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.

Ex Input:
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 IB degradation and NFB 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 IKK 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 NFB via IKK activated by caspase-8 and -10. Also PKR signaling results in NFB 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 NFB activation. Type III IFN are induced by TLR3, TLR9, and via RIG-I and peroxisomal-resident IPS-1. Especially IRF1, but also NFB, IRF3, and IRF7 are implicated in IFN- production, with the latter being stabilized by Med23.

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

Ex Input:
Acute respiratory failure contributes significantly to nonrelapse mortality after allogeneic hematopoietic stem cell transplantation. Although there is a trend of improved survival over time, mortality remains unacceptably high. An understanding of the pathophysiology of early respiratory failure, opportunities for targeted therapy, assessment of the patient at risk, optimal use of noninvasive positive pressure ventilation, strategies to improve alveolar recruitment, appropriate fluid management, care of the patient with chronic lung disease, and importantly, a team approach between critical care and transplantation services may improve outcomes. O

Ex Output:
A Critical Care and Transplantation-Based Approach to Acute Respiratory Failure after Hematopoietic Stem Cell Transplantation in Children

Ex Input:
In this study, we report the complete genome sequence of two contemporary human coronavirus OC43 (HCoV-OC43) strains detected in 2003 and 2004, respectively. Comparative genetic analyses of the circulating strains and the prototype HCoV-OC43 strain (ATCC VR759) were performed. Remarkably, a lower than expected similarity is found between the complete genomes and more in particular between the spike genes of the BE03 and BE04 strains. This finding suggests the existence of two genetically distinct HCoV-OC43 strains, circulating in Belgium in 2003 and 2004. Spike gene sequencing of three additional 2003 and two additional 2004 HCoV-OC43 strains, and subsequent phylogenetic analysis confirm this assumption. Compared to the ATCC prototype HCoV-OC43 strain, an important amino acid substitution is present in the potential cleavage site sequence of the spike protein of all contemporary strains, restoring the N-RRXRR-C motif, associated with increased spike protein cleavability in bovine coronaviruses. We here describe specific characteristics associated with circulating HCoV-OC43 strains, and we provide substantial evidence for the genetic variability of HCoV-OC43. D

Ex Output:
Circulation of genetically distinct contemporary human coronavirus OC43 strains