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.

[EX Q]: Several kinds of pressure can lead to the emergence of infectious diseases. In the case of zoonoses emerging from livestock, one of the most significant changes that has taken place since the mid twentieth century is what has been termed the "livestock revolution", whereby the stock of food animals, their productivity and their trade has increased rapidly to feed rising and increasingly wealthy and urbanized populations. Further increases are projected in the future in low and middle-income countries. Using avian influenza as an example, we discuss how the emergence of avian influenza H5N1 and H7N9 in China was linked to rapid intensification of the poultry sector taking place in landscapes rich in wetland agriculture and wild waterfowls habitats, providing an extensive interface with the wild reservoir of avian influenza viruses. Trade networks and live-poultry markets further exacerbated the spread and persistence of avian influenza as well as human exposure. However, as the history of emergence of highly pathogenic avian influenza (HPAI) demonstrates in high-income countries such as the USA, Canada, Australia, the United Kingdom or the Netherlands, this is by no way specific to low and middle-income countries. Many HPAI emergence events took place in countries with generally good biosecurity standards, and the majority of these in regions hosting intensive poultry production systems. Emerging zoonoses are only one of a number of externalities of intensive livestock production systems, alongside antimicrobial consumption, disruption of nutrient cycles and greenhouse gases emissions, with direct or indirect impacts on human health. In parallel, livestock production is essential to nutrition and livelihoods in many low-income countries. Deindustrialization of the most intensive production systems in high-income countries and sustainable intensifications in low-income countries may converge to a situation where the nutritional and livelihood benefits of livestock production would be less overshadowed by its negative impacts on human an ecosystem health.
[EX A]: Intensifying poultry production systems and the emergence of avian influenza in China: a 'One Health/Ecohealth' epitome

[EX Q]: showing signs of disease in southern China during the period from 2013-2015. The nucleotide and amino acid sequences from the isolated field strains were compared to 42 published references. Nucleotide homologies ranged from 63.1-99.9% and amino acid homologies ranging from 60.2-100%. At least seven IBV genotypes were co-circulating in commercial chicken farms in southern China. The IBV isolates were genetically diverse and underwent continuing evolution. The QX-type, TW I-type, and 4/91-type were the most common genotypes during the three-year observation period and accounted for 88.8% of the isolated strains. Notably, the prevalence of the TW I-type strains has been increasing in recent years and has become the most common genotype in China. The emergence of variant IBV strains can be attributed to recombination. Serologic analysis and antigenic 3D cartography of 4 reference and 14 field isolated strains indicated the surveyed IBVs had diverse serology types and that the serotype of the isolated QX-type and TW I-type strains was distinct from the vaccines strains. Therefore, long-term continuing surveillance is necessary for IBV prevention and control. Avian infectious bronchitis (IB) is an acute and highly contagious disease caused by the avian infectious bronchitis virus (IBV). IB causes substantial economic losses throughout the poultry industry worldwide. IBV affects chickens of all ages causing upper respiratory disease, nephritic syndromes, and decreased egg production 1 . IBV has been circulating in China since 1982. The epidemiology of IBV in China is complicated due to the large geographical area, and multiple IBV genotypes and serotypes are known to coexist 2 . Our previous epidemiology monitoring during 2004 to 2012, found at least seven genotypes of IBV circulating. In that study, the QX-like IBV genotype that causes nephritis had become predominant in China 3-6 . Although IBV vaccines are widely used and most commercial chickens have been vaccinated, there are still frequent outbreaks of IB that cause clinical disease and production problems 7-9 . For example, widespread use of vaccines derived from Massachusetts (Mass) serotypes such as H120 and H52 did not prevent frequent outbreaks of IB in chicken flocks 10, 11 . IBV belongs to the genus Gammacoronavirus, family Coronaviridae, and order Nidovirales. Its genome is linear, non-segmented, positive-sense, single-stranded RNA that is approximately 27.6 kilobases (kb) in length. As with other coronaviruses, the IBV S1 glycoprotein contains virus neutralizing epitopes and serotype-specific sequences 12, 13 . The S1 protein is involved in infectivity and plays an important role in attachment to the host cell, as well as induction of neutralizing antibodies 14 . Given the importance of the S1 protein virus/host interactions, IBV genetic analysis and research of IBV has been primarily based on the S1 gene 15 . Variation in the S1 protein is the basis for genotype and serotype classification, defines antigen characteristics, contributes to emergence of IBV variants, and poor vaccine protection 13, 16 . S1 variability is due in part to the lack of proofreading by the RNA-dependent RNA polymerase (RDRP) that introduces mutations into the viral genome during replication. Variation is also introduced by the specific template switching mechanism used by coronaviruses, which frequently leads to genetic recombination 17, 18 . At least 30 serotypes of IBV have been identified worldwide. Vaccine cross-protection between serotypes is minimal 19 . Therefore, phylogenetic and genetic analyses have become tools for monitoring the molecular evolution of IBV and provide a fast and accurate method for genotype classification. In some studies, the genotype analyses have been used to predict IBV serotype and used to inform vaccine selection 20 . In this study, long-term surveillance was conducted with the aim of identifying IBV strains isolated from commercial chicken farms in south China. During 2013-2015, IBV strains were isolated from flocks with clinical outbreaks. Genetic, phylogenetic, and recombination analyses were performed to study the genetic diversity of the S1 gene in field isolated IBV strains. Cross-neutralization tests and antigenic cartography were performed to determine the serological and antigenic relationship between a part of the isolated and vaccine strains.
[EX A]: Epidemiology and characterization of avian infectious bronchitis virus strains circulating in southern China during the period from 2013-2015 OPEN

[EX Q]: The location of autocrine interactions between the v-sis protein and PDGF receptors remains uncertain and controversial. To examine whether receptor-ligand interactions can occur intracellularly, we have constructed fusion proteins that anchor v-sis to specific intracellular membranes. Fusion of a cis-Golgi retention signal from a coronavirus E1 glycoprotein to v-sis protein completely abolished its transforming ability when transfected into NIH3T3 cells. Fusion proteins incorporating mutations in this retention signal were not retained within the Golgi complex but instead were transported to the cell surface, resulting in efficient transformation. All chimeric proteins were shown to dimerize properly. Derivatives of some of these constructs were also constructed bearing the cytoplasmic tail from the glycoprotein of vesicular stomatitis virus (VSV-G). These constructs allowed examination of subcellular localization by double-label immunofluorescence, using antibodies that distinguish between the extraceUular PDGF-related domain and the VSV-G cytoplasmic tail. Colocalization of sis-E1-G with Golgi markers confirmed its targeting to the early Golgi complex. The sis-E1 constructs, targeted to the early Golgi complex, exhibited no proteo-lyric processing whereas the mutant forms of sis-E1 exhibited normal proteolytic processing. Treatment with suramin, a polyanionic compound that disrupts ligand/receptor interactions at the cell surface, was able to revert the transformed phenotype induced by the mutant sis-E1 constructs described here. Our results demonstrate that autocrine interactions between the v-sis oncoprotein and PDGF receptors within the early Golgi complex do not result in functional signal transduction. Another v-sis fusion protein was constructed by attaching the transmembrane domain and COOHterminus of TGN38, a protein that localizes to the trans-Golgi network (TGN). This construct was primarily retained intracellularly, although some of the fusion protein reached the surface. Deletion of the COOH-terminal region of the TGN38 retention signal abrogated the TGN-localization, as evidenced by very prominent cell surface localization, and resulted in increased transforming activity. The behavior of the sis-TGN38 derivatives is discussed within the context of the properties of TGN38 itself, which is known to recycle from the cell surface to the TGN.
[EX A]:
The v-sis Oncoprotein Loses Transforming Activity When Targeted to the Early Golgi Complex