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: Background: Influenza is a zoonotic disease that infects millions of people each year resulting in hundreds of thousands of deaths, and in turn devastating pandemics. Influenza is caused by influenza viruses, including influenza A virus (IAV). There are many subtypes of IAV but only a few seem to be able to adapt to humans and to cause disease. In 2013, an H7N9 IAV subtype emerged in China that does not cause clinical symptoms in its chicken host but leads to severe infections when transmitted into humans. Since 2013, there have been six epidemic waves of H7N9 with 1567 laboratory-confirmed human infections and 615 deaths. Pathogenicity of IAV is complex, but a crucial feature contributing to virulence is the activation of the hemagglutinin (HA) fusion protein by host proteases that triggers membrane fusion and leads to subsequent virus propagation. : 293T, VERO, and MDCK cells were used to conduct Western blot analysis, immunofluorescence assays, and pseudoparticle and live virus infections, and to evaluate H7N9 HA cleavage-activation. Results/Conclusions: We show that human matriptase/ST 14 is able to cleave H7N9 HA. Cleavage of H7N9 HA expressed in cell culture results in fusogenic HA and syncytia formation. In infection studies with viral pseudoparticles carrying matriptase/ ST 14-activated H7N9 HA, we observed a high infectivity of cells. Finally, human matriptase/ST 14 also activated H7N9 live virus which resulted in high infectivity. Our data demonstrate that human matriptase/ST 14 is a likely candidate protease to promote H7N9 infections in humans.

Answer: Human matriptase/ST 14 proteolytically cleaves H7N9 hemagglutinin and facilitates the activation of influenza A/Shanghai/2/2013 virus in cell culture

Question: Acute cough is a major symptom of viral respiratory tract infection and causes excessive morbidity in human populations across the world. A wide variety of viruses play a role in the development of cough after acute infection and all of these manifest a similar clinical picture across different age groups. Despite the large disease burden surprisingly little is known about the mechanism of acute cough following viral infection. Both in vitro and in vivo experiments show that increased production of neuropeptides and leukotrienes mediate cough after viral infection, along with altered expression of neural receptors. Increased airway mucus production is also likely to play a significant role. This work is reviewed in this article. Following the recent development of a mouse model for rhinovirus infection and the establishment of experimental models of rhinovirus challenge in human subjects with both asthma and COPD the field is expanding to translate in vitro research into clinical studies and hopefully eventually into clinical practice. Developing a clearer understanding of the mechanisms underlying virus induced cough may lead to more specific and effective therapies.

Answer: Cough and viruses in airways disease: Mechanisms

Question: Introduction: Type-I interferons (IFNs) have been used to treat several types of cancers including follicular lymphoma, hairy cell leukemia and chronic myeloid leukemia. Treatment with type-I IFNs is however associated with significant toxic side effects due to the ubiquitous expression of type-I IFN receptors. Type-III IFNs elicit similar cellular responses as type-I IFNs, but restricted expression of type-III receptors may limit potential side effects of treatment with type-III IFNs. A number of studies are now exploring the use of type-III IFNs, specifically IFN-k3, as anticancer agents. IFN-k4 is a newly discovered type-III IFN that is genetically regulated and produced in a subset of individuals. Previously, we showed that IFN-k4 inhibits proliferation in a hepatoma cell line, however its anticancer potential has not been explored in comparison to other type-III IFNs. Methods: We developed stable human hepatoma (HepG2) and B-cell lymphoma (Raji) cell lines, engineered to express either IFN-k4-GFP or IFN-k3-GFP upon induction by doxycycline. We compared antiproliferative activity of IFN-k3 and IFN-k4 by measuring BRDU incorporation before and after induction of IFN-k expression. We also compared cell viability, apoptosis, and changes in cell cycle between IFN-k3 and IFN-k4 expressing cell lines. RNAseq and pathway analysis were used to explore the antiproliferative effect induced by IFN-k4. We show that IFN-k4 has higher antiproliferative activity compared to IFN-k3 in Raji and HepG2 cell lines and this can be explained by inhibition of the cell cycle. IFN-k4 expressing cell lines showed increased apoptotic cell death compared to IFN-k3 expressing cell lines. We also show that antiproliferative activity of IFN-k4 may be a result of inhibition of the MAPK pathway. Conclusion: This study demonstrates that IFN-k4 has a more potent antiproliferative activity than IFN-k3 in hepatoma and B cell lymphoma cell lines and the anticancer potential of IFN-k4 should be further explored. Introduction: Interleukin-1b (IL-1b) is a potent proinflammatory cytokine that is implicated both in acute and chronic viral infection. Persistent hepatic inflammation is the hallmark of hepatitis C virus (HCV) infection wherein it serves as a platform for progressive liver injury and onset of liver cancer. We examined the role of IL-1b role in HCV-induced hepatic inflammation by first assessing the transcriptional profile of chronic HCV patient liver by next-gen sequencing (RNAseq) staged by inflammation and fibrosis score. (microenvironment) role of IRF5 in mammary tumor initiation and progression.

Answer:
P001 IFN-K4 HAS A POTENT ANTIPROLIFERATIVE ACTIVITY IN B-CELL LYMPHOMA AND HEPATOMA CELL LINES HCV CORE PROTEIN TRIGGERS IL-1B PRODUCTION VIA THE NLRP3 INFLAMMASOME P004 LOSS OF IRF5 INDUCES SPONTANEOUS MAMMARY TUMORIGEN- ESIS P005 PROTEOLYTIC ORIGIN OF THE SOLUBLE HUMAN IL-6R IN VIVO AND A DECISIVE ROLE OF N-GLYCOSYLATION DISTINCT ROLES FOR IRF5 IN MAMMARY EPITHELIAL CELLS AND HOST TUMOR IMMUNITY: LOSS OF IRF5 IN EITHER COMPART- MENT LEADS TO TUMORIGENESIS SEXUALLY DIMORPHIC ROLES OF STAT3 IN PEDIATRIC BRAIN CANCER P008 DISRUPTION OF PD-1/PD-L1 SIGNALING IN 2D VS. 3D COLORECTAL CANCER COCULTURE MODEL REVEALED BY RNAI HIGH THROUGH- PUT SCREEN