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: Respiratory syncytial virus (RSV) is the leading cause of bronchiolitis and viral pneumonia in infants and young children worldwide. In the Middle East and Arab countries, the burden of RSV-associated hospitalizations is not well characterized. We sought to determine the burden and clinical/epidemiological characteristics of RSV hospitalization in young children in Amman, Jordan. We investigated risk factors for severity including vitamin D levels. Methods: We conducted viral surveillance with clinical and demographic data in children <2 years admitted with respiratory symptoms and/or fever at the Al-Bashir Government Hospital from March16, 2010 to March 31, 2013. Nasal/throat swabs were obtained and placed into lysis buffer, and frozen at −80 • C until testing by real-time RT-PCR for 11 respiratory viruses. Heel stick blood or sera samples for 25hydroxyvitamin D [25(OH)D] levels were obtained and sent to a central laboratory for mass spectrometry. Results: Of the 3168 children, >80% testing positive for one virus, with RSV the most common virus detected (44%). The RSV-associated hospitalization rate was highest in children <6 months with an annual range of 21.1-25.9 per 1000, compared to 6.0-8.0 in 6-11-month-olds and 1.6-2.5 in 12-23-month-olds. RSV-positive children compared with RSV-negative were more likely to be previously healthy without underlying medical conditions, less likely to be born prematurely, had a higher frequency of supplemental oxygen use, and had lower median vitamin D levels. Risk factors for oxygen use in RSV-positive children included underlying medical conditions, lack of breastfeeding, younger age, and higher viral load. Conclusion: RSV is a major cause of illness in hospitalized Jordanian children and is associated with increased severity compared to other respiratory viruses. Children with RSV in the Middle East would benefit from future RSV vaccines and antiviral therapy.

SOLUTION: Natural history and epidemiology of respiratory syncytial virus infection in the Middle East: Hospital surveillance for children under age two in Jordan

PROBLEM: Keywords: interferon, interferon-stimulated genes, tumor necrosis factor-related apoptosis-inducing ligand, acute lung injury, innate immunity, influenza, respiratory syncytial virus, coronavirus FiGURe 1 | PRRs and their downstream signaling pathways in virus-induced iFN induction. In viral infection, type I IFNs are induced by TLR, RLR, CLR, and cytosolic nucleic acid sensors. Cell membrane-located TLRs ligate to viral envelope proteins (e.g., TLR2/herpes simplex virus), upon which they recruit MyD88. MyD88 interacts with IRAK kinase (IRAK-1, -2, or -4) that either directly activate IRF1 or interact with TRAF6, which induces IRF7 or assembles with TAK1. TAK1 forms a complex with TAB-1/-2 and -3 and subsequently either activates the MAPK kinases p38 and JNK, leading to AP-1 phosphorylation and nuclear translocation, or induces ubiquitination of NEMO followed by IκB degradation and NFκB activation. Endosomal TLRs recognizing viral nucleic acid and signal via the adaptor protein MyD88 (for TLR7/8/9) or interact with TRIF (for TLR3) followed by TRAF3, TANK, and TBK1 activation. TBK1 and IKKε then phosphorylate and activate IRF3 and IRF7. Additionally, TRIF can interact with TRAF6 to initiate TAK1 signaling. Both RLRs, RIG-I and MDA-5, recognize nucleic acid contents in the cytoplasm and stimulate the mitochondrial anchored IPS-1 for dimerization followed by TRADD recruitment that acts via TRAF3 on IRF3 and IRF7. Additionally, IPS-1 can interact with FADD and RIP1 to activate NFκB via IKK activated by caspase-8 and -10. Also PKR signaling results in NFκB activation and nuclear translocation. The dsDNA sensor cGAS produces cGAMP that activates ER-located STING that via TBK1 induces IRF3 translocation and type I IFN production. CLRs play a minor role in viral recognition; however, DC-SIGN activates the small GTPase Ras and Raf protein kinase, followed by NFκB activation. Type III IFN are induced by TLR3, TLR9, and via RIG-I and peroxisomal-resident IPS-1. Especially IRF1, but also NFκB, IRF3, and IRF7 are implicated in IFN-λ production, with the latter being stabilized by Med23.

SOLUTION: The impact of the interferon/TNF- Related Apoptosis-inducing Ligand Signaling Axis on Disease Progression in Respiratory viral infection and Beyond

PROBLEM: The SARS-associated human coronavirus (SARS-HCoV) is a newly described, emerging virus conclusively established as the etiologic agent of the severe acute respiratory syndrome (SARS). This study presents a single-tube RT-PCR assay that can detect with high analytical sensitivity the SARS-HCoV, as well as several other coronaviruses including other known human respiratory coronaviruses (HCoV-OC43 and HCoV-229E). Species identification is provided by sequencing the amplicon, although a rapid screening test by restriction enzyme analysis has proved to be very useful for the analysis of samples obtained during the SARS outbreak in Toronto, Canada.

SOLUTION:
Comprehensive detection and identification of human coronaviruses, including the SARS-associated coronavirus, with a single RT-PCR assay