TASK DEFINITION: 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.
PROBLEM: The Middle East respiratory syndrome coronavirus (MERS-CoV) closely resembled severe acute respiratory syndrome coronavirus (SARS-CoV) in disease manifestation as rapidly progressive acute pneumonia with multi-organ dysfunction. Using monocyte-derived-dendritic cells (Mo-DCs), we discovered fundamental discrepancies in the outcome of MERS-CoV-and SARS-CoV-infection. First, MERS-CoV productively infected Mo-DCs while SARS-CoV-infection was abortive. Second, MERS-CoV induced significantly higher levels of IFN-γ, IP-10, IL-12, and RANTES expression than SARS-CoV. Third, MERS-CoV-infection induced higher surface expression of MHC class II (HLA-DR) and the co-stimulatory molecule CD86 than SARS-CoV-infection. Overall, our data suggests that the dendritic cell can serve as an important target of viral replication and a vehicle for dissemination. MERS-CoV-infection in DCs results in the production of a rich combination of cytokines and chemokines, and modulates innate immune response differently from that of SARS-CoV-infection. Our findings may help to explain the apparent discrepancy in the pathogenicity between MERS-CoV and SARS-CoV.

SOLUTION: Productive replication of Middle East respiratory syndrome coronavirus in monocyte-derived dendritic cells modulates innate immune response

PROBLEM: with the pathological structure of BPD, as seen in the lungs of preterm infants who died and in animal models (3, 7). As the authors note, this study was limited in that the subjects with BPD were stable outpatients younger than 3 years who did not require oxygen therapy at the time of the study. Whether their findings hold true in infants with persistent severe BPD, including those with chronic ventilator-dependent hypoxemic respiratory failure, is not clear. In addition, BPD classification was based on clinical decision making, rather than a physiologic assessment such as the oxygen reduction test (11). In an earlier article, members of this group studied DL CO and its components, DM and Vc, in full-term infants without lung disease and showed that DL CO and Vc (but not DM) correlated with the level of proangiogenic circulating hematopoietic stem/progenitor cells (pCHSPCs) (12). However, this study did not include preterm infants with or without BPD. Both pCHSPCs, also referred to as circulating progenitor cells, as well as late-outgrowth endothelial colony-forming cells, are decreased in the cord blood of preterm infants who later develop moderate or severe BPD (13, 14) . Together, these findings suggest that early disruptions in the number and function of angiogenic progenitor cells, possibly by maternal complications of pregnancy known to be associated with BPD risk, may lead to impaired development of the pulmonary vasculature and sustained impaired gas exchange in preterm infants with BPD. This study shows how a physiologic assessment, such as infant pulmonary function testing, may be used in the clinical setting to provide an estimation of impaired gas exchange in preterm infants with varying degrees of lung injury. Combining functional assays such as this with measurement of pCHSPCs and other angiogenic biomarkers in the cord blood, as well as novel imaging techniques such as quantitative pulmonary magnetic resonance imaging (15), will lead to improved disease phenotyping of preterm infants at risk for BPD. Given the spectrum of disease severity among infants with severe BPD (as determined by the currently accepted diagnostic criteria), novel methods such as these will help identify preterm neonates more accurately, permit targeted therapies for the most severely affected infants, and provide quantitative evidence of the efficacy of these interventions in young children after preterm birth (16). n

SOLUTION: Jobe AH, Bancalari E. Bronchopulmonary dysplasia

PROBLEM: Background: The novel influenza A pandemic virus (H1N1pdm) caused considerable morbidity and mortality worldwide in 2009. The aim of the present study was to evaluate the clinical course, duration of viral shedding, H1N1pdm evolution and emergence of antiviral resistance in hospitalized cancer patients with severe H1N1pdm infections during the winter of 2009 in Brazil. We performed a prospective single-center cohort study in a cancer center in Rio de Janeiro, Brazil. Hospitalized patients with cancer and a confirmed diagnosis of influenza A H1N1pdm were evaluated. The main outcome measures in this study were in-hospital mortality, duration of viral shedding, viral persistence and both functional and molecular analyses of H1N1pdm susceptibility to oseltamivir. Results: A total of 44 hospitalized patients with suspected influenza-like illness were screened. A total of 24 had diagnosed H1N1pdm infections. The overall hospital mortality in our cohort was 21%. Thirteen (54%) patients required intensive care. The median age of the studied cohort was 14.5 years (3-69 years). Eighteen (75%) patients had received chemotherapy in the previous month, and 14 were neutropenic at the onset of influenza. A total of 10 patients were evaluated for their duration of viral shedding, and 5 (50%) displayed prolonged viral shedding (median 23, range = 11-63 days); however, this was not associated with the emergence of a resistant H1N1pdm virus. Viral evolution was observed in sequentially collected samples. Conclusions: Prolonged influenza A H1N1pdm shedding was observed in cancer patients. However, oseltamivir resistance was not detected. Taken together, our data suggest that severely ill cancer patients may constitute a pandemic virus reservoir with major implications for viral propagation.

SOLUTION:
H1N1pdm Influenza Infection in Hospitalized Cancer Patients: Clinical Evolution and Viral Analysis