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.

[Q]: In this paper, a modified susceptible infected susceptible (SIS) epidemic model is proposed on community structure networks considering birth and death of node. For the existence of node's death would change the topology of global network, the characteristic of network with death rate is discussed. Then we study the epidemiology behavior based on the mean-field theory and derive the relationships between epidemic threshold and other parameters, such as modularity coefficient, birth rate and death rates (caused by disease or other reasons). In addition, the stability of endemic equilibrium is analyzed. Theoretical analysis and simulations show that the epidemic threshold increases with the increase of two kinds of death rates, while it decreases with the increase of the modularity coefficient and network size.
[A]: The Journal of China Universities of Posts and Telecommunications Modeling and analysis of epidemic spreading on community network with node's birth and death


[Q]: Duck plague virus (DPV) is a representative pathogen transmitted among aquatic animals that causes gross lesions and immune inhibition in geese and ducks. The mechanism of organ tropism and innate immune evasion of DPV has not been completely deciphered due to a lack of cell models to study the innate immune manipulation and pathogenicity of aquatic viruses. In the present study, we isolated five types of duck primary cells [duck embryo fibroblasts (DEFs), neurons, astrocytes, peripheral blood mononuclear cells (PBMCs), and monocytes/macrophages] to identify appropriate cell models for DPV, using tropism infection and innate immunologic assays. Cells responded differently to stimulation with DNA viruses or RNA virus analogs. DPV infection exhibited broad tropism, as the recombinant virulent strain (CHv-GFP) infected DEFs, neurons, astrocytes, and monocytes/macrophages, but not the PBMCs, as the expression of EGFP was negligible. The basal levels of innate immunity molecules were highest in monocytes/macrophages and lower in DEFs and astrocytes. Conversely, the titer and genomic copy number of the attenuated virus strain was higher in DEFs and astrocytes than in neurons and monocytes/macrophages. The titer and genomic copy number of the attenuated virus strain were higher compared with the virulent strain in DEFs, neurons, and astrocytes. The innate immune response was not significantly induced by either DPV strain in DEFs, neurons, or astrocytes. The virulent strain persistently infected monocytes/macrophages, but the attenuated strain did so abortively, and this was accompanied by the phenomenon of innate immune inhibition and activation by the virulent and attenuated strains, respectively. Blockage of IFNAR signaling promoted replication of the attenuated strain. Pre-activation of IFNAR signaling inhibited infection by the virulent strain. The selection assay results indicated that induction of innate immunity plays an essential role in controlling DPV infection, and monocytes/macrophages are an Tian et al. Duck Primary Cells Infection Models important cell model for further investigations. Our study provided practical methods for isolating and culturing duck primary cells, and our results will facilitate further investigations of organ tropism, innate immune responses, latent infection, and the effectiveness of antiviral drugs for treating DPV and potentially other aerial bird pathogens.
[A]: Isolation and Selection of Duck Primary Cells as Pathogenic and Innate Immunologic Cell Models for Duck Plague Virus


[Q]: Antigenically related feline coronaviruses cause two distinct disease manifestations in infected cats. The diseases are feline infectious peritonitis (FIP), in which the virus is widely disseminated, and feline enteric coronavirus (FECV), a mild disease in which the virus is usually limited to the villi. These two viruses were found to differ in their growth in cell culture. FIPV grows to higher titer, forms larger plaques and switches offhost cell protein synthesis more effectively than FECV. Cross neutralization studies showed antigenic differences between the strains. There also appeared to be a difference in the nucleoprotein molecular weight of the viruses causing these two different disease syndromes.
[A]:
Archives of Virology Antigenic and biological diversity of feline coronaviruses: feline infectious peritonitis and feline enteritis virus*