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 Input:
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 Output:
Intensifying poultry production systems and the emergence of avian influenza in China: a 'One Health/Ecohealth' epitome

Ex Input:
Hepatitis C virus (HCV) is a blood-borne pathogen causing acute and chronic hepatitis. A significant number of people chronically infected with HCV develop cirrhosis and/or liver cancer. The pathophysiologic mechanisms of hepatocyte damage associated with chronic HCV infection are not fully understood yet, mainly due to the lack of an in vitro system able to recapitulate the stages of infection in vivo. Several studies underline that HCV virus replication depends on redox-sensitive cellular pathways; in addition, it is known that virus itself induces alterations of the cellular redox state. However, the exact interplay between HCV replication and oxidative stress has not been elucidated. In particular, the role of reduced glutathione (GSH) in HCV replication and infection is still not clear. We set up an in vitro system, based on low m.o.i. of Huh7.5 cell line with a HCV infectious clone (J6/JFH1), that reproduced the acute and persistent phases of HCV infection up to 76 days of culture. We demonstrated that the acute phase of HCV infection is characterized by the elevated levels of reactive oxygen species (ROS) associated in part with an increase of NADPH-oxidase transcripts and activity and a depletion of GSH accompanied by high rates of viral replication and apoptotic cell death. Conversely, the chronic phase is characterized by a reestablishment of reduced environment due to a decreased ROS production and increased GSH content in infected cells that might concur to the establishment of viral persistence. Treatment with the prooxidant auranofin of the persistently infected cultures induced the increase of viral RNA titer, suggesting that a prooxidant state could favor the reactivation of HCV viral replication that in turn caused cell damage and death. Our results suggest that targeting the redox-sensitive host-cells pathways essential for viral replication and/or persistence may represent a promising option for contrasting HCV infection.

Ex Output:
Counteraction of HCV-Induced Oxidative Stress Concurs to Establish Chronic Infection in Liver Cell Cultures

Ex Input:
Hepatitis C virus (HCV) infection is a major cause of chronic liver disease and has become a global health threat. No HCV vaccine is currently available and treatment with antiviral therapy is associated with adverse side effects. Moreover, there is no preventive therapy for recurrent hepatitis C post liver transplantation. The NS3 serine protease is necessary for HCV replication and represents a prime target for developing anti HCV therapies. Recently we described a therapeutic approach for eradication of HCV infected cells that is based on protein delivery of two NS3 protease-activatable recombinant toxins we named ''zymoxins''. These toxins were inactivated by fusion to rationally designed inhibitory peptides via NS3-cleavable linkers. Once delivered to cells where NS3 protease is present, the inhibitory peptide is removed resulting in re-activation of cytotoxic activity. The zymoxins we described suffered from two limitations: they required high levels of protease for activation and had basal activities in the un-activated form that resulted in a narrow potential therapeutic window. Here, we present a solution that overcame the major limitations of the ''first generation zymoxins'' by converting MazF ribonuclease, the toxic component of the E. coli chromosomal MazEF toxin-antitoxin system, into an NS3-activated zymoxin that is introduced to cells by means of gene delivery. We constructed an expression cassette that encodes for a single polypeptide that incorporates both the toxin and a fragment of its potent natural antidote, MazE, linked via an NS3-cleavable linker. While covalently paired to its inhibitor, the ribonuclease is well tolerated when expressed in naive, healthy cells. In contrast, activating proteolysis that is induced by even low levels of NS3, results in an eradication of NS3 expressing model cells and HCV infected cells. Zymoxins may thus become a valuable tool in eradicating cells infected by intracellular pathogens that express intracellular proteases.

Ex Output:
Removal of Hepatitis C Virus-Infected Cells by a Zymogenized Bacterial Toxin