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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.
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Objective: The aim of this study was to further clarify clinical characteristics and predict mortality risk among patients with viral pneumonia. Methods: A total of 528 patients with viral pneumonia at RuiJin hospital in Shanghai from May 2015 to May 2019 were recruited. Multiplex real-time RT-PCR was used to detect respiratory viruses. Demographic information, comorbidities, routine laboratory examinations, immunological indexes, etiological detections, radiological images and treatment were collected on admission. Results: 76 (14.4%) patients died within 90 days in hospital. A predictive MuLBSTA score was calculated on the basis of a multivariate logistic regression model in order to predict mortality with a weighted score that included multilobular infiltrates (OR = 5.20, 95% CI 1.41-12.52, p = 0.010; 5 points), lymphocyte 0.8 * 10 9 /L (OR = 4.53, 95% CI 2.55-8.05, p < 0.001; 4 points), bacterial coinfection (OR = 3.71, 95% CI 2.11-6.51, p < 0.001; 4 points), acute-smoker (OR = 3.19, 95% CI 1.34-6.26, p = 0.001; 3 points), quit-smoker (OR = 2.18, 95% CI 0.99-4.82, p = 0.054; 2 points), hypertension (OR = 2.39, 95% CI 1.55-4.26, p = 0.003; 2 points) and age 60 years (OR = 2.14, 95% CI 1.04-4.39, p = 0.038; 2 points). 12 points was used as a cut-off value for mortality risk stratification. This model showed sensitivity of 0.776, specificity of 0.778 and a better predictive ability than CURB-65 (AUROC = 0.773 vs. 0.717, p < 0.001). Conclusion: Here, we designed an easy-to-use clinically predictive tool for assessing 90-day mortality risk of viral pneumonia. It can accurately stratify hospitalized patients with viral pneumonia into relevant risk categories and could provide guidance to make further clinical decisions.
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Citation: Clinical Features Predicting Mortality Risk in Patients With Viral Pneumonia: The MuLBSTA Score

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Coxsackieviruses are enteric viruses that frequently infect humans. To examine coxsackievirus pathogenesis, we orally inoculated mice with the coxsackievirus B3 (CVB3) Nancy strain. Using HeLa cell plaque assays with agar overlays, we noticed that some fecal viruses generated plaques >100 times as large as inoculum viruses. These large-plaque variants emerged following viral replication in several different tissues. We identified a single amino acid change, N63Y, in the VP3 capsid protein that was sufficient to confer the large-plaque phenotype. Wild-type CVB3 and N63Y mutant CVB3 had similar plaque sizes when agarose was used in the overlay instead of agar. We determined that sulfated glycans in agar inhibited plaque formation by wildtype CVB3 but not by N63Y mutant CVB3. Furthermore, N63Y mutant CVB3 bound heparin, a sulfated glycan, less efficiently than wild-type CVB3 did. While N63Y mutant CVB3 had a growth defect in cultured cells and reduced attachment, it had enhanced replication and pathogenesis in mice. Infection with N63Y mutant CVB3 induced more severe hepatic damage than infection with wild-type CVB3, likely because N63Y mutant CVB3 disseminates more efficiently to the liver. Our data reinforce the idea that culture-adapted laboratory virus strains can have reduced fitness in vivo. N63Y mutant CVB3 may be useful as a platform to understand viral adaptation and pathogenesis in animal studies. IMPORTANCE Coxsackieviruses frequently infect humans, and although many infections are mild or asymptomatic, there can be severe outcomes, including heart inflammation. Most studies with coxsackieviruses and other viruses use laboratory-adapted viral strains because of their efficient replication in cell culture. We used a cell culture-adapted strain of CVB3, Nancy, to examine viral replication and pathogenesis in orally inoculated mice. We found that mice shed viruses distinct from input viruses because they formed extremely large plaques in cell culture. We identified a single mutation, VP3 N63Y, that was sufficient for large-plaque formation. N63Y mutant viruses have reduced glycan binding and replication in cell culture; however, they have enhanced replication and virulence in mice. We are now using N63Y mutant CVB3 as an improved system for viral pathogenesis studies. Citation Wang Y, Pfeiffer JK. 2016. Emergence of a large-plaque variant in mice infected with coxsackievirus B3. mBio 7(2):e00119-16.
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Emergence of a Large-Plaque Variant in Mice Infected with Coxsackievirus B3

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induced host immune response , but the relative contribution of each remains largely unknown. For example , C57BL/6 (B6) mice infected with mouse hepatitis virus (JHM strain , JHMV) develop severe encephalitis , with death occurring within 7 days. Here, we show that the host response to a single JHMVspecific immunodominant CD4 T-cell epitope is critical for severe disease. We engineered a recombinant JHMV with mutations in the immunodominant CD4 T-cell epitope (rJ.M Y135Q ). Infection of naive B6 mice with this virus resulted in mild disease with no mortality. However , introduction of a CD4 T-cell epitope from Listeria monocytogenes into rJ.M Y135Q generated a highly virulent virus. The decrease in disease severity was not due to a switch from Th1 to Th2 predominance in rJ.M Y135Q -infected mice , an effect on CD8 T-cell function , or differential expression of tumor necrosis factor- by JHMV-specific CD4 T cells. These results show that the response to a single virus-specific CD4 T-cell epitope may contribute to a pathogenic host response in the setting of acute viral disease and that abrogation of this response ameliorates clinical disease without diminishing virus clearance.
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Pathogenic Role for Virus-Specific CD4 T Cells in Mice with Coronavirus-Induced Acute Encephalitis