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Several viruses have the ability to form large multinucleated cells known as syncytia. Many properties of syncytia and the role they play in the evolution of a viral infection are not well understood. One basic question that has not yet been answered is how quickly syncytia form. We use a novel mathematical model of cell-cell fusion assays and apply it to experimental data from SARS-CoV-2 fusion assays to provide the first estimates of virus-mediated cell fusion rate. We find that for SARS-CoV2, the fusion rate is in the range of 6 × 10−4–12×10−4/h. We also use our model to compare fusion rates when the protease TMPRSS2 is overexpressed (2–4 times larger fusion rate), when the protease furin is removed (one third the original fusion rate), and when the spike protein is altered (1/10th the original fusion rate). The use of mathematical models allows us to provide additional quantitative information about syncytia formation. • A mathematical model is used to analyze SARS-CoV-2 cell-cell fusion assays. • This allows us to estimate the virus-mediated fusion rate for the first time. • Estimates are used to quantify the effect of TMPRSS2 and furin on cell fusion. • Removal of the spike cleavage site causes a ten-fold reduction in fusion rate. [ABSTRACT FROM AUTHOR]

The World Health Organization (WHO) on December 31, 2019, was informed of several cases of respiratory diseases of unknown origin in the city of Wuhan in the Chinese Province of Hubei, the clinical manifestations of which were similar to those of viral pneumonia and manifested as fever, cough, and shortness of breath. And, the disease caused by the virus is named the new coronavirus disease 2019 and it will be abbreviated as 2019-nCoV and COVID-19. As of January 30, 2020, the WHO classified this epidemic as a global health emergency (Chung et al. in Radiology 295(1):202–207, 2020). It is an international real-life problem. Due to deaths, globally everyone is under fear. Now, it is the responsibility of researchers to give hope to the people. In this article, we aim to better protect people and general pandemic preparedness by predicting the lifetime of the disease-causing virus using three mathematical models. This article deals with a complex real-life problem people face all over the world, an international real-life problem. The main focus is on the USA due to large infection and death due to coronavirus and thereby the life of every individual is uncertain. The death counts of the USA from February 29 to April 22, 2020, are used in this article as a data set. The death counts of the USA are fitted by the solutions of three mathematical models and a solution to an international problem is achieved. Based on the death rate, the lifetime of the coronavirus COVID-19 is predicted as 1464.76 days from February 29, 2020. That is, after March 2024 there will be no death in the USA due to COVID-19 if everyone follows the guidelines of WHO and the advice of healthcare workers. People and government can get prepared for this situation and many lives can be saved. It is the contribution of soft computing. Finally, this article suggests several steps to control the spread and severity of the disease. The research work, the lifetime prediction presented in this article is entirely new and differs from all other articles in the literature. [ABSTRACT FROM AUTHOR]

COVID-19 pandemic has underlined the impact of emergent pathogens as a major threat to human health. The development of quantitative approaches to advance comprehension of the current outbreak is urgently needed to tackle this severe disease. Considering different starting times of infection, mathematical models are proposed to represent SARS-CoV-2 dynamics in infected patients. Based on the target cell limited model, the within-host reproductive number for SARS-CoV-2 is consistent with the broad values of human influenza infection. The best model to fit the data was including immune cell response, which suggests a slow immune response peaking between 5 to 10 days post-onset of symptoms. The model with the eclipse phase, time in a latent phase before becoming productively infected cells, was not supported. Interestingly, model simulations predict that SARS-CoV-2 may replicate very slowly in the first days after infection, and viral load could be below detection levels during the first 4 days post infection. A quantitative comprehension of SARS-CoV-2 dynamics and the estimation of standard parameters of viral infections is the key contribution of this pioneering work. These models can serve for future evaluation of control theoretical approaches to tailor new drugs against COVID-19. [ABSTRACT FROM AUTHOR]

In December 2019, the first case of infection with a new virus COVID-19 (SARS-CoV-2), named coronavirus, was reported in the city of Wuhan, China. At that time, almost nobody paid any attention to it. The new pathogen, however, fast proved to be extremely infectious and dangerous, resulting in about 3–5% mortality. Over the few months that followed, coronavirus has spread over entire world. At the end of March, the total number of infections is fast approaching the psychological threshold of one million, resulting so far in tens of thousands of deaths. Due to the high number of lives already lost and the virus high potential for further spread, and due to its huge overall impact on the economies and societies, it is widely admitted that coronavirus poses the biggest challenge to the humanity after the second World war. The COVID-19 epidemic is provoking numerous questions at all levels. It also shows that modern society is extremely vulnerable and unprepared to such events. A wide scientific and public discussion becomes urgent. Some possible directions of this discussion are suggested in this article. [ABSTRACT FROM AUTHOR]

• We measure infection of human (A549-ACE2) and animal (Vero-E6) cells by SARS-CoV-2. • We use mathematical modelling to estimate SARS-CoV-2 infection parameters. • SARS-CoV-2 infection rate of A549-ACE2 cells is lower than that of Vero E6 cells. • Latent phase of infected A549-ACE2 cells is longer than that of Vero E6 cells. • We conclude that Vero-E6 cells are not suitable for long-term drug screening assays. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV -2), a causative agent of COVID-19 disease, poses a significant threat to public health. Since its outbreak in December 2019, Wuhan, China, extensive collection of diverse data from cell culture and animal infections as well as population level data from an ongoing pandemic, has been vital in assessing strategies to battle its spread. Mathematical modelling plays a key role in quantifying determinants that drive virus infection dynamics, especially those relevant for epidemiological investigations and predictions as well as for proposing efficient mitigation strategies. We utilized a simple mathematical model to describe and explain experimental results on viral replication cycle kinetics during SARS-CoV-2 infection of animal and human derived cell lines, green monkey kidney cells, Vero-E6, and human lung epithelium cells, A549-ACE2, respectively. We conducted cell infections using two distinct initial viral concentrations and quantified viral loads over time. We then fitted the model to our experimental data and quantified the viral parameters. We showed that such cellular tropism generates significant differences in the infection rates and incubation times of SARS-CoV-2, that is, the times to the first release of newly synthesised viral progeny by SARS-CoV-2-infected cells. Specifically, the rate at which A549-ACE2 cells were infected by SARS-CoV-2 was 15 times lower than that in the case of Vero-E6 cell infection and the duration of latent phase of A549-ACE2 cells was 1.6 times longer than that of Vero-E6 cells. On the other hand, we found no statistically significant differences in other viral parameters, such as viral production rate or infected cell death rate. Since in vitro infection assays represent the first stage in the development of antiviral treatments against SARS-CoV-2, discrepancies in the viral parameter values across different cell hosts have to be identified and quantified to better target vaccine and antiviral research. [ABSTRACT FROM AUTHOR]