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.
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Question: 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.

Answer: Epidemiology and characterization of avian infectious bronchitis virus strains circulating in southern China during the period from 2013-2015 OPEN


Question: 2 The abbreviations used are: S, spike; SARS-CoV, severe acute respiratory syndrome coronavirus; MLV, murine leukemia virus; DC-SIGN, dendritic cell-specific intercellular adhesion molecule-3-gubbing non-integrin, ACE2, argiotensin I conserting enzyme 2. FIGURE 4. Introduction of alanine residues in the S2 region modulates elastase-induced virus entry mediated by SARS-CoV S. A and B, pseudotyped virion infections were performed as described for Fig. 2. Infection was induced by treatment with elastase (A) or trypsin (B). Results are presented as relative light units (RLU). Error bars represent the S.E. of three independent experiments. C, cleavage of SARS-CoV by elastase. HEK293T cells expressing the wild type (WT) or mutant SARS-CoV spike protein were treated with 50 g/ml elastase. Cell surface proteins were biotinylated and precipitated, and cleavage products of the SARS-CoV spike protein were analyzed in Western blot with an antibody recognizing the C9 tag at the C terminus of the protein.

Answer: Elastase-mediated Activation of the Severe Acute Respiratory Syndrome Coronavirus Spike Protein at Discrete Sites within the S2 Domain * □ S


Question: The primary intracellular protein degradation systems, including the ubiquitin-proteasome and the lysosome pathways, have been emerging as central regulators of viral infectivity, inflammation, and viral pathogenicity. Viral myocarditis is an inflammatory disease of the myocardium caused by virus infection in the heart. The disease progression of viral myocarditis occurs in three distinct stages: acute viral infection, immune cell infiltration, and cardiac remodelling. Growing evidence suggests a crucial role for host proteolytic machineries in the regulation of the pathogenesis and progression of viral myocarditis in all three stages. Cardiotropic viruses evolve different strategies to subvert host protein degradation systems to achieve successful viral replication. In addition, these proteolytic systems play important roles in the activation of innate and adaptive immune responses during viral infection. Recent evidence also suggests a key role for the ubiquitin-proteasome and lysosome systems as the primary effectors of protein quality control in the regulation of cardiac remodelling. This review summarizes the recent advances in understanding the direct interaction between cardiotropic viruses and host proteolytic systems, with an emphasis on coxsackievirus B3, one of the primary aetiological agents causing viral myocarditis, and highlights possible roles of the host degradation systems in the pathogenesis of viral myocarditis and its progression to dilated cardiomyopathy. ---

Answer:
SPOTLIGHT REVIEW Protein degradation systems in viral myocarditis leading to dilated cardiomyopathy