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: Background. Before kidney transplantation, donors and recipients are routinely screened for viral pathogens using specific tests. Little is known about unrecognized viruses of the urinary tract that potentially result in transmission. Using an open metagenomic approach, we aimed to comprehensively assess virus transmission in living-donor kidney transplantation. Methods. Living kidney donors and their corresponding recipients were enrolled at the time of transplantation. Follow-up study visits for recipients were scheduled 4-6 weeks and 1 year thereafter. At each visit, plasma and urine samples were collected and transplant recipients were evaluated for signs of infection or other transplant-related complications. For metagenomic analysis, samples were enriched for viruses, amplified by anchored random polymerase chain reaction (PCR), and sequenced using high-throughput metagenomic sequencing. Viruses detected by sequencing were confirmed using real-time PCR. Results. We analyzed a total of 30 living kidney donor and recipient pairs, with a follow-up of at least 1 year. In addition to viruses commonly detected during routine post-transplant virus monitoring, metagenomic sequencing detected JC polyomavirus (JCPyV) in the urine of 7 donors and their corresponding recipients. Phylogenetic analysis confirmed infection with the donor strain in 6 cases, suggesting transmission from the transplant donor to the recipient, despite recipient seropositivity for JCPyV at the time of transplantation. Conclusions. Metagenomic sequencing identified frequent transmission of JCPyV from kidney transplant donors to recipients. Considering the high incidence rate, future studies within larger cohorts are needed to define the relevance of JCPyV infection and the donor's virome for transplant outcomes.

A: Clinical Infectious Diseases Metagenomic Virome Sequencing in Living Donor and Recipient Kidney Transplant Pairs Revealed JC Polyomavirus Transmission
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Q: Background: Despite the seriousness of dengue-related disease, with an estimated 50-100 million cases of dengue fever and 250,000-500,000 cases of dengue hemorrhagic fever/dengue shock syndrome each year, a clear understanding of dengue pathogenesis remains elusive. Because of the lack of a disease model in animals and the complex immune interaction in dengue infection, the study of host response and immunopathogenesis is difficult. The development of genomics technology, microarray and high throughput quantitative PCR have allowed researchers to study gene expression changes on a much broader scale. We therefore used this approach to investigate the host response in dengue virusinfected cell lines and in patients developing dengue fever. Methodology/Principal Findings: Using microarray and high throughput quantitative PCR method to monitor the host response to dengue viral replication in cell line infection models and in dengue patient blood samples, we identified differentially expressed genes along three major pathways; NF-kB initiated immune responses, type I interferon (IFN) and the ubiquitin proteasome pathway. Among the most highly upregulated genes were the chemokines IP-10 and I-TAC, both ligands of the CXCR3 receptor. Increased expression of IP-10 and I-TAC in the peripheral blood of ten patients at the early onset of fever was confirmed by ELISA. A highly upregulated gene in the IFN pathway, viperin, was overexpressed in A549 cells resulting in a significant reduction in viral replication. The upregulation of genes in the ubiquitin-proteasome pathway prompted the testing of proteasome inhibitors MG-132 and ALLN, both of which reduced viral replication. Conclusion/Significance: Unbiased gene expression analysis has identified new host genes associated with dengue infection, which we have validated in functional studies. We showed that some parts of the host response can be used as potential biomarkers for the disease while others can be used to control dengue viral replication, thus representing viable targets for drug therapy.

A: Host Gene Expression Profiling of Dengue Virus Infection in Cell Lines and Patients
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Q: Two species of membrane-associated glycoproteins have been identified in the coronavirus virion. They are readily distinguished on the basis of size, radiolabeling characteristics, and location in relation to the lipid bilayer. The larger glycoprotein is highly labeled by both radiolabeled fucose and glucosamine. This species is found in two forms, GP180 and GP90, with apparent molecular weights of 180,000 and 90,000. GP180 can be converted to GP90 in vitro by treatment of virions with trypsin. Analysis of tryptic digests of GP90 and GPl80 give identical peptide patterns. Based on pronase and bromelain sensitiyities, GP180/90 is the only protein which is located entirely external to the viral envelope. It appears to comprise the characteristic long, petal-shaped peplomers of the virion. The smaller glycoprotein, GP23, has an apparent molecular weight of 23,000 and is labeled by radiolabeled glucosamine but not by fucose. The level of glucosamine-labeling of GP23 is about l/10 that of GP180/90. GP23 appears to possess two distinct domains: a smaller, carbohydrate containing region which is found outside the viral envelope, and a larger portion, highly labeled by methionine, which is integrally associated with the viral membrane. A new nomenclature is proposed for the three major coronavirus structural proteins. The two envelope glycoproteins, GP23 and GP180/90 are designated El and E2, respectively; the inner core protein, ~~50, is designated N.

A:
Characterization of a Coronavirus' II. Glycoproteins of the Viral Envelope: Tryptic Peptide Analysis
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