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.

Input: Consider Input: 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 B (NF-B) 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)/ IB kinase epsilon (IKK) kinases 13-17 . NF-B, mainly p65/p50, activation during SeV and RSV infections occurs through IB kinase (IKK)-dependent phosphorylation of the NF-B inhibitor protein IB 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 PP1 and PP1 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/IKK 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.

Output: DUSP1 regulates apoptosis and cell migration, but not the JIP1- protected cytokine response, during Respiratory Syncytial Virus and Sendai Virus infection OPEN

Input: Consider Input: Contact networks are convenient models to investigate epidemics, with nodes and links representing potential hosts and infection pathways, respectively. The outcomes of outbreak simulations on networks are driven both by the underlying epidemic model, and by the networks' structural properties, so that the same pathogen can generate different epidemic dynamics on different networks. Here we ask whether there are general properties that make a contact network intrinsically vulnerable to epidemics (that is, regardless of specific epidemiological parameters). By conducting simulations on a large set of modelled networks, we show that, when a broad range of network topologies is taken into account, the effect of specific network properties on outbreak magnitude is stronger than that of fundamental pathogen features such as transmission rate, infection duration, and immunization ability. Then, by focusing on a large set of real world networks of the same type (potential contacts between field voles, Microtus agrestis), we showed how network structure can be used to accurately assess the relative, intrinsic vulnerability of networks towards a specific pathogen, even when those have limited topological variability. These results have profound implications for how we prevent disease outbreaks; in many real world situations, the topology of host contact networks can be described and used to infer intrinsic vulnerability. Such an approach can increase preparedness and inform preventive measures against emerging diseases for which limited epidemiological information is available, enabling the identification of priority targets before an epidemic event.

Output: The intrinsic vulnerability of networks to epidemics

Input: Consider Input: Houttuynia cordata is an important traditional Chinese herb with unresolved genetics and taxonomy, which lead to potential problems in the conservation and utilization of the resource. Inter-simple sequence repeat (ISSR) markers were used to assess the level and distribution of genetic diversity in 226 individuals from 15 populations of H. cordata in China. ISSR analysis revealed low genetic variations within populations but high genetic differentiations among populations. This genetic structure probably mainly reflects the historical association among populations. Genetic cluster analysis showed that the basal clade is composed of populations from Southwest China, and the other populations have continuous and eastward distributions. The structure of genetic diversity in H. cordata demonstrated that this species might have survived in Southwest China during the glacial age, and subsequently experienced an eastern postglacial expansion. Based on the results of genetic analysis, it was proposed that as many as possible targeted populations for conservation be included.
Output: Genetic Variation and Population Differentiation in a Medical Herb Houttuynia cordata in China Revealed by Inter-Simple Sequence Repeats (ISSRs)