how does the coronavirus respond to changes in the weather

Genome analyses help track coronavirus' moves

Genome analyses help track coronavirus' moves.

Will heat kill the coronavirus?

We don't know if changing seasons will help stem the outbreak, says Michael Le Page

Regulation of Stress Responses and Translational Control by Coronavirus

Similar to other viruses, coronavirus infection triggers cellular stress responses in infected host cells. The close association of coronavirus replication with the endoplasmic reticulum (ER) results in the ER stress responses, which impose a challenge to the viruses. Viruses, in turn, have come up with various mechanisms to block or subvert these responses. One of the ER stress responses is inhibition of the global protein synthesis to reduce the amount of unfolded proteins inside the ER lumen. Viruses have evolved the capacity to overcome the protein translation shutoff to ensure viral protein production. Here, we review the strategies exploited by coronavirus to modulate cellular stress response pathways. The involvement of coronavirus-induced stress responses and translational control in viral pathogenesis will also be briefly discussed.

Do Humidity and Temperature Impact the Spread of the Novel Coronavirus?

What next for the coronavirus response?

Photopolarimetrical properties of coronavirus model particles: spike proteins number influence

Coronavirus virions have spherical shape surrounded by spike proteins. The coronavirus spike proteins are very effective molecular mechanisms, which provide the coronavirus entrance to the host cell. The number of these spikes is different; it dramatically depends on external conditions and determines the degree of danger of the virus. A larger number of spike proteins makes the virus infectivity stronger. This paper describes a mathematical model of the shape of coronavirus virions. Based on this model, the characteristics of light scattered by the coronavirus virions were calculated. It was found two main features of coronavirus model particles in the spectral region near 200nm: a minimum of intensity and a sharp leap of the linear polarization degree. The effect of the spike protein number on the intensity and polarization properties of the scattered light was studied. It was determined that when the number of spike proteins decreases, both the intensity minimum and the position of the linear polarization leap shift to shorter wavelengths. This allows us to better evaluate the shape of the coronavirus virion, and, therefore, the infectious danger of the virus. It was shown that the shorter the wavelength of scattered light, the more reliably one can distinguish viruses from non-viruses. The developed model and the light scattering simulations based on it can be applied not only to coronaviruses, but also to other objects of a similar structure, for example, pollen.

Photopolarimetrical properties of coronavirus model particles: Spike proteins number influence

Abstract Coronavirus virions have spherical shape surrounded by spike proteins. The coronavirus spike proteins are very effective molecular mechanisms, which provide the coronavirus entrance to the host cell. The number of these spikes is different; it dramatically depends on external conditions and determines the degree of danger of the virus. A larger number of spike proteins makes the virus infectivity stronger. This paper describes a mathematical model of the shape of coronavirus virions. Based on this model, the characteristics of light scattered by the coronavirus virions were calculated. It was found two main features of coronavirus model particles in the spectral region near 200 nm: a minimum of intensity and a sharp leap of the linear polarization degree. The effect of the spike protein number on the intensity and polarization properties of the scattered light was studied. It was determined that when the number of spike proteins decreases, both the intensity minimum and the position of the linear polarization leap shift to shorter wavelengths. This allows us to better evaluate the shape of the coronavirus virion, and, therefore, the infectious danger of the virus. It was shown that the shorter the wavelength of scattered light, the more reliably one can distinguish viruses from non-viruses. The developed model and the light scattering simulations based on it can be applied not only to coronaviruses, but also to other objects of a similar structure, for example, pollen.

[Bats, viruses and humans: coronaviruses on the rise?].

The outbreak of the SARS coronavirus in 2002/2003 and the recent disease cases with a new human coronavirus (originally designated EMC-CoV, recently renamed MERS-CoV) have put the focus onto the virus family Coronaviridae. Both viruses appeared to have managed to jump over the species barrier from a bat reservoir to the human population. Bats are considered to serve as a natural reservoir for coronaviruses infecting mammals. An important factor for crossing the species-barrier is the adaptation to a new receptor on cells of the new host species. During evolution coronaviruses have developed a large diversity of binding specificities demonstrating the high flexibility of the coronaviral spike protein, which is responsible for binding to target cells.

Mechanisms of Coronavirus Cell Entry Mediated by the Viral Spike Protein

Coronaviruses are enveloped positive-stranded RNA viruses that replicate in the cytoplasm. To deliver their nucleocapsid into the host cell, they rely on the fusion of their envelope with the host cell membrane. The spike glycoprotein (S) mediates virus entry and is a primary determinant of cell tropism and pathogenesis. It is classified as a class I fusion protein, and is responsible for binding to the receptor on the host cell as well as mediating the fusion of host and viral membranes—A process driven by major conformational changes of the S protein. This review discusses coronavirus entry mechanisms focusing on the different triggers used by coronaviruses to initiate the conformational change of the S protein: receptor binding, low pH exposure and proteolytic activation. We also highlight commonalities between coronavirus S proteins and other class I viral fusion proteins, as well as distinctive features that confer distinct tropism, pathogenicity and host interspecies transmission characteristics to coronaviruses.

Heat and coronavirus can be twin killers

Isothermal evaporation rate of deposited liquid aerosols and the SARS-CoV-2 coronavirus survival

It is shown that the evaporation rate of a liquid sample containing the culture of coronavirus affects its survival on a substrate. Possible mechanisms of such influence can be due to the appearance of large, about 140 bar, non comprehensive capillary pressures and the associated dynamic forces during the movement of the evaporation front in a sample with the virus. A simulation of isothermal evaporation of a thin liquid sample based on the Stefan problem was performed. The comparison of simulation data and recent experiments on the coronavirus survival on various surfaces showed that the rate of isothermal evaporation of aqueous samples, which is higher for heat-conducting materials, correlates well with the lifetime of the coronavirus on these surfaces.

The Effects of Temperature and Relative Humidity on the Viability of the SARS Coronavirus

The main route of transmission of SARS CoV infection is presumed to be respiratory droplets. However the virus is also detectable in other body fluids and excreta. The stability of the virus at different temperatures and relative humidity on smooth surfaces were studied. The dried virus on smooth surfaces retained its viability for over 5 days at temperatures of 22–25°C and relative humidity of 40–50%, that is, typical air-conditioned environments. However, virus viability was rapidly lost (>3 log(10)) at higher temperatures and higher relative humidity (e.g., 38°C, and relative humidity of >95%). The better stability of SARS coronavirus at low temperature and low humidity environment may facilitate its transmission in community in subtropical area (such as Hong Kong) during the spring and in air-conditioned environments. It may also explain why some Asian countries in tropical area (such as Malaysia, Indonesia or Thailand) with high temperature and high relative humidity environment did not have major community outbreaks of SARS.

Coronavirus come of age

Beyond the science of covid-19

Models of the new coronavirus's spread are imperfect, so factors other than the science play an important role too, says David Adam

This newly recognized coronavirus makes one wonder why we were so unprepared

Heat and coronavirus can be twin killers.

The Weather Impacts the Outbreak of COVID-19 in Mainland China

Recent literature has suggested that climate conditions have considerably significant influences on the transmission of coronavirus COVID-19. However, there is a lack of comprehensive study that investigates the relationships between multiple weather factors and the development of COVID-19 pandemic while excluding the impact of social factors. In this paper, we study the relationships between six main weather factors and the infection statistics of COVID-19 on 250 cities in Mainland China. Our correlation analysis using weather and infection statistics indicates that all the studied weather factors are correlated with the spread of COVID-19, where precipitation shows the strongest correlation. We also build a weather-aware predictive model that forecasts the number of infected cases should there be a second wave of the outbreak in Mainland China. Our predicted results show that cities located in different geographical areas are likely to be challenged with the second wave of COVID-19 at very different time periods and the severity of the outbreak varies to a large degree, in correspondence with the varying weather conditions.

Coronavirus, as a source of pandemic pathogens

The coronavirus and the influenza virus have similarities and differences. In order to comprehensively compare them, their genome sequencing data were examined by principal component analysis. Variations in coronavirus were smaller than those in a subclass of the influenza virus. In addition, differences among coronaviruses in a variety of hosts were small. These characteristics may have facilitated the infection of different hosts. Although many of the coronaviruses were more conservative, those repeatedly found among humans showed annual changes. If SARS-CoV-2 changes its genome like the Influenza H type, it will repeatedly spread every few years. In addition, the coronavirus family has many other candidates for subsequent pandemics. One Sentence Summary The genome data of coronavirus were compared to influenza virus, to investigate its spreading mechanism and future status. Coronavirus would repeatedly spread every few years. In addition, the coronavirus family has many other candidates for subsequent pandemics.

Uncertainty in the Time of Coronavirus

A Multiscale and Comparative Model for Receptor Binding of 2019 Novel Coronavirus and the Implication of its Life Cycle in Host Cells

The respiratory syndrome caused by a new type of coronavirus has been emerging from China and caused more than 1000 death globally since December 2019. This new virus, called 2019 novel coronavirus (2019-nCoV) uses the same receptor called Angiotensinconverting enzyme 2 (ACE2) to attack humans as the coronavirus that caused the severe acute respiratory syndrome (SARS) seventeen years ago. Both viruses recognize ACE2 through the spike proteins (S-protein) on their surfaces. It was found that the S-protein from the SARS coronavirus (SARS-CoV) bind stronger to ACE2 than 2019-nCoV. However, function of a bio-system is often under kinetic, rather than thermodynamic, control. To address this issue, we constructed a structural model for complex formed between ACE2 and the S-protein from 2019-nCoV, so that the rate of their association can be estimated and compared with the binding of S-protein from SARS-CoV by a multiscale simulation method. Our simulation results suggest that the association of new virus to the receptor is slower than SARS, which is consistent with the experimental data obtained very recently. We further integrated this difference of association rate between virus and receptor into a mathematical model which describes the life cycle of virus in host cells and its interplay with the innate immune system. Interestingly, we found that the slower association between virus and receptor can result in longer incubation period, while still maintaining a relatively higher level of viral concentration in human body. Our computational study therefore provides, from the molecular level, one possible explanation that the new disease by far spread much faster than SARS.

Spread of SARS-CoV-2 Coronavirus likely to be constrained by climate

As new cases of COVID-19 are being confirmed pressure is mounting to increase understanding of the factors underlying the spread the disease. Using data on local transmissions until the 23rd of March 2020, we develop an ensemble of 200 ecological niche models to project monthly variation in climate suitability for spread of SARS-CoV-2 throughout a typical climatological year. Although cases of COVID-19 are reported all over the world, most outbreaks display a pattern of clustering in relatively cool and dry areas. The predecessor SARS-CoV-1 was linked to similar climate conditions. Should the spread of SARS CoV-2 continue to follow current trends, asynchronous seasonal global outbreaks could be expected. According to the models, temperate warm and cold climates are more favorable to spread of the virus, whereas arid and tropical climates are less favorable. However, model uncertainties are still high across much of sub- Saharan Africa, Latin America and South East Asia. While models of epidemic spread utilize human demography and mobility as predictors, climate can also help constrain the virus. This is because the environment can mediate human-to-human transmission of SARS-CoV-2, and unsuitable climates can cause the virus to destabilize quickly, hence reducing its capacity to become epidemic.

Spatial modeling cannot currently differentiate SARS-CoV-2 coronavirus and human distributions on the basis of climate in the United States

The SARS-CoV-2 coronavirus is wreaking havoc globally, yet knowledge of its biology is limited. Climate and seasonality influence the distributions of many diseases, and studies suggest a link between SARS-CoV-2 and cool weather. One such study, building species distribution models (SDMs), predicted SARS-CoV-2 risk may remain concentrated in the Northern Hemisphere, shifting northward in summer months. Others have highlighted issues with SARS-CoV-2 SDMs, notably: the primary niche of the virus is the host it infects, climate may be a weak distributional predictor, global prevalence data have issues, and the virus is not in a population equilibrium. While these issues should be considered, climate still may be important for predicting the future distribution of SARS-CoV-2. To further examine if there is a link, we model with raw cases and population scaled cases for SARS-CoV-2 county-level data from the United States. We show that SDMs built from population scaled cases data cannot be distinguished from control models built from raw human population data, while SDMs built on raw data fail to predict the current known distribution of cases in the US. The population scaled analyses indicate that climate may not play a central role in current US viral distribution and that human population density is likely a primary driver. Still, we do find slightly more population scaled viral cases in cooler areas. This coupled with our geographically constrained focus make it so we cannot rule out climate as a partial driver of the US SARS-CoV-2 distribution. Climate's role on SARS-CoV-2 should continue to be cautiously examined, but at this time we should assume that SARS-CoV-2 can spread anywhere in the US.

Inactivation of coronaviruses by heat

Coronavirus replication factories

Coronavirus.

All roads lead to coronavirus.

Investigation of the effect of temperature on the structure of SARS-Cov-2 Spike Protein by Molecular Dynamics Simulations

Statistical and epidemiological data imply temperature sensitivity of the SARS-CoV-2 coronavirus. However, the molecular level understanding of the virus structure at different temperature is still not clear. Spike protein is the outermost structural protein of the SARS-CoV-2 virus which interacts with the Angiotensin Converting Enzyme 2 (ACE2), a human receptor, and enters the respiratory system. In this study, we performed an all atom molecular dynamics simulation to study the effect of temperature on the structure of the Spike protein. After 200ns of simulation at different temperatures, we came across some interesting phenomena exhibited by the protein. We found that the solvent exposed domain of Spike protein, namely S1, is more mobile than the transmembrane domain, S2. Structural studies implied the presence of several charged residues on the surface of N-terminal Domain of S1 which are optimally oriented at 10-30 °C. Bioinformatics analyses indicated that it is capable of binding to other human receptors and should not be disregarded. Additionally, we found that receptor binding motif (RBM), present on the receptor binding domain (RBD) of S1, begins to close around temperature of 40 °C and attains a completely closed conformation at 50 °C. The closed conformation disables its ability to bind to ACE2, due to the burying of its receptor binding residues. Our results clearly show that there are active and inactive states of the protein at different temperatures. This would not only prove beneficial for understanding the fundamental nature of the virus, but would be also useful in the development of vaccines and therapeutics. Graphical Abstract Highlights Statistical and epidemiological evidence show that external climatic conditions influence the SARS-CoV infectivity, but we still lack a molecular level understanding of the same. Here, we study the influence of temperature on the structure of the Spike glycoprotein, the outermost structural protein, of the virus which binds to the human receptor ACE2. Results show that the Spike’s S1 domain is very sensitive to external atmospheric conditions compared to the S2 transmembrane domain. The N-terminal domain comprises of several solvent exposed charged residues that are capable of binding to human proteins. The region is specifically stable at temperatures ranging around 10-30° C. The Receptor Binding Motif adopts a closed conformation at 40°C and completely closes at higher temperatures making it unsuitable of binding to human receptors

Parallel problems

Our fight against climate change offers useful lessons for tackling the coronavirus

Mini organs reveal how the coronavirus ravages the body.

PDA Responds to the Novel Coronavirus Situation.

Coronavirus disruptions reverberate through research

Shedding ultraviolet light on coronavirus

Coronavirus

The Evolution of Computational Chemistry Along with Coronaviruses.

Why does the coronavirus spread so easily between people?

Coronavirus and Malta: weathering the storm

Forecasting the timeframe of 2019-nCoV and human cells interaction with reverse engineering

In December 2019, an atypical pneumonia invaded the city of Wuhan, China, and the causative agent of this disease turned out to be a new coronavirus. In January 2020, the World Health Organization named the new coronavirus 2019-nCoV and subsequently it is referred to as SARS-CoV2 and the related disease as CoViD-19 (Lai et al., 2020). Very quickly, the epidemic led to a pandemic and it is now a worldwide emergency requiring the creation of new antiviral therapies and a related vaccine. The purpose of this article is to review and investigate further the molecular mechanism by which the SARS-CoV2 virus infection proceeds via the formation of a hetero-trimer between its protein S, the ACE2 receptor and the B0AT1 protein, which is the "entry receptor" for the infection process involving membrane fusion (Li et al., 2003). A reverse engineering process uses the formalism of the Hill function to represent the functions related to the dynamics of the biochemical interactions of the viral infection process. Then, using a logical evaluation of viral density that measures the rate at which the cells are hijacked by the virus (and they provide a place for the virus to replicate) and considering the "time delay" given by the interaction between cell and virus, the expected duration of the incubation period is predicted. The conclusion is that the density of the virus varies from the "exposure time" to the "interaction time" (virus-cells). This model can be used both to evaluate the infectious condition and to analyze the incubation period. BACKGROUND: The ongoing threat of the new coronavirus SARS-CoV2 pandemic is alarming and strategies for combating infection are highly desired. This RNA virus belongs to the ß-coronavirus genus and is similar in some features to SARS-CoV. Currently, no vaccine or approved medical treatment is available. The complex dynamics of the rapid spread of this virus can be demonstrated with the aid of a computational framework. METHODS: A mathematical model based on the principles of cell-virus interaction is developed in this manuscript. The amino acid sequence of S proein and its interaction with the ACE-2 protein is mimicked with the aid of Hill function. The mathematical model with delay is solved with the aid of numerical solvers and the parametric values are obtained with the help of MCMC algorithm. RESULTS: A delay differential equation model is developed to demonstrate the dynamics of target cells, infected cells and the SARS-CoV2. The important parameters and coefficients are demonstrated with the aid of numerical computations. The resulting thresholds and forecasting may prove to be useful tools for future experimental studies and control strategies. CONCLUSIONS: From the analysis, I is concluded that control strategy via delay is a promising technique and the role of Hill function formalism in control strategies can be better interpreted in an inexpensive manner with the aid of a theoretical framework.

Whose coronavirus strategy worked best? Scientists hunt most effective policies.

Coronavirus disruptions reverberate through research.

What could coronavirus teach us?

Another Decade, Another Coronavirus

Coronavirus envelope assembly is sensitive to changes in the terminal regions of the viral M protein.

Recently we demonstrated that the co-expressed coronavirus membrane proteins have the capacity to assemble viral envelopes which are similar to normal virus particles in dimensions and appearance, and which can form independent of a nucleocapsid (Vennema et al., 1996). For the formation of these particles only the M and the E protein are required; the S protein is dispensable but is incorporated when present. As we illustrate here, this virus-like particle assembly system is an ideal tool to study the interactions between the essential assembly partners M and E in molecular detail. Taking a mutagenetic approach we demonstrate that envelope assembly is critically sensitive to changes in the primary structure of both terminal domains of the M protein. The effects were most dramatically observed after mutation of the carboxy-terminal domain where the deletion of just one single amino acid at the extreme terminus abolished particle formation almost completely. But also some subtle mutations in the amino-terminal domain were severely inhibitory to the assembly process. Interestingly, mutant M proteins that were themselves incompetent to support particle formation appeared to inhibit, in a concentration dependent manner, the assembly of particles by wild-type M and E protein.

Predicting the receptor-binding domain usage of the coronavirus based on kmer frequency on spike protein

Is the coronavirus airborne? Experts can't agree

Changes in human nasal mucosa during experimental coronavirus common colds.

Twenty-four adult volunteers were inoculated with nasal drops containing a coronavirus of 229E serotype to determine the differences in the clinical and physiological reactions which occur between clinically infected, sub-clinically infected and non-infected individuals. Thirteen volunteers were clinically infected, 8 had sub-clinical infections and 3 were uninfected. Nasal airway resistance and the temperature of the nasal mucosa increased in all infected subjects both with and without symptoms: the core temperature increased also but to a lesser extent. Mucosal blood flow and nasal secretion increased only in those with symptoms. The albumin content of the nasal secretion increased in the clinically infected, suggesting that it was derived, partially at least, from the circulation. The nasal cycle of variation in airway resistance between the two sides of the nose was observed in all three groups but increased only in those clinically infected.

Science in the time of coronavirus.

Mathematical Modeling of Coronavirus Reproduction Rate with Policy and Behavioral Effects

In this paper a modified mathematical model based on the SIR model used which can predict the spreading of the corona virus disease (COVID-19) and its effects on people in the days ahead. This model takes into account all the death, infected and recovered characteristics of this disease. To determine the extent of the risk posed by this novel coronavirus; the transmission rate (R0) is utilized for a time period from the beginning of spreading virus. In particular, it includes a novel policy to capture the R0 response in the virus spreading over time. The model estimates the vulnerability of the pandemic with a prediction of new cases by estimating a time-varying R0 to capture changes in the behavior of SIR model implies to new policy taken at different times and different locations of the world. This modified SIR model with the different values of R0 can be applied to different country scenario using the real time data report provided by the authorities during this pandemic. The effective evaluation of R0 can forecast the necessity of lockdown as well as reopening the economy.

Susceptible supply limits the role of climate in the early SARS-CoV-2 pandemic

Preliminary evidence suggests that climate may modulate the transmission of SARS-CoV-2. Yet it remains unclear whether seasonal and geographic variations in climate can substantially alter the pandemic trajectory, given high susceptibility is a core driver. Here, we use a climate-dependent epidemic model to simulate the SARS-CoV-2 pandemic probing different scenarios based on known coronavirus biology. We find that while variations in weather may be important for endemic infections, during the pandemic stage of an emerging pathogen the climate drives only modest changes to pandemic size. A preliminary analysis of non-pharmaceutical control measures indicates that they may moderate the pandemic-climate interaction via susceptible depletion. Our findings suggest, without effective control measures, strong outbreaks are likely in more humid climates and summer weather will not substantially limit pandemic growth.

The SARS-CoV-2 exerts a distinctive strategy for interacting with the ACE2 human receptor

The COVID-19 disease has plagued over 110 countries and has resulted in over 4,000 deaths within 10 weeks. We compare the interaction between the human ACE2 receptor and the SARS-CoV-2 spike protein with that of other pathogenic coronaviruses using molecular dynamics simulations. SARS-CoV, SARS-CoV-2, and HCoV-NL63 recognize ACE2 as the natural receptor but present a distinct binding interface to ACE2 and a different network of residue-residue contacts. SARS-CoV and SARS-CoV-2 have comparable binding affinities achieved by balancing energetics and dynamics. The SARS-CoV-2–ACE2 complex contains a higher number of contacts, a larger interface area, and decreased interface residue fluctuations relative to SARS-CoV. These findings expose an exceptional evolutionary exploration exerted by coronaviruses toward host recognition. We postulate that the versatility of cell receptor binding strategies has immediate implications on therapeutic strategies. One Sentence Summary Molecular dynamics simulations reveal a temporal dimension of coronaviruses interactions with the host receptor.

All roads lead to coronavirus

Host Factors in Coronavirus Replication

Coronaviruses are pathogens with a serious impact on human and animal health. They mostly cause enteric or respiratory disease, which can be severe and life threatening, e.g., in the case of the zoonotic coronaviruses causing severe acute respiratory syndrome (SARS) and Middle East Respiratory Syndrome (MERS) in humans. Despite the economic and societal impact of such coronavirus infections, and the likelihood of future outbreaks of additional pathogenic coronaviruses, our options to prevent or treat coronavirus infections remain very limited. This highlights the importance of advancing our knowledge on the replication of these viruses and their interactions with the host. Compared to other +RNA viruses, coronaviruses have an exceptionally large genome and employ a complex genome expression strategy. Next to a role in basic virus replication or virus assembly, many of the coronavirus proteins expressed in the infected cell contribute to the coronavirus-host interplay. For example, by interacting with the host cell to create an optimal environment for coronavirus replication, by altering host gene expression or by counteracting the host’s antiviral defenses. These coronavirus–host interactions are key to viral pathogenesis and will ultimately determine the outcome of infection. Due to the complexity of the coronavirus proteome and replication cycle, our knowledge of host factors involved in coronavirus replication is still in an early stage compared to what is known for some other +RNA viruses. This review summarizes our current understanding of coronavirus–host interactions at the level of the infected cell, with special attention for the assembly and function of the viral RNA-synthesising machinery and the evasion of cellular innate immune responses.

How Volunteers Are Dealing With Coronavirus Issues

Coronavirus misinformation needs researchers to respond

The coronaviruslike superfamily.

Concerns Over the Coronavirus Spread to the Oil Industry

Coronavirus misinformation needs researchers to respond.

New coronavirus

The role of programmed-1 ribosomal frameshifting in coronavirus propagation.

Coronaviruses have the potential to cause significant economic, agricultural and health problems. The severe acute respiratory syndrome (SARS) associated coronavirus outbreak in late 2002, early 2003 called attention to the potential damage that coronaviruses could cause in the human population. The ensuing research has enlightened many to the molecular biology of coronaviruses. A programmed -1 ribosomal frameshift is required by coronaviruses for the production of the RNA dependent RNA polymerase which in turn is essential for viral replication. The frameshifting signal encoded in the viral genome has additional features that are not essential for frameshifting. Elucidation of the differences between coronavirus frameshift signals and signals from other viruses may help our understanding of these features. Here we summarize current knowledge and add additional insight regarding the function of the programmed -1 ribosomal frameshift signal in the coronavirus lifecycle.

Coronavirus receptor specificity.

Molecular evolution of SARS coronavirus tracked

Coronavirus: just imagine

The Molecular Biology of Coronaviruses

Publisher Summary This chapter discusses the manipulation of clones of coronavirus and of complementary DNAs (cDNAs) of defective-interfering (DI) RNAs to study coronavirus RNA replication, transcription, recombination, processing and transport of proteins, virion assembly, identification of cell receptors for coronaviruses, and processing of the polymerase. The nature of the coronavirus genome is nonsegmented, single-stranded, and positive-sense RNA. Its size ranges from 27 to 32 kb, which is significantly larger when compared with other RNA viruses. The gene encoding the large surface glycoprotein is up to 4.4 kb, encoding an imposing trimeric, highly glycosylated protein. This soars some 20 nm above the virion envelope, giving the virus the appearance-with a little imagination-of a crown or coronet. Coronavirus research has contributed to the understanding of many aspects of molecular biology in general, such as the mechanism of RNA synthesis, translational control, and protein transport and processing. It remains a treasure capable of generating unexpected insights.

Coronavirus lockdowns have changed the way Earth moves

Variational-LSTM Autoencoder to forecast the spread of coronavirus across the globe

Modelling the spread of coronavirus globally while learning trends at global and country levels remains crucial for tackling the pandemic. We introduce a novel variational LSTM-Autoencoder model to predict the spread of coronavirus for each country across the globe. This deep spatio-temporal model does not only rely on historical data of the virus spread but also includes factors related to urban characteristics represented in locational and demographic data (such as population density, urban population, and fertility rate), an index that represent the governmental measures and response amid toward mitigating the outbreak (includes 13 measures such as: 1) school closing, 2) workplace closing, 3) cancelling public events, 4) close public transport, 5) public information campaigns, 6) restrictions on internal movements, 7) international travel controls, 8) fiscal measures, 9) monetary measures, 10) emergency investment in health care, 11) investment in vaccines, 12) virus testing framework, and 13) contact tracing). In addition, the introduced method learns to generate graph to adjust the spatial dependences among different countries while forecasting the spread. We trained two models for short and long-term forecasts. The first one is trained to output one step in future with three previous timestamps of all features across the globe, whereas the second model is trained to output 10 steps in future. Overall, the trained models show high validation for forecasting the spread for each country for short and long-term forecasts, which makes the introduce method a useful tool to assist decision and policymaking for the different corners of the globe.

Weathering the pandemic: How the Caribbean Basin can use viral and environmental patterns to predict, prepare, and respond to COVID-19

The 2020 coronavirus pandemic is developing at different paces throughout the world. Some areas, like the Caribbean Basin, have yet to see the virus strike at full force. When it does, there is reasonable evidence to suggest the consequent COVID-19 outbreaks will overwhelm healthcare systems and economies. This is particularly concerning in the Caribbean as pandemics can have disproportionately higher mortality impacts on lower and middle-income countries. Preliminary observations from our team and others suggest that temperature and climatological factors could influence the spread of this novel coronavirus, making spatiotemporal predictions of its infectiousness possible. This review studies geographic and time-based distribution of known respiratory viruses in the Caribbean Basin in an attempt to foresee how the pandemic will develop in this region. This review is meant to aid in planning short- and long-term interventions to manage outbreaks at the international, national, and subnational levels in the region.

Keep up with the latest coronavirus research.

Coronavirus can infect cats - dogs, not so much

The Evolution of Computational Chemistry Along with Coronaviruses

Coronavirus can infect cats - dogs, not so much.

Coronavirus: the first three months as it happened

Investigation of effective climatology parameters on COVID-19 outbreak in Iran

SARS CoV-2 (COVID-19) Coronavirus cases are confirmed throughout the world and millions of people are being put into quarantine. A better understanding of the effective parameters in infection spreading can bring about a logical measurement toward COVID-19. The effect of climatic factors on spreading of COVID-19 can play an important role in the new Coronavirus outbreak. In this study, the main parameters, including the number of infected people with COVID-19, population density, intra-provincial movement, and infection days to end of the study period, average temperature, average precipitation, humidity, wind speed, and average solar radiation investigated to understand how can these parameters effects on COVID-19 spreading in Iran? The Partial correlation coefficient (PCC) and Sobol'-Jansen methods are used for analyzing the effect and correlation of variables with the COVID-19 spreading rate. The result of sensitivity analysis shows that the population density, intra-provincial movement have a direct relationship with the infection outbreak. Conversely, areas with low values of wind speed, humidity, and solar radiation exposure to a high rate of infection that support the virus's survival. The provinces such as Tehran, Mazandaran, Alborz, Gilan, and Qom are more susceptible to infection because of high population density, intra-provincial movements and high humidity rate in comparison with Southern provinces.

Does the coronavirus a global threat?

PDA Responds to the Novel Coronavirus Situation

Computers against COVID-19

It took scientists only a few days in January to deduce the genome of the novel coronavirus, SARS-CoV-2, giving researchers around the world blueprints to the virus’s molecular tools and machinery But for computational chemists and biophysicists, the hard work is just beginning They have spent the past 2 months using those blueprints to build computer models of the virus’s proteins These models could help them figure out how the proteins interact with human cells and could help them find therapies to prevent infections or treat COVID-19, the disease caused by the virus The scientists are now beginning to deploy these carefully crafted models Accurately modeling the thousands of atoms in proteins like the polymerase that SARS-CoV-2 uses to replicate its RNA can require significant computing power The need for computing power increases further when scientists want to simulate interactions between proteins or between proteins and molecules, and it increases

Coronavirus?

Un nuevo coronavirus emerge

Koronaviruset kjenner ingen grenser./ Koronaviruset kjenner ingen grenser./ The coronavirus knows no borders

Science in the time of coronavirus

Science in the Time of Coronavirus

Coronavirus entry and release in polarized epithelial cells: a review

Most coronaviruses cause respiratory or intestinal infections in their animal or human host. Hence, their interaction with polarized epithelial cells plays a critical role in the onset and outcome of infection. In this paper, we review the knowledge regarding the entry and release of coronaviruses, with particular emphasis on the severe acute respiratory syndrome and Middle East respiratory syndrome coronaviruses. As these viruses approach the epithelial surfaces from the apical side, it is not surprising that coronavirus cell receptors are exposed primarily on the apical domain of polarized epithelial cells. With respect to release, all possibilities appear to occur. Thus, most coronaviruses exit through the apical surface, several through the basolateral one, although the Middle East respiratory syndrome coronavirus appears to use both sides. These observations help us understand the local or systematic spread of the infection within its host as well as the spread of the virus within the host population. Copyright © 2014 John Wiley & Sons, Ltd.

Forecasting the timeframe of coronavirus and human cells interaction with reverse engineering

Abstract In December 2019, an atypical pneumonia invaded the city of Wuhan, China, and the causative agent of this disease turned out to be a new coronavirus. In January 2020, the World Health Organization named the new coronavirus 2019-nCoV and subsequently it is referred to as SARS-CoV2 and the related disease as CoViD-19 [9]. Very quickly, the epidemic led to a pandemic and it is now a worldwide emergency requiring the creation of new antiviral therapies and a related vaccine. The purpose of this article is to review and investigate further the molecular mechanism by which the SARS-CoV2 virus infection proceeds via the formation of a hetero-trimer between its protein S, the ACE2 receptor and the B0AT1 protein, which is the “entry receptor” for the infection process involving membrane fusion [10]. A reverse engineering process uses the formalism of the Hill function to represent the functions related to the dynamics of the biochemical interactions of the viral infection process. Then, using a logical evaluation of viral density that measures the rate at which the cells are hijacked by the virus (and they provide a place for the virus to replicate) and considering the “time delay” given by the interaction between cell and virus, the expected duration of the incubation period is predicted. The conclusion is that the density of the virus varies from the “exposure time” to the “interaction time” (virus-cells). This model can be used both to evaluate the infectious condition and to analyze the incubation period. Background The ongoing threat of the new coronavirus SARS-CoV2 pandemic is alarming and strategies for combating infection are highly desired. This RNA virus belongs to the β-coronavirus genus and is similar in some features to SARS-CoV. Currently, no vaccine or approved medical treatment is available. The complex dynamics of the rapid spread of this virus can be demonstrated with the aid of a computational framework. Methods A mathematical model based on the principles of cell-virus interaction is developed in this manuscript. The amino acid sequence of S proein and its interaction with the ACE-2 protein is mimicked with the aid of Hill function. The mathematical model with delay is solved with the aid of numerical solvers and the parametric values are obtained with the help of MCMC algorithm. Results A delay differential equation model is developed to demonstrate the dynamics of target cells, infected cells and the SARS-CoV2. The important parameters and coefficients are demonstrated with the aid of numerical computations. The resulting thresholds and forecasting may prove to be useful tools for future experimental studies and control strategies. Conclusions From the analysis, I is concluded that control strategy via delay is a promising technique and the role of Hill function formalism in control strategies can be better interpreted in an inexpensive manner with the aid of a theoretical framework.

Changes in nucleolar morphology and proteins during infection with the coronavirus infectious bronchitis virus

The nucleolus is a dynamic subnuclear structure involved in ribosome subunit biogenesis, cell cycle control and mediating responses to cell stress, among other functions. While many different viruses target proteins to the nucleolus and recruit nucleolar proteins to facilitate virus replication, the effect of infection on the nucleolus in terms of morphology and protein content is unknown. Previously we have shown that the coronavirus nucleocapsid protein will localize to the nucleolus. In this study, using the avian infectious bronchitis coronavirus, we have shown that virus infection results in a number of changes to the nucleolus both in terms of gross morphology and protein content. Using confocal microscopy coupled with fluorescent labelled nucleolar marker proteins we observed changes in the morphology of the nucleolus including an enlarged fibrillar centre. We found that the tumour suppressor protein, p53, which localizes normally to the nucleus and nucleolus, was redistributed predominately to the cytoplasm.

Generation coronavirus?

How scientific conferences will survive the coronavirus shock.

Chaos with Coronavirus

An uncommon cold

The covid-19 virus isn't the first coronavirus to jump from animals to humans. What can we learn from previous encounters, asks Anthony King.

Susceptible supply limits the role of climate in the COVID-19 pandemic

Preliminary evidence suggests that climate may modulate the transmission of SARS-CoV-2. Yet it remains unclear whether seasonal and geographic variations in climate can substantially alter the pandemic trajectory, given high susceptibility is a core driver. Here, we use a climate-dependent epidemic model to simulate the SARS-CoV-2 pandemic probing different scenarios of climate-dependence based on known coronavirus biology. We find that while variations in humidity may be important for endemic infections, during the pandemic stage of an emerging pathogen such as SARS-CoV-2 climate may drive only modest changes to pandemic size and duration. Our results suggest that, in the absence of effective control measures, significant cases in the coming months are likely to occur in more humid (warmer) climates, irrespective of the climate-dependence of transmission and that summer temperatures will not substantially limit pandemic growth.

Interactions Between Sars Coronavirus and its Receptor

The molecular biology of intracellular events during Coronavirus infection cycle

CoV-2 which is the causative agent of COVID-19 belongs to genus betacoronaviruses. The sequence analysis of S protein of CoV-2 has shown that it has acquired a ‘polybasic cleavage site’ consisting of 12 aminoacids that has been predicted to enable its cleavage by other cellular proteases possibly increasing its transmissibility. The aminoacids present in receptor binding domain of S protein of SARS CoV which are critical for its binding to cellular receptor are different in CoV-2. The presence of heptanucleotide slippery sequence in ORF1 resulting in ribosomal frameshifting, and presence of transcription regulatory sequences between ORFs resulting in discontinuous transcription, are peculiar features of Coronavirus infection cycle. The exonuclease activity of nsp14 provides possible proofreading ability to RNA polymerase makes coronaviruses different from other RNA viruses allowing coronaviruses to maintain their relatively large genome size. This mini-review summarizes the peculiar features of Coronaviruses genome and the critical events during the infection cycle with focus on CoV-2.

Coronavirus is the trigger, but the immune response is deadly

The Environmental Impacts of the Coronavirus

The Covid-19 coronavirus pandemic has resulted in global lockdowns, sharply curtailing economic activity. It is a unique experiment with substantial impacts that will form the agenda for research. There are five sets of questions: the short-term impacts on emissions, the natural environment and environmental policy, including regulations and COP26; longer-term consequences from the deployment of macroeconomic monetary and fiscal stimuli, and investment in green deals; possible further deglobalisation and its impact on climate change and nature; intergenerational environmental impacts including debt and pollution burdens on future generations; and possible behavioural changes to the environment, both positive and negative.

WHO sets up expert committee to advise on coronavirus.

Seasonality of Respiratory Viral Infections.

The seasonal cycle of respiratory viral diseases has been widely recognized for thousands of years, as annual epidemics of the common cold and influenza disease hit the human population like clockwork in the winter season in temperate regions. Moreover, epidemics caused by viruses such as severe acute respiratory syndrome coronavirus (SARS-CoV) and the newly emerging SARS-CoV-2 occur during the winter months. The mechanisms underlying the seasonal nature of respiratory viral infections have been examined and debated for many years. The two major contributing factors are the changes in environmental parameters and human behavior. Studies have revealed the effect of temperature and humidity on respiratory virus stability and transmission rates. More recent research highlights the importance of the environmental factors, especially temperature and humidity, in modulating host intrinsic, innate, and adaptive immune responses to viral infections in the respiratory tract. Here we review evidence of how outdoor and indoor climates are linked to the seasonality of viral respiratory infections. We further discuss determinants of host response in the seasonality of respiratory viruses by highlighting recent studies in the field. Expected final online publication date for the Annual Review of Virology, Volume 7 is September 29, 2020. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

The structure and replication of coronaviruses.

[Coronaviruses].

Coronaviruses contain positive-stranded RNA with ca. 30 kb as a genome, which is wrapped by the envelope, and constitute Nidovirales together with Arteriviridae. The feature of viruses in Nidovirales is the unique structure of the mRNA set, called 3' co-terminal nested set. Coronaviruses have several to more than 10 different species of subgenomic mRNA and generally only the OFR located in the 5' end of each mRNA is translated. The 5' 20 kb of the coronavirus genome or mRNA-1 consists of two ORFs, 1a and 1b, between that there is a unique RNA structure called pseudoknot. From mRNA-1, 1a as well as 1a+1b are translated; the latter 1a+1b results from the translation due to ribosomal frame-shifting facilitated by the pseudoknot structure. From those two proteins, totally 16 proteins are produced as a result of auto-cleavage by the proteases included in la protein. Those proteins exhibit different functions, such as RNA-dependent RNA polymerase, helicase, proteases and proteins that regulate cellular functions, mRNAs smaller than mRNA-2 translate in general the structural proteins, nucleocapsid (N) protein, spike (S) protein, integrated membrane (M) protein and envelope (E) proteins. Those proteins assemble to the vesicles located from ER to Golgi (ER Golgi intermediate compartment) and virions bud into the vesicles. Those virions are released from infected cells via exocytosis.

CoV-2 which is the causative agent of COVID-19 belongs to genus betacoronaviruses. The sequence analysis of S protein of CoV-2 has shown that it has acquired a 'polybasic cleavage site' consisting of 12 aminoacids that has been predicted to enable its cleavage by other cellular proteases possibly increasing its transmissibility. The aminoacids present in receptor binding domain of S protein of SARS CoV which are critical for its binding to cellular receptor are different in CoV-2. The presence of heptanucleotide slippery sequence in ORF1 resulting in ribosomal frameshifting, and presence of transcription regulatory sequences between ORFs resulting in discontinuous transcription, are peculiar features of Coronavirus infection cycle. The exonuclease activity of nsp14 provides possible proofreading ability to RNA polymerase makes coronaviruses different from other RNA viruses allowing coronaviruses to maintain their relatively large genome size. This mini-review summarizes the peculiar features of Coronaviruses genome and the critical events during the infection cycle with focus on CoV-2.

Coronavirus lockdowns have changed the way Earth moves.

Mathematical modelling for coronavirus disease (COVID-19) in predicting future behaviours and sensitivity analysis

Nowadays, there are a variety of descriptive studies of available clinical data for coronavirus disease (COVID-19) Mathematical modelling and computational simulations are effective tools that help global efforts to estimate key transmission parameters The model equations often require computational tools and dynamical analysis that play an important role in controlling the disease This work reviews some models for coronavirus first, that can address important questions about the global health care and suggest important notes Then, we model the disease as a system of differential equations We develop previous models for the coronavirus, some key computational simulations and sensitivity analysis are added Accordingly, the local sensitivities for each model state with respect to the model parameters are computed using three different techniques: non-normalizations, half normalizations and full normalizations Results based on sensitivity analysis show that almost all model parameters may have role on spreading this virus among susceptible, exposed and quarantined susceptible people More specifically, communicate rate person-to-person, quarantined exposed rate and transition rate of exposed individuals have an effective role in spreading this disease One possible solution suggests that healthcare programs should pay more attention to intervention strategies, and people need to self-quarantine that can effectively reduce the disease