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.

Input: Consider Input: Hepatitis C virus (HCV) is thought to be involved in the pathogenesis of autoimmune hepatitis (AIH) type 2, which is defined by the presence of type I antiliver kidney microsome autoantibodies directed mainly against cytochrome P450 (CYP)2D6 and by autoreactive liver infiltrating T cells. Virus-specific CD8 ϩ cytotoxic T lymphocytes (CTLs) that recognize infected cells and contribute to viral clearance and tissue injury during HCV infection could be involved in the induction of AIH. To explore whether the antiviral cellular immunity may turn against self-antigens, we characterized the primary CTL response against an HLA-A * 0201-restricted HCV-derived epitope, i.e., HCV core 178-187, which shows sequence homology with human CYP2A6 and CYP2A7 8-17. To determine the relevance of these homologies for the pathogenesis of HCV-associated AIH, we used synthetic peptides to induce primary CTL responses in peripheral blood mononuclear cells of healthy blood donors and patients with chronic HCV infection. We found that the naive CTL repertoire of both groups contains cross-reactive CTLs inducible by the HCV peptide recognizing both CYP2A6 and CYP2A7 peptides as well as endogenously processed CYP2A6 protein. Importantly, we failed to induce CTLs with the CYPderived peptides that showed a lower capacity to form stable complexes with the HLA-A2 molecule. These findings demonstrate the potential of HCV to induce autoreactive CD8 ϩ CTLs by molecular mimicry, possibly contributing to virus-associated autoimmunity.

Output: Molecular Mimicry of Human Cytochrome P450 by Hepatitis C Virus at the Level of Cytotoxic T Cell Recognition


Input: Consider Input: We have previously reported that the apathogenic Tula hantavirus induces apoptosis in Vero E6 epithelial cells. To assess the molecular mechanisms behind the induced apoptosis we studied the effects of hantavirus infection on cellular signaling pathways which promote cell survival. We previously also observed that the Tula virus-induced cell death process is augmented by external TNF-α. Since TNF-α is involved in the pathogenesis of hantavirus-caused hemorrhagic fever with renal syndrome (HFRS) we investigated its effects on HFRS-causing hantavirus-infected cells. We studied both apathogenic (Tula and Topografov) and pathogenic (Puumala and Seoul) hantaviruses for their ability to regulate cellular signaling pathways and observed a direct virusmediated down-regulation of external signal-regulated kinases 1 and 2 (ERK1/2) survival pathway activity, which was dramatically enhanced by TNF-α. The fold of ERK1/2 inhibition correlated with viral replication efficiencies, which varied drastically between the hantaviruses studied. We demonstrate that in the presence of a cytokine TNF-α, which is increased in HFRS patients, hantaviruses are capable of inactivating proteins that promote cell survival (ERK1/ 2). These results imply that hantavirus-infected epithelial cell barrier functions might be compromised in diseased individuals and could at least partially explain the mechanisms of renal dysfunction and the resulting proteinuria seen in HFRS patients.

Output: Virology Journal Hantaviruses and TNF-alpha act synergistically to induce ERK1/2 inactivation in Vero E6 cells


Input: Consider Input: Supplementary Text 1: Details of specimen collection, processing, polymerase chain reaction 34 assays, quality control measures, and assay parameters used to identify respiratory viruses. Specimen collection 36 All swabs were collected using a plastic-shaft, rayon-budded swab in a transport tube with a foam 37 pad reservoir soaked with viral transport medium (Virocult MW950, Medical Wire & Equipment, 38 Wiltshire, England). A single swab was used to sample both nostrils. 39 Quality Control measures 40 A known amount of whole equine herpesvirus (EHV) spiked into each sample assessed nucleic 41 acid extraction quality and presence of polymerase chain reaction (PCR) inhibitors. 1 Any extract 42 having a >3 cycle-threshold (Ct) difference to that of the expected value by EHV real-time PCR 43 assays was considered to have failed quality control and the sample was re-extracted. Specimen quality was assessed by testing for a marker of human genomic DNA, endogenous 46 retrovirus-3 (ERV-3). 2 We have demonstrated previously that among specimens with an ERV-3 Ct a adjusted for clustering using sandwich estimators to account for within-infant correlation between observations; b Individual rhinovirus species do not add up to 'All rhinovirus' detections because of a combination of more than one rhinovirus species detected within the same ARI episode, or single new virus detection episodes where HRV positive specimens could not be sequenced.


Output: Viruses causing lower respiratory symptoms in children younger than 2-years of age: 1 findings from the ORChID birth cohort. 2