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 Q]: The host antiviral response involves the induction of interferons and proinflammatory cytokines, but also the activation of cell death pathways, including apoptosis, to limit viral replication and spreading. This host defense is strictly regulated to eliminate the infection while limiting tissue damage that is associated with virus pathogenesis. Post-translational modifications, most notably phosphorylation, are key regulators of the antiviral defense implying an important role of protein phosphatases. Here, we investigated the role of the dual-specificity phosphatase 1 (DUSP1) in the host defense against human respiratory syncytial virus (RSV), a pathogenic virus of the Pneumoviridae family, and Sendai virus (SeV), a model virus being developed as a vector for anti-RSV vaccine. We found that DUSP1 is upregulated before being subjected to proteasomal degradation. DUSP1 does not inhibit the antiviral response, but negatively regulates virus-induced JNK/p38 MAPK phosphorylation. Interaction with the JNK-interacting protein 1 scaffold protein prevents dephosphorylation of JNK by DUSP1, likely explaining that AP-1 activation and downstream cytokine production are protected from DUSP1 inhibition. Importantly, DUSP1 promotes SeV-induced apoptosis and suppresses cell migration in RSVinfected cells. Collectively, our data unveils a previously unrecognized selective role of DUSP1 in the regulation of tissue damage and repair during infections by RSV and SeV. Respiratory syncytial virus (RSV) belongs to the Pneumoviridae family of large enveloped negative-sense ssRNA viruses that includes important human pathogens 1,2 . RSV is a leading cause of acute lower respiratory tract infections associated with morbidity and mortality in infants, children and elderly, but also adults of all-age with a compromised immune system, cardiopulmonary diseases or following transplantation 3,4 . The capacity of the host to mount an appropriate antiviral defense aimed at limiting virus replication and spreading is critical to determine the outcome of the infection. As a consequence, the inability of the host to sustain an antiviral response leads to failure in eradicating the infection. Conversely, uncontrolled duration or intensity of the response is harmful to the host and is associated with the development of virus-associated pathogenesis, chronic inflammatory diseases and various autoimmune diseases 5,6 . Therefore, these responses need to reach the ideal intensity and duration for efficient fighting of the infection while limiting tissue damage and promote tissue repair 7 . To this aim, the various components of the host antiviral defense, including the transcriptional induction of interferons (IFNs) and proinflammatory cytokines and chemokines, but also the activation of cell death pathways, such as apoptosis, are subjected to stringent regulation by both positive and negative mechanisms 8,9 . Published: xx xx xxxx OPEN www.nature.com/scientificreports/ 2 Scientific RepoRts | 7: 17388 | Upon virus entry and sensing by the cytosolic pathogen recognition receptors (PRRs) retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated protein 5 (MDA-5), the mitochondrial membrane-associated adaptor (MAVS) coordinates multiple signalling pathways ultimately leading to the activation of the transcription factors IFN regulatory factors (IRF) 3/7, Nuclear Factor κB (NF-κB) and Activator Protein 1 (AP-1) 10-12 . Activation of IRF3 relies on a complex set of phosphorylations mainly mediated by the TANK-binding kinase 1 (TBK1)/ IκB kinase epsilon (IKKε) kinases 13-17 . NF-κB, mainly p65/p50, activation during SeV and RSV infections occurs through IκB kinase (IKK)-dependent phosphorylation of the NF-κB inhibitor protein IκBα and of the p65 subunit 18, 19 . The signaling cascade leading to AP-1 activation is more elusive, but ultimately results in the phosphorylation of the nuclear Activating Transcription Factor 2 (ATF-2) and c-Jun subunits by JNK and p38 Mitogen-Activated Protein Kinases (MAPKs) 10,20,21 . The activation of these transcription factors promotes the transcription of early antiviral genes, type I/III IFNs and proinflammatory cytokines and chemokines 12, 22, 23 . In response to IFNs, hundreds of interferon-stimulated genes (ISGs) are induced to limit virus replication through enhancement of virus detection and innate immune signaling, cytoskeleton remodelling, inhibition of protein translation, induction of apoptosis, amongst other antiviral functions 24-26 . These same PRRs have also been shown to activate IFN-independent cell death pathways, including apoptosis 8 . Post-translational modifications (PTMs), including phosphorylation, ubiquitylation and acetylation, of signal transduction proteins involved in the pathways engaged downstream of virus sensing are crucial to reach a fine-tuned regulation of the innate immune response 27 . In light of the very well documented importance of phosphorylation PTMs in the regulation of the antiviral response, the protein phosphatases negatively regulating the signaling events have started to be identified. The exact role of the Ser/Thr protein phosphatase 1 (PP1) in the antiviral response remains elusive as PP1α and PP1γ were found to dephosphorylate MDA-5 and RIG-I leading to their activation 28 , while they were also described to be responsible for the dephosphorylation of key C-terminal phosphoresidues of IRF3 leading to its inhibition 29 . Most likely reflecting the complexity of IRF3 regulation through phosphorylation at multiple C-terminal phosphoacceptor sites, two other phosphatases, the Ser/Thr protein phosphatase 2 (PP2A) and MAPK phosphatase (MKP) 5, dephosphorylate IRF3 to terminate its activation 30-32 . The Ser/Thr protein phosphatase, Mg 2+ /Mn 2+ -dependent (PPM) 1B acts as a TBK1 phosphatase to inhibit IRF3 activation, while PPM1A targets both TBK1/IKKε and MAVS for dephosphorylation to negatively regulate the antiviral response 33,34 . In the present study, we sought to address the role of the MKP-1/DUSP1 dual phosphatase (referred to thereafter as DUSP1) in the regulation of the host-defense against RSV and Sendai virus (SeV), a model paramyxovirus that is currently evaluated as a replication-competent backbone for the development of an RSV vaccine 3 . We demonstrate that DUSP1 is a negative regulator of RSV-and SeV-induced JNK/p38 MAPK phosphorylation. However, this function is neither linked to the inhibition of the antiviral response nor to the induction of a cytokine and chemokine response elicited during virus infection. Interestingly, we found that interaction of JNK by the JNK interacting protein (JIP) 1 scaffold protein, previously shown to be critical for AP-1 and downstream cytokine production specifically, protects JNK from dephosphorylation by DUSP1. Although we confirmed that a JNK/p38 signalling module is involved in the induction of virus-induced apoptosis, our data suggests that DUSP1 has a pro-apoptotic function independently of JNK and p38 during SeV infection. Finally, we found that DUSP1 dampens cell migration during RSV infection. Altogether, these findings point to a previously unrecognized role of DUSP1 in functions that have an impact on virus-associated tissue damage and repair.
[EX A]: DUSP1 regulates apoptosis and cell migration, but not the JIP1- protected cytokine response, during Respiratory Syncytial Virus and Sendai Virus infection OPEN

[EX Q]: Acute respiratory tract infections (ARI) are a major burden in pediatric long-term care. We analyzed the financial impact of ARI in 2012-2013. Costs associated with ARI during the respiratory viral season were ten times greater than during the non-respiratory viral season, $31 224 and $3242 per 1000 patient-days, respectively (P < 0Á001). ARI are burdensome for pediatric long-term care facilities not only because of the associated morbidity and mortality, but also due to the great financial costs of prevention. Please cite this paper as: Murray et al. (2016) Direct costs of acute respiratory infections in a pediatric long-term care facility. Influenza and Other Respiratory Viruses 10(1), 34-36.
[EX A]: Direct costs of acute respiratory infections in a pediatric long-term care facility

[EX Q]: Numerous reviews on dog zonoses address long-lasting lists of zoonotic infections, observed worldwide or very specifically in certain regions only. Here we describe the average family dog in the Western hemisphere owned by an average family without sufficient knowledge about potential hazards their pet might transmit to family members. This chapter is based on semi quantitative risk analysis in order to rank potential health risk transmitted from family dogs to human. Surprisingly every day risk is different from the generally expected potential risk according to traditional ranking of hazards (zoonoses) in dogs in general. Attention is given to human behavior regarding the family dog and responsible dog ownership. Modern trends include pet travel or pet import from endemic to non-endemic areas, without sufficient knowledge amongst pet owners or public health institutes. Of great value is information provided by ESCCAP (www.esccap.org) with information for European countries (veterinarians and pet-owners) on prevalences and prevention of parasitic infections in dogs and cats in the major languages of Europe. Eventually attention is paid to new trends in dog feed such as feeding bones and raw meat. This may have serious consequences for the spread of ordinary zoonoses like Salmonella and parasitic infections not only between dogs, but also to family members. A last point of attention is the prevention of attracting wild life zoonoses via dogs to family members (eg. Echinococcus multilocularis and Baylisascaris spp.). Authorities responsible for public health should be encouraged to pay more attention, not only in providing more regulations, but primary in enforcement of existing rules and stimulating responsible pet-ownership. Companion animal veterinarians and (local) public health authorities, including physicians, should contribute equally in zoonoses prevention programs ('One health' approach). 575 
[EX A]:
Dogs and Transmission of Infection to Man, "Respected Member of the Family?"