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Summary: Since cases first emerged in December 2019, COVID‐19 (a type of coronavirus) has rapidly become pandemic. This fast‐tracked paper (published quickly) from China on COVID‐19 is written by dermatologists at the epicentre of the outbreak in Wuhan. Dermatology clinic staff may be at risk because protective equipment is not routinely available, and skin lesions might possibly transmit the virus indirectly. These authors suggest preventive measures based on experience in this and previous coronavirus outbreaks. Online consultation for non‐urgent patients reduces the numbers of patients attending clinics. Nurse‐led triage, to identify patients with possible COVID‐19, at the entrances of hospital and skin clinics directs patients with a cough or fever to a specific COVID‐19 area and a dermatologist is consulted if the fever might be related to skin disease. Clinic staff wear N95 masks and observe hand hygiene during consultations. Patients are admitted to a ward only if routine blood tests and chest CT scans exclude COVID‐19. Triage will not detect patients who are showing no symptoms but who are developing the disease, so the hospital should provide an on‐call expert team to discuss inpatients suspected or diagnosed with COVID‐19 and refer them to radiology, respiratory or intensive care colleagues as required. Confirmed cases are managed following local policies. Skin disorders in COVID‐19 inpatients can usually be managed remotely using photographs, email and teleconferencing. If necessary a multidisciplinary team (a team of medical staff from different specialties) can meet in the clean area of the isolation ward. If the dermatologist must see the patient, all records should be provided in advance to minimise exposure time. With these precautions, as of 20th February 2020 no infected patients were detected in the Wuhan Dermatology Department. This is a summary of the study: Emergency management for preventing and controlling nosocomial infection of 2019 novel coronavirus: implications for the dermatology department Linked Article: Tao et al. Br J Dermatol 2020; 182:1477–1478 [ABSTRACT FROM AUTHOR]

The lack of an identifiable intermediate host species for the proximal animal ancestor of SARS-CoV-2, and the large geographical distance between Wuhan and where the closest evolutionary related coronaviruses circulating in horseshoe bats (members of the Sarbecovirus subgenus) have been identified, is fueling speculation on the natural origins of SARS-CoV-2. We performed a comprehensive phylogenetic study on SARS-CoV-2 and all the related bat and pangolin sarbecoviruses sampled so far. Determining the likely recombination events reveals a highly reticulate evolutionary history within this group of coronaviruses. Distribution of the inferred recombination events is nonrandom with evidence that Spike, the main target for humoral immunity, is beside a recombination hotspot likely driving antigenic shift events in the ancestry of bat sarbecoviruses. Coupled with the geographic ranges of their hosts and the sampling locations, across southern China, and into Southeast Asia, we confirm that horseshoe bats, Rhinolophus , are the likely reservoir species for the SARS-CoV-2 progenitor. By tracing the recombinant sequence patterns, we conclude that there has been relatively recent geographic movement and cocirculation of these viruses' ancestors, extending across their bat host ranges in China and Southeast Asia over the last 100 years. We confirm that a direct proximal ancestor to SARS-CoV-2 has not yet been sampled, since the closest known relatives collected in Yunnan shared a common ancestor with SARS-CoV-2 approximately 40 years ago. Our analysis highlights the need for dramatically more wildlife sampling to: 1) pinpoint the exact origins of SARS-CoV-2's animal progenitor, 2) the intermediate species that facilitated transmission from bats to humans (if there is one), and 3) survey the extent of the diversity in the related sarbecoviruses' phylogeny that present high risk for future spillovers. [ABSTRACT FROM AUTHOR]

Motivation The outbreak of novel severe acute respiratory syndrome coronavirus (SARS-CoV-2, also known as COVID-19) in Wuhan has attracted worldwide attention. SARS-CoV-2 causes severe inflammation, which can be fatal. Consequently, there has been a massive and rapid growth in research aimed at throwing light on the mechanisms of infection and the progression of the disease. With regard to this data science is playing a pivotal role in in silico analysis to gain insights into SARS-CoV-2 and the outbreak of COVID-19 in order to forecast, diagnose and come up with a drug to tackle the virus. The availability of large multiomics, radiological, bio-molecular and medical datasets requires the development of novel exploratory and predictive models, or the customisation of existing ones in order to fit the current problem. The high number of approaches generates the need for surveys to guide data scientists and medical practitioners in selecting the right tools to manage their clinical data. Results Focusing on data science methodologies, we conduct a detailed study on the state-of-the-art of works tackling the current pandemic scenario. We consider various current COVID-19 data analytic domains such as phylogenetic analysis, SARS-CoV-2 genome identification, protein structure prediction, host–viral protein interactomics, clinical imaging, epidemiological research and drug discovery. We highlight data types and instances, their generation pipelines and the data science models currently in use. The current study should give a detailed sketch of the road map towards handling COVID-19 like situations by leveraging data science experts in choosing the right tools. We also summarise our review focusing on prime challenges and possible future research directions. Contact hguzzi@unicz.it , sroy01@cus.ac.in [ABSTRACT FROM AUTHOR]

The novel coronavirus or COVID-19 has first been found in Wuhan, China, and became pandemic. Angiotensin-converting enzyme 2 (ACE2) plays a key role in the host cells as a receptor of Spike-I Glycoprotein of COVID-19 which causes final infection. ACE2 is highly expressed in the bladder, ileum, kidney and liver, comparing with ACE2 expression in the lung-specific pulmonary alveolar type II cells. In this study, the single-cell RNAseq data of the five tissues from different humans are curated and cell types with high expressions of ACE2 are identified. Subsequently, the protein–protein interaction networks have been established. From the network, potential biomarkers which can form functional hubs, are selected based on k-means network clustering. It is observed that angiotensin PPAR family proteins show important roles in the functional hubs. To understand the functions of the potential markers, corresponding pathways have been researched thoroughly through the pathway semantic networks. Subsequently, the pathways have been ranked according to their influence and dependency in the network using PageRank algorithm. The outcomes show some important facts in terms of infection. Firstly, renin-angiotensin system and PPAR signaling pathway can play a vital role for enhancing the infection after its intrusion through ACE2. Next, pathway networks consist of few basic metabolic and influential pathways, e.g. insulin resistance. This information corroborate the fact that diabetic patients are more vulnerable to COVID-19 infection. Interestingly, the key regulators of the aforementioned pathways are angiontensin and PPAR family proteins. Hence, angiotensin and PPAR family proteins can be considered as possible therapeutic targets. Contact: sagnik.sen2008@gmail.com, umaulik@cse.jdvu.ac.in Supplementary information: Supplementary data are available online. [ABSTRACT FROM AUTHOR]

Background The new coronavirus (COVID-19) rapidly resulted in a pandemic. We report the characteristics of patients with severe or critical severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in Wuhan city, China, and the risk factors related to infection severity and death. Methods We extracted the demographic and clinical data of 7283 patients with severe COVID-19 infection from designated Wuhan hospitals as of 25 February 2020. Factors associated with COVID-19 critical illness and mortality were analysed using logistic- and Cox-regression analyses. Results We studied 6269 patients with severe COVID-19 illness and 1014 critically ill patients. The median (IQR) age was 64 (53–71) years; 51.2% were male, 38.9% were retirees and 7.4% had self-reported histories of chronic disease. Up to the end of the study, 1180 patients (16.2%) recovered and were discharged, 649 (8.9%) died and the remainder were still receiving treatment. The number of daily confirmed critical cases peaked between 23 January and 1 February 2020. Patients with advanced age [odds ratio (OR), 1.03; 95% confidence intervals (CIs), 1.03–1.04], male sex (OR, 1.57; 95% CI, 1.33–1.86) and pre-existing diabetes (OR, 2.11), hypertension (OR, 2.72), cardiovascular disease (OR, 2.15) or respiratory disease (OR, 3.50) were more likely to be critically ill. Compared with those who recovered and were discharged, patients who died were older [hazard ratio (HR), 1.04; 95% CI, 1.03–1.05], more likely to be male (HR, 1.74; 95% CI, 1.44–2.11) and more likely to have hypertension (HR, 5.58), cardiovascular disease (HR, 1.83) or diabetes (HR, 1.67). Conclusion Advanced age, male sex and a history of chronic disease were associated with COVID-19 critical illness and death. Identifying these risk factors could help in the clinical monitoring of susceptible populations. [ABSTRACT FROM AUTHOR]

Background Novel coronavirus disease 2019 (COVID-19) emerged in Wuhan and rapidly spread, affecting >10 million cases worldwide. Caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and primarily manifesting as an acute respiratory failure with interstitial and alveolar pneumonia, it can also affect multiple organs. Kidney involvement was underestimated in early reports and its role remains controversial. The aim of this study was to analyse the role of kidney damage in COVID-19 outcome. Methods This is a prospective cohort study of 1603 consecutive patients admitted in a University Reference Hospital in the heart of the European outbreak. Results Median age was 64 years, 40.4% were female, 15.2% presented diabetes mellitus, 35.7% hypertension and 20.3% obesity. On admission, the prevalence of elevated serum creatinine (sCr), proteinuria, leucocyturia and haematuria were 21.0, 37.8, 31.8 and 45.6%, respectively. In total, 43.5% of those with an elevated sCr had previous chronic kidney disease (CKD) and 11.4% of those with normal sCr developed an in-hospital acute kidney injury (AKI); 17 patients needed acute haemodialysis; and 197 patients died during hospitalization. Cox proportional hazard regression confirmed that elevated baseline sCr [hazard ratio (95% confidence interval) 2.40 (1.79–3.22)], previous CKD [1.59 (1.06-2.37)], haematuria [1 + 1.68 (0.92–3.06), 2–3 + 2.69 (1.49–4.87)] and in-hospital AKI [1.50 (0.92–2.44)] were independent risk factors for in-hospital death after adjusting for age, sex and comorbidity. Conclusion The prevalence of acute and chronic kidney disease on admission and in-hospital AKI is higher than previously reported in Wuhan, and is associated with high in-hospital mortality. We should increase our awareness towards kidney involvement and design specific strategies for management of COVID-19 in these patients. [ABSTRACT FROM AUTHOR]

A recent outbreak of pneumonia in Wuhan, China was found to be caused by a 2019 novel coronavirus (2019-nCoV or SARS-CoV-2 or HCoV-19). We previously reported the clinical features of 12 patients with 2019-nCoV infections in Shenzhen, China. To further understand the pathogenesis of COVID-19 and find better ways to monitor and treat the disease caused by 2019-nCoV, we measured the levels of 48 cytokines in the blood plasma of those 12 COVID-19 patients. Thirty-eight out of the 48 measured cytokines in the plasma of 2019-nCoV-infected patients were significantly elevated compared to healthy individuals. Seventeen cytokines were linked to 2019-nCoV loads. Fifteen cytokines, namely M-CSF, IL-10, IFN-α2, IL-17, IL-4, IP-10, IL-7, IL-1ra, G-CSF, IL-12, IFN-γ, IL-1α, IL-2, HGF and PDGF-BB, were strongly associated with the lung-injury Murray score and could be used to predict the disease severity of 2019-nCoV infections by calculating the area under the curve of the receiver-operating characteristics. Our results suggest that 2019-nCoV infections trigger extensive changes in a wide array of cytokines, some of which could be potential biomarkers of disease severity of 2019-nCoV infections. These findings will likely improve our understanding of the immunopathologic mechanisms of this emerging disease. Our results also suggest that modulators of cytokine responses may play a therapeutic role in combating the disease once the functions of these elevated cytokines have been characterized. [ABSTRACT FROM AUTHOR]

Novel coronavirus disease 2019 (COVID-19) was first identified in Wuhan, China, and declared by World Health Organization as a pandemic in March 2020. Since then, it has been well known for COVID-19 patients to present with clinical manifestations of severe acute respiratory syndrome (SARS-CoV-2) similar to the influenza. However, in the course of the disease, various pathological complications of high clinical significance have remained unknown. Impaired blood supply to the visceral vascular system can cause serious life-threatening acute damage. We report a case of a 60-year-old female with difficulty in breathing and extensive acute intestinal ischemia confirmed to be associated with SARS-CoV-2 infection. The patient developed a sudden abdominal pain and succumbed shortly after admission before imaging studies were performed. Autopsy revealed massive bowel ischemia. This case highlights the importance of paying attention to serious and less known clinical manifestations other than pulmonary symptoms and fever. [ABSTRACT FROM AUTHOR]