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.

A novel betacoronavirus associated with lethal respiratory and renal complications was recently identified in patients from several countries in the Middle East. We report the deep genome sequencing of the virus directly from a patient's sputum sample. Our high-throughput sequencing yielded a substantial depth of genome sequence assembly and showed the minority viral variants in the specimen. Detailed phylogenetic analysis of the virus genome (England/ Qatar/2012) revealed its close relationship to European bat coronaviruses circulating among the bat species of the Vespertilionidae family. Molecular clock analysis showed that the 2 human infections of this betacoronavirus in June 2012 (EMC/2012) and September 2012 (England/Qatar/2012) share a common virus ancestor most likely considerably before early 2012, suggesting the human diversity is the result of multiple zoonotic events. T he ability of coronaviruses (CoVs) to infect multiple species and to rapidly change through recombination presents a continuing human health threat. The epidemic of severe acute respiratory syndrome (SARS) during 2003-2004 during which a CoV transmitted from bats to civet cats and then to humans demonstrated this potential (reviewed in [1, 2] ). Recently, a novel human betacoronavirus (betaCoV) was found to be associated with at least 13 human infections, 7 of which were fatal (3-7). One of the viruses, EMC/2012, has been sequenced, and its sequence similarity to several bat CoVs suggested an animal origin, but a definitive bat species of origin has not yet been identified (3). Additional genome sequences from this virus are needed to aid diagnostics, monitor population dynamics, identify the animal source, and characterize mechanisms of pathogenesis. The large size (30,000 nt) and high variability of CoV RNA genomes present a challenge for sequencing. We describe a strategy for rapidly designing the primers necessary for reverse transcription and cDNA amplification of such diverse RNA viruses and report the full-genome determination of the novel CoV directly from patient sputum using next-generation short-read sequencing. Full genomes from 2 epidemiologically unlinked novel CoV infections separated in time by >2 months were analyzed to gain clues to 2 major questions: what are the precursors of the virus, and how long has the virus been circulating in its current form? Materials and Methods Fifteen betaCoV full genomes with the closest homology to EMC/2012 (GenBank accession no. JX869059) were analyzed to identify all possible primer-like sequences (melting temperature 58°C-60°C, guanine plus cytosine content 35%-60%) yielding 357,198 potential primers. The 30-kb JX869059 CoV genome was divided into fifteen 2.5-kb overlapping amplicons, and the 2 highest frequency sequences mapping in the 5′ and 3′ 250 bp of each amplicon were selected. Reverse complements of the 3′ mapping sequences were prepared, resulting in a set of 60 primers for the 15 amplicons (4 primers/amplicon). Three additional primers were added for the extreme termini of the genome. The algorithm also prepared a virtual PCR map of the predicted binding and amplicon size for the primer set on CoV genomes. A map of the primer mapping positions
Full-Genome Deep Sequencing and Phylogenetic Analysis of Novel Human Betacoronavirus

('filoviruses') that cause severe hemorrhagic fever with human case fatality rates of up to 90%. Filovirus infection requires fusion of the host cell and virus membranes, a process that is mediated by the envelope glycoprotein (GP). GP contains two subunits, the surface subunit (GP1), which is responsible for cell attachment, and the transmembrane subunit (GP2), which catalyzes membrane fusion. The GP2 ectodomain contains two heptad repeat regions, N-terminal and C-terminal (NHR and CHR, respectively) that adopt a six-helix bundle during the fusion process. The refolding of this six-helix bundle provides the thermodynamic driving force to overcome barriers associated with membrane fusion. Here we report the crystal structure of the MARV GP2 core domain in its post-fusion (six-helix bundle) conformation at 1.9 Å resolution. The MARV GP2 core domain backbone conformation is virtually identical to that of EBOV GP2 (reported previously), and consists of a central NHR core trimeric coiled-coil packed against peripheral CHR α-helices and an intervening loop/helix-turn-helix segment. We previously reported that the stability of the MARV GP2 post-fusion structure is highly pH-dependent, with increasing stability at lower pH [Harrison, J.S.; Koellhoffer, J. K.; Chandran, K.; and Lai, J. R. Biochemistry, 2012Biochemistry, , 51, 2515Biochemistry, -2525. We hypothesized that this pH-dependent stability provides a mechanism for conformational control such that the post-fusion six helix bundle is promoted in the environments of appropriately matured endosomes. In this report, a structural rationale for this pH-dependent stability is described, and involves a high-density array of core and surface acidic side chains at the midsection of the structure, termed the 'anion stripe.' In addition, many surface-exposed salt bridges likely contribute to stabilizing the post-fusion structure at low pH. These results provide structural insights into the mechanism of MARV GP2-mediated membrane fusion.
Crystal Structure of the Marburg Virus GP2 Core Domain in its Post-Fusion Conformation †

A total of 116 hospitalized patients with confirmed COVID-19 pneumonia and SARS-CoV-2-specific immunoglobulins tested in Tongji hospital were retrospectively investigated. Clinical, laboratory, radiological characteristics and outcomes data were compared between mild-moderate group and died group. Further, a paired case-control study was conducted where each deceased case was matched to three mild-moderate patients of similar age. Among 116 subjects included, 101 mild-moderate patients survived and 15 cases died. SARS-CoV-2-specific IgM levels peaked in forth week after onset of COVID-19 pneumonia, while serum IgG levels increased over 8 weeks. Serum IgM levels were higher in deceased patients than mild-moderate patients (P = 0.024), but not IgG. Serum IgM levels were negatively correlated with clinical outcome, eosinophil count and albumin levels (r = -0.269, P = 0.003; r = -0.188, P = 0.043; and r = -0.198, P = 0.033, resp.). The area under the ROC curve (AUC) for IgM antibody was 0.681 (95% CI: 0.517-0.845, P = 0.024). In case-control study paired by age, serum IgM was higher in deceased patients than mild-moderate patients (P = 0.019), positively correlated with leucocyte count (r = 0.260, P = 0.045), while negatively correlated with clinical outcome and albumin levels (r = -0.337, P = 0.008; r = -0.265, P = 0.041). AUC for IgM levels was 0.704 (95% CI: 0.534-0.873, P = 0.019). These results indicate that dynamics of SARS-CoV-2 specific IgM and IgG antibodies was similar with that of SARS-CoV, while elevated serum IgM levels indicate poor outcome in patients with COVID-19 pneumonia. All rights reserved. No reuse allowed without permission. author/funder, who has granted medRxiv a license to display the preprint in perpetuity.

Elevated serum IgM levels indicate poor outcome in patients with coronavirus disease 2019 pneumonia: A retrospective case-control study