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: 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.

A: Counteraction of HCV-Induced Oxidative Stress Concurs to Establish Chronic Infection in Liver Cell Cultures
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Q: The Tasmanian devil (Sarcophilus harrisii), so named for its blood-curdling, nocturnal shrieks and snarls, is the largest of the carnivorous marsupials. Although once widely persecuted, concerted efforts are now being made to save the devil from extinction following the emergence of a fatal transmissible malignancy known as devil facial tumour disease (DFTD). DFTD is unusual in that the infectious agent is the cancer cell itself. This chapter discusses the aetiology and pathogenesis of DFTD as well as the profound impact the spread of DFTD has had on the devil's conservation status. Strategies for managing DFTD and conserving the devil will be explored and the contribution of new sequencing technology to the field of conservation genetics and genomics will be examined with regard to the Tasmanian devil and DFTD.

A: Devil Facial Tumour Disease (DFTD): Using Genetics and Genomics to Investigate Infectious Disease in an Endangered Marsupial
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Q: Background: Feline leishmaniosis caused by Leishmania infantum is considered a rare disease in endemic areas, whereas subclinical infections are common. Immune response plays a key role in driving the course of L. infantum infection in other host species; however, the feline cell-mediated immune response to L. infantum infection has not yet been investigated. The aim of this study was to determine the cell-mediated immune response specific to L. infantum by means of interferon (IFN)-γ release in whole blood assay from cats living in endemic areas (66 in Sicily and 113 in Catalonia) and to compare with antibody levels to L. infantum [enzyme-linked immunosorbent assay (ELISA) and immunofluorescence antibody test (IFAT)], blood parasite load and retroviral infections. Results: Most cats (n = 140) were L. infantum antibody negative and only 22% (n = 39) were positive. Only 9 and 2% of tested cats had a feline immunodeficency virus (FIV) infection or a feline leukemia virus (FeLV) infection, respectively. Thirty-two cats out of 179 (18%) produced IFN-γ after stimulation with L. infantum soluble antigen (LSA) while the majority of cats (93%) produced IFN-γ after stimulation with concanavalin A (ConA). Six LSA-IFN-γ-producer cats were seropositive (three to ELISA and five to IFAT) but they were polymerase chain reaction (PCR) negative, while only one cat was antibody-and PCR-positive. Significant positive correlations were found between IFN-γ concentrations after stimulation with LSA and ConA, and between serology and PCR testing. No association was found between FIV status and LSA or ConA-IFN-γ production. Combining PCR, serology and specific IFN-γ concentration results, we found that 36% of cats studied were exposed to L. infantum. As expected, cats from endemic areas produce IFN-γ after ex vivo blood stimulation with LSA and therefore are able to activate a cell-mediated adaptive immune response against the parasite that is variably associated with antibody or blood PCR positivity. The association of this assay to serological and molecular tests provides a better estimate of cat exposure to L. infantum.

A:
Leishmania infantum-specific IFN-γ production in stimulated blood from cats living in areas where canine leishmaniosis is endemic
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