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: Murine norovirus-1 (MNV-1) is known to subvert host cell division inducing an accumulation of cells in the G 0 /G 1 phase, creating conditions where viral replication is favored. This study identified that NS5 (VPg), is capable of inducing cell cycle arrest in the absence of viral replication or other viral proteins in an analogous manner to MNV-1 infection. NS5 expression induced an accumulation of cells in the G 0 /G 1 phase in an asynchronous population by inhibiting progression at the G 1 /S restriction point. Furthermore, NS5 expression resulted in a down-regulation of cyclin A expression in asynchronous cells and inhibited cyclin A expression in cells progressing from G 1 to S phase. The activity of NS5 on the host cell cycle occurs through an uncharacterized function. Amino acid substitutions of NS5(Y26A) and NS5(F123A) that inhibit the ability for NS5 to attach to RNA and recruit host eukaryotic translation initiation factors, respectively, retained the ability to induce an accumulation of cells in the G 0 /G 1 phase as identified for wild-type NS5. To the best of our knowledge, this is the first report of a VPg protein manipulating the host cell cycle.

A: Expression of the NS5 (VPg) Protein of Murine Norovirus Induces a G1/S Phase Arrest
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Q: Objective: Healthcare providers in emergency departments should wear respirators for infection protection. However, the wearer's vigorous movements during cardiopulmonary resuscitation may affect the protective performance of the respirator. Herein, we aimed to assess the effects of chest compressions (CCs) on the protective performance of respirators. Methods: This crossover study evaluated 30 healthcare providers from 1 emergency department who performed CC with real-time feedback. The first, second, and third groups started with a cup-type, fold-type, and valve-type respirator, respectively, after which the respirators were randomized for each group. The fit factors were measured using a quantitative fit testing device before and during the CC in each experiment. The protection rate was defined as the proportion of respirators achieving a fit factor ≥100. Results: The fold-type respirator had a significantly greater protection rate at baseline (100.0% ± 0.0%) compared to the cup-type (73.6% ± 39.6%, P = .003) and valve-type respirators (87.5% ± 30.3%, P = .012). During the CC, the fit factor values significantly decreased for the cup-type (44.9% ± 42.8%, P < .001) and valve-type respirators (59.5% ± 41.7%, P = .002), but not for the fold-type respirator (93.2% ± 21.7%, P = .095). Conclusions: The protective performances of respirators may be influenced by CC. Healthcare providers should identify the respirator that provides the best fit for their intended tasks. Abbreviations: CC = Chest compression, CPR = Cardiopulmonary resuscitation, MERS = Middle East Respiratory Syndrome, NIOSH = National Institute for Occupational Safety and Health.

A: Comparing the protective performances of 3 types of N95 filtering facepiece respirators during chest compressions A randomized simulation study
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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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