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.

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

ORF la of lactate dehydrogenase-elevating virus, strain P (LDV-P), encodes a protein of 2206 amino acids. Eisenberg hydrophobic moment analysis of the protein predicted the presence of eleven transmembrane segments in the C-terminal half of the molecule (amino acids 980-1852) that flank the serine protease domain, cDNAs encoding ORF la protein segments encompassing transmembrane segments 5 to 11 and its amphipathic C-terminal end as well as the N-terminal 80 amino acids of the downstream ORF lb protein were transcribed and the transcripts in vitro translated in the absence and presence of microsomal membranes. The synthesis of the protein products with putative transmembrane segments was enhanced by the presence of the microsomal membranes and the proteins became membrane associated. When synthesized in the absence of membranes they were recovered in the supernatant upon ultracentrifugation of the translation reaction mixtures, whereas they were recovered in the membrane pellet when synthesized in the presence of membranes. Furthermore, the latter proteins were not released from the membranes by disruption of the membrane vesicles in carbonate buffer, pH 11.5, and large portions of the proteins were resistant to digestion by trypsin, chymotrypsin and proteinase K. No N-glycosylation was observed and only little, if any, processing of the protein by the putative serine protease. The results indicate that the C-terminal half of the ORF la protein represents a non-glycosylated integral membrane protein. Potential modes of synthesis and function of the protein are discussed. In addition, the results showed that the synthesis of the ORF la protein was generally terminated at its termination codon, but that read-through into the ORF lb gene occurred with low frequency.
Membrane association of the C-terminal half of the open reading frame la protein of lactate dehydrogenase-elevating virus Brief Report

Background: Taiwan experienced one of the most serious outbreaks of severe acute respiratory syndrome (SARS) during the 2003 epidemic. Public health nurses faced unprecedented challenges in implementing an extensive quarantine policy to prevent disease spread. Their professional confidence, however, was shattered during the SARS crisis. This paper assesses factors related to public health nurses' confidence in managing community SARS control programs. Methods: In May 2003, we sent structured questionnaires to all 361 health centers in Taiwan and asked the public health nurses responsible for epidemic control to complete. A total of 312 completed surveys were returned for a response rate of 86.4%. Descriptive methods and logistic regression were used to analyze the data. Results: Most public health nurses (71.9%) expressed a general lack of confidence in handling the SARS epidemic. Confidence was significantly associated with perceived epidemic severity (OR, 0.58; 95% CI: 0.35-0.99), daily epidemic updates (OR, 2.26; 95% CI: 1.28-3.98), and number of cases in the community (OR, 2.21; 95% CI: 1.13-4.31). Conclusion: Nurses' individual risk perception and prompt update of epidemic information significantly affect levels of professional confidence, a key factor influencing quarantine implementation success. Strategies to promote productive interagency collaboration and advocate participatory policy making involving health workers at all levels are needed to control effectively infectious disease outbreaks. (Am J Infect Control 2006;34:176-81.) 

Confidence in controlling a SARS outbreak: Experiences of public health nurses in managing home quarantine measures in Taiwan