In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.

Ebola virus (EboV) belongs to the Filoviridae family of viruses that causes severe and fatal hemhorragic fever. Infection by EboV involves fusion between the virus and host cell membranes mediated by the envelope glycoprotein GP2 of the virus. Similar to the envelope glycoproteins of other viruses, the central feature of the GP2 ectodomain postfusion structure is a six-helix bundle formed by the protein's N-and C-heptad repeat regions (NHR and CHR, respectively). Folding of this six-helix bundle provides the energetic driving force for membrane fusion; in other viruses, designed agents that disrupt formation of the six-helix bundle act as potent fusion inhibitors. To interrogate determinants of EboV GP2-mediated membrane fusion, we designed model proteins that consist of the NHR and CHR segments linked by short protein linkers. Circular dichroism and gel filtration studies indicate that these proteins adopt stable ahelical folds consistent with design. Thermal denaturation indicated that the GP2 six-helix bundle is highly stable at pH 5.3 (melting temperature, T m , of 86.8 6 2.0°C and van't Hoff enthalpy, DH vH , of 228.2 6 1.0 kcal/mol) and comparable in stability to other viral membrane fusion six-helix bundles. We found that the stability of our designed a-helical bundle proteins was dependent on buffering conditions with increasing stability at lower pH. Small pH differences (5.3-6.1) had dramatic effects (DT m 5 37°C) suggesting a mechanism for conformational control that is dependent on environmental pH. These results suggest a role for low pH in stabilizing six-helix bundle formation during the process of GP2-mediated viral membrane fusion.
Designed protein mimics of the Ebola virus glycoprotein GP2 a-helical bundle: Stability and pH effects

This study shows that the disease free equilibrium ( ) for COVID-19 coronavirus does not satisfy the criteria for a locally or globally asymptotic stability. This implies that as a pandemic as declared by WHO (2020) the COVID-19 coronavirus does not have a curative vaccine yet and precautionary measures are advised through quarantine and observatory procedures. Also, the Basic Reproductive number ( 0 < 1) by Equation (33) shows that there is a chance of decline of secondary infections when the ratio between the incidence rate in the population and the total number of infected population quarantined with observatory procedure. The effort to evaluate the disease equilibrium shows that unless there is a dedicated effort from government, decision makers and stakeholders, the world would hardly be reed of the COVID-19 coronavirus and further spread is eminent and the rate of infection will continue to increase despite the increased rate of recovery because of the absence of vaccine at the moment.
MATHEMATICAL PREDICTIONS FOR COVID-19 AS A GLOBAL PANDEMIC

Graphical Abstract Highlights d Combined measurements of host-viral scRNA-seq during in vivo influenza infection d High prevalence of infection in a variety of immune and nonimmune cell types d Extensive cellular heterogeneity exists within infected and bystander cells d Generic and cell-type-specific differences between infected and bystander cells SUMMARY The influenza virus is a major cause of morbidity and mortality worldwide. Yet, both the impact of intracellular viral replication and the variation in host response across different cell types remain uncharacterized. Here we used single-cell RNA sequencing to investigate the heterogeneity in the response of lung tissue cells to in vivo influenza infection. Analysis of viral and host transcriptomes in the same single cell enabled us to resolve the cellular heterogeneity of bystander (exposed but uninfected) as compared with infected cells. We reveal that all major immune and non-immune cell types manifest substantial fractions of infected cells, albeit at low viral transcriptome loads relative to epithelial cells. We show that all cell types respond primarily with a robust generic transcriptional response, and we demonstrate novel markers specific for influenza-infected as opposed to bystander cells. These findings open new avenues for targeted therapy aimed exclusively at infected cells.

Dissection of Influenza Infection In Vivo by Single- Cell RNA Sequencing