus disease 2019 (COVID‐19). Methods A retrospective cohort of COVID‐19 patients admitted to a designated hospital in Beijing was analyzed to study the factors affecting the duration of viral shedding. Results The median duration of viral shedding was 11 days (IQR, 8‐14.3 days) as measured from illness onset. Univariate regression analysis showed that disease severity, corticosteroid therapy, fever (temperature>38.5℃), and time from onset to hospitalization were associated with prolonged duration of viral shedding ( p <0.05). Multivariate regression analysis showed that fever (temperature>38.5℃) (OR 5.1, 95%CI: 1.5‐18.1), corticosteroid therapy (OR 6.3, 95%CI: 1.5‐27.8), and time from onset to hospitalization (OR 1.8, 95%CI: 1.19‐2.7) were associated with increased odds of prolonged duration of viral shedding. Conclusions Corticosteroid treatment, fever (temperature>38.5℃), and longer time from onset to hospitalization were associated with prolonged viral shedding in COVID‐19 patients. This article is protected by copyright. All rights reserved.

Background: On March 11, 2020, the World Health Organization (WHO) officially announced that the coronavirus disease 2019 (COVID-19) had reached global pandemic status. Current studies have found that angiotensin-converting enzyme 2 (ACE2) is a cell surface receptor of the novel coronavirus that plays a vital role in the pathogenesis of COVID-19. It is of immense importance for the prevention of virus transmission and treatment to clarify the distribution and expression of ACE2 in various tissues and organs of the body.Methods: RNAseq transcriptome data and sex data were obtained from the genotype-tissue expression (GTEx) and the Cancer Genome Atlas (TCGA) databases. We separately analyzed the distribution of ACE2 expression in different tissues in the GTEx and TCGA database, and explored the correlation between sex and ACE2 expression levels. Next, the expression levels of ACE2 in different tissues and organs and its correlation with sex were analyzed once again after combing all samples from the two databases.Results: ACE2 expression data were collected from the GTEx database for 6738 normal tissues. Six hundred eighteen tumor tissue data were collected from the TCGA database. The results of the analysis are consistent from different databases. The results indicated that the expression of ACE2 was the highest in the small intestines, higher in tissues such as salivary glands in the testicular, kidney, heart, thyroid and adipose tissues, while the expression of ACE2 was lower in tissues such as the spleen, brain, muscle, pituitary, and skin. There were no significant differences in the expression of ACE2 in the different organs when it came to the individual's sex.Conclusions: Our study deeply explored the distribution and expression of ACE2 in various tissues of the human body. The tissues and organs with high ACE2 expression were consistent with the current clinical and basic research results of the novel coronavirus. Our study is conducive to the discovery of potential target organs for viral infection, to provide a reference for the development of clinical progress of patients with novel coronavirus infection.

A recent study indicated that apamin-sensitive current (I KAS, mediated by apamin-sensitive small conductance calcium-activated potassium channels subunits) density significantly increased in heart failure and led to recurrent spontaneous ventricular fibrillation. While the underlying molecular correlation with SK channels is still undetermined, we hypothesized that they are remodeled in HF and that bisoprolol could reverse the remodeling. Volume-overload models were created on male Sprague-Dawley rats by producing an abdominal arteriovenous fistula. Confocal microscopy, quantitative real-time PCR, and western blot were performed to investigate the expression of SK channels and observe the influence of β-blocker bisoprolol on the expression of SK channels I KAS, and the effect of bisoprolol on I KAS and the sensitivity of I KAS to [Ca(2+)]i at single isolated cells were also explored using whole-cell patch clamp techniques. SK channels were remodeled in HF rats, displaying the significant increase of SK1 and SK3 channel expression. After the treatment of HF rats with bisoprolol, the expression of SK1 and SK3 channels was significantly downregulated, and bisoprolol effectively downregulated I KAS density as well as the sensitivity of I KAS to [Ca(2+)]i. Our data indicated that the expression of SK1 and SK3 increased in HF. Bisoprolol effectively attenuated the change and downregulated I KAS density as well as the sensitivity of I KAS to [Ca(2+)]i.