By 27 February 2020, the outbreak of coronavirus disease 2019 (COVID‐19) caused 82 623 confirmed cases and 2858 deaths globally, more than severe acute respiratory syndrome (SARS) (8273 cases, 775 deaths) and Middle East respiratory syndrome (MERS) (1139 cases, 431 deaths) caused in 2003 and 2013, respectively. COVID‐19 has spread to 46 countries internationally. Total fatality rate of COVID‐19 is estimated at 3.46% by far based on published data from the Chinese Center for Disease Control and Prevention (China CDC). Average incubation period of COVID‐19 is around 6.4 days, ranges from 0 to 24 days. The basic reproductive number (R0) of COVID‐19 ranges from 2 to 3.5 at the early phase regardless of different prediction models, which is higher than SARS and MERS. A study from China CDC showed majority of patients (80.9%) were considered asymptomatic or mild pneumonia but released large amounts of viruses at the early phase of infection, which posed enormous challenges for containing the spread of COVID‐19. Nosocomial transmission was another severe problem. A total of 3019 health workers were infected by 12 February 2020, which accounted for 3.83% of total number of infections, and extremely burdened the health system, especially in Wuhan. Limited epidemiological and clinical data suggest that the disease spectrum of COVID‐19 may differ from SARS or MERS. We summarize latest literatures on genetic, epidemiological, and clinical features of COVID‐19 in comparison to SARS and MERS and emphasize special measures on diagnosis and potential interventions. This review will improve our understanding of the unique features of COVID‐19 and enhance our control measures in the future.

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Infection with many mammalian orthoreovirus (MRV) strains results in shutoff of host, but not viral, protein synthesis via protein kinase R (PKR) activation and phosphorylation of translation initiation factor eIF2␣. Following inhibition of protein synthesis, cellular mRNAs localize to discrete structures in the cytoplasm called stress granules (SGs), where they are held in a translationally inactive state. We examined MRV-infected cells to characterize SG formation in response to MRV infection. We found that SGs formed at early times following infection (2 to 6 h postinfection) in a manner dependent on phosphorylation of eIF2␣. MRV induced SG formation in all four eIF2␣ kinase knockout cell lines, suggesting that at least two kinases are involved in induction of SGs. Inhibitors of MRV disassembly prevented MRV-induced SG formation, indicating that viral uncoating is a required step for SG formation. Neither inactivation of MRV virions by UV light nor treatment of MRV-infected cells with the translational inhibitor puromycin prevented SG formation, suggesting that viral transcription and translation are not required for SG formation. Viral cores were found to colocalize with SGs; however, cores from UV-inactivated virions did not associate with SGs, suggesting that viral core particles are recruited into SGs in a process that requires the synthesis of viral mRNA. These results demonstrate that MRV particles induce SGs in a step following viral disassembly but preceding viral mRNA transcription and that core particles are themselves recruited to SGs, suggesting that the cellular stress response may play a role in the MRV replication cycle.

In response to mammalian orthoreovirus (MRV) infection, cells initiate a stress response that includes eIF2␣ phosphorylation and protein synthesis inhibition. We have previously shown that early in infection, MRV activation of eIF2␣ phosphorylation results in the formation of cellular stress granules (SGs). In this work, we show that as infection proceeds, MRV disrupts SGs despite sustained levels of phosphorylated eIF2␣ and, further, interferes with the induction of SGs by other stress inducers. MRV interference with SG formation occurs downstream of eIF2␣ phosphorylation, suggesting the virus uncouples the cellular stress signaling machinery from SG formation. We additionally examined mRNA translation in the presence of SGs induced by eIF2␣ phosphorylation-dependent and -independent mechanisms. We found that irrespective of eIF2␣ phosphorylation status, the presence of SGs in cells correlated with inhibition of viral and cellular translation. In contrast, MRV disruption of SGs correlated with the release of viral mRNAs from translational inhibition, even in the presence of phosphorylated eIF2␣. Viral mRNAs were also translated in the presence of phosphorylated eIF2␣ in PKR ؊/؊ cells. These results suggest that MRV escape from host cell translational shutoff correlates with virus-induced SG disruption and occurs in the presence of phosphorylated eIF2␣ in a PKR-independent manner.The nonfusogenic mammalian orthoreoviruses (MRV) are members of a large family of animal and plant viruses (Reoviridae) that includes many members that are of considerable importance in human, animal, and plant disease. Following infection with many viruses from this family, including MRV, the host cell initiates a stress response that culminates in shutoff of protein translation (10,34,43). Viral mRNAs are able to escape this inhibition and continue to be translated in the shutoff environment (40,41,52). In the case of MRV, the innate immune response has been implicated in host translational shutoff via activation of the double-stranded RNA (dsRNA) kinase PKR (12,37,40,45). PKR is activated by binding dsRNA, at which point it homodimerizes and undergoes autophosphorylation (51). Activated PKR phosphorylates serine 51 on the alpha subunit of the cellular translation initiation factor eIF2 (23). In the absence of cellular stress, eIF2␣ binds to GTP and initiator methionyl-tRNA (met-tRNA i ) to form a ternary complex, which subsequently binds to the 40S ribosomal complex to form the 43S preinitiation complex. As translational initiation proceeds, eIF2-bound GTP is hydrolyzed to release initiation factors from the ribosome. The released GDP bound to eIF2 must be exchanged for GTP in a reaction catalyzed by the guanine nucleotide exchange factor, eIF2B. Upon this exchange, eIF2-GTP can again bind mettRNA i to initiate a new round of translation. When phosphorylated, eIF2␣ changes from a substrate to a competitive inhibitor of eIF2B, preventing the exchange of GDP for GTP. This results in global inhibition of protein synthesis (reviewed in r...

Renin–angiotensin–aldosterone system (RAAS) inhibitors, including angiotensin‐converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) are one of the most prescribed antihypertensive medications. Previous studies showed RAAS inhibitors increase the expression of ACE2, a cellular receptor for severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), which provokes a concern that the use of ACEI and ARB in hypertensive individuals might lead to increased mortality and severity of coronavirus disease 2019 (COVID‐19). To further investigate the effects of ACEI/ARB on COVID‐19 patients, we systematically reviewed relevant studies that met predetermined inclusion criteria in search of PubMed, Embase, Cochrane Library databases, medRxiv, and bioRxiv. The search strategy included clinical data published through October 12, 2020. Twenty‐six studies involving 8104 hypertensive patients in ACEI/ARB‐treated group and 8203 hypertensive patients in non‐ACEI/ARB‐treated group were analyzed. Random‐effects meta‐analysis showed ACEI/ARB treatment was significantly associated with a lower risk of mortality in hypertensive COVID‐19 patients (odds ratio [OR] = 0.624, 95% confidence interval [CI] = 0.457–0.852, p = .003, I2 = 74.3%). Meta‐regression analysis showed that age, gender, study site, Newcastle–Ottawa Scale scores, comorbidities of diabetes, coronary artery disease, chronic kidney disease, or cancer has no significant modulating effect of ACEI/ARB treatment on the mortality of hypertensive COVID‐19 patients (all p > .1). In addition, the ACEI/ARB treatment was associated with a lower risk of ventilatory support (OR = 0.682, 95% CI = 0.475–1.978, p = .037, I2 = 0.0%). In conclusion, these results suggest that ACEI/ARB medications should not be discontinued for hypertensive patients in the context of COVID‐19 pandemic.

Background Evidence suggests that the outbreak of the coronavirus disease 2019 (COVID-19) and the prevention/control measures for COVID-19 may cause insomnia during the acute phase of COVID-19 pandemic in China. However, it is unclear whether insomnia sustains during the later phases of the pandemic. Methods We searched PubMed/Medline, EMBASE, PsycINFO and China National Knowledge Infrastructure from the 27 th December 2019 to the 2 nd February 2021. As early stage studies on COVID-19 pandemic in China were defined as those conducted prior to April 1 st , 2020, while late stage studies were those conducted after April 1 st , 2020. Results A total of 98 studies with 193,889 participants were included. The pooled prevalence of insomnia symptoms among all populations was 39.1%; the pooled prevalence of insomnia symptoms during the early and late stages of COVID-19 in China were 37.0% (95% CI 34.1-39.9%) and 41.8% (95% CI 33.6-50.0%), respectively. Importantly, there was no significant difference regarding the prevalence of insomnia symptoms between the early and late stages of COVID-19. Meta-regression showed that healthcare workers, COVID-19 patients, patients with chronic medical conditions and patients with mental disorders had a higher prevalence of insomnia symptoms compared to the general population. This association remained significant in healthcare workers and patients with chronic medical conditions after adjusting for age, gender, areas of high or low prevalence of COVID-19 cases, anxiety and depression. Conclusions Over one third of our sample presented insomnia symptoms during the early stage of COVID-19 pandemic in China. Interestingly, prevalence of insomnia symptoms sustained high during the late stage of the pandemic despite the control of the disease and the amelioration of its adverse effects. Our findings suggest that insomnia symptoms related to COVID-19 appear to persist of over time.

The nondoped Mg2SnO4 material with inverse spinel structure was synthesized by solid state reaction. This phosphor showed a broad green emission band covering 470–550 nm under 291 nm excitation, which was due to the recombination of F centers with holes. Stimulated by 980 nm infrared laser, the green photostimulated luminescence was first observed in a nondoped oxide. After ultraviolet irradiation, the green persistent luminescence of Mg2SnO4 could be seen in darkness for about 5 h. The decay curves revealed that the long persistent luminescence was governed by tunneling mechanism and it proved the presence of different trap clusters in Mg2SnO4. These trap clusters (such as [SnMg••–Oi″], [SnMg••–2e′], and [SnMg••–e″]) induced the trap levels with different depths in band gap and corresponded to the three components (at 110, 168, and 213 °C) of the thermoluminescence glow curve of Mg2SnO4. These trap levels with different depths were proved to be not independent. It revealed that the shallow traps (110 °C) and part of the deep traps (168 and 213 °C) were involved in the persistent luminescence. Meanwhile, all the shallow and deep traps were responsible for the photostimulated luminescence. Accordingly, the photoluminescence, persistent, and photostimulated luminescence mechanisms of the nondoped Mg2SnO4 material were first proposed.

Background The 2019 coronavirus disease (COVID-19) has disrupted millions of lives and commerce. We investigated psychological reactions and insomnia during the COVID-19 outbreak in adults with mental health disorders (MDs). Methods A self-reported psychological and sleep online survey was conducted in China between February 5th to 19th, 2020. A total of 244 adults with MDs and 1116 controls matched for age, gender and sites were included. Worsened symptoms of anxiety, depressive and insomnia were defined when severity levels shifted to a more severe category compared to pre-COVID-19. Results During the COVID-19 outbreak, we found significantly increased prevalence of anxiety (MDs: 54.9% vs. 49.6%, controls: 25.5% vs. 14.3%), depression (MDs: 63.9% vs. 61.5%, controls: 29.9% vs. 21.2%) and insomnia (MDs: 66.0% vs. 57.8%, controls: 31.5% vs. 24.8%) compared to pre-COVID-19 period (all P-value < 0.001). Furthermore, adults with MDs had higher odds for developing COVID-19-related stress (OR = 3.41, 95% CI 2.49 ~ 4.67), worsened anxiety (OR = 1.95, 95% CI 1.38 ~ 2.76), depression (OR = 2.04, 95% CI 1.43 ~ 2.93) and insomnia (OR = 2.22, 95% CI 1.53 ~ 3.21) during the COVID-19 outbreak compared to controls. Moreover, higher COVID-19-related stress and lower levels of pre-COVID-19 anxiety, depressive and insomnia symptoms were predictors for worsened anxiety, depression and insomnia in adults with MDs, respectively. Conclusions Our findings suggest that adverse psychological reactions and insomnia are more pronounced in adults with mental health disorders during the COVID-19 outbreak, thus more attention need to be provided.