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.

Q: The coronavirus (CoV) responsible for severe acute respiratory syndrome (SARS), SARS-CoV, encodes two large polyproteins (pp1a and pp1ab) that are processed by two viral proteases to yield mature non-structural proteins (nsps). Many of these nsps have essential roles in viral replication, but several have no assigned function and possess amino acid sequences that are unique to the CoV family. One such protein is SARS-CoV nsp1, which is processed from the N-terminus of both pp1a and pp1ab. The mature SARS-CoV protein is present in cells several hours post-infection and co-localizes to the viral replication complex, but its function in the viral life cycle remains unknown. Furthermore, nsp1 sequences are highly divergent across the CoV family, and it has been suggested that this is due to nsp1 possessing a function speciWc to viral interactions with its host cell or acting as a host speciWc virulence factor. In order to initiate structural and biophysical studies of SARS-CoV nsp1, a recombinant expression system and a puriWcation protocol have been developed, yielding milligram quantities of highly puriWed SARS-CoV nsp1. The puriWed protein was characterized using circular dichroism, size exclusion chromatography, and multi-angle light scattering.

A: Expression, puriWcation and characterization of recombinant severe acute respiratory syndrome coronavirus non-structural protein 1
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Q: Acute cough is a major symptom of viral respiratory tract infection and causes excessive morbidity in human populations across the world. A wide variety of viruses play a role in the development of cough after acute infection and all of these manifest a similar clinical picture across different age groups. Despite the large disease burden surprisingly little is known about the mechanism of acute cough following viral infection. Both in vitro and in vivo experiments show that increased production of neuropeptides and leukotrienes mediate cough after viral infection, along with altered expression of neural receptors. Increased airway mucus production is also likely to play a significant role. This work is reviewed in this article. Following the recent development of a mouse model for rhinovirus infection and the establishment of experimental models of rhinovirus challenge in human subjects with both asthma and COPD the field is expanding to translate in vitro research into clinical studies and hopefully eventually into clinical practice. Developing a clearer understanding of the mechanisms underlying virus induced cough may lead to more specific and effective therapies.

A: Cough and viruses in airways disease: Mechanisms
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Q: The contribution of distinct central nervous system (CNS) resident cells to protective alpha/beta interferon (IFN-␣/␤) function following viral infections is poorly understood. Based on numerous immune regulatory functions of astrocytes, we evaluated the contribution of astrocyte IFN-␣/␤ signaling toward protection against the nonlethal glia-and neuronotropic mouse hepatitis virus (MHV) strain A59. Analysis of gene expression associated with IFN-␣/␤ function, e.g., pattern recognition receptors (PRRs) and interferon-stimulated genes (ISGs), revealed lower basal mRNA levels in brain-derived astrocytes than in microglia. Although astrocytes poorly induced Ifn␤ mRNA following infection, they upregulated various mRNAs in the IFN-␣/␤ pathway to a higher extent than microglia, supporting effective IFN-␣/␤ responsiveness. Ablation of the IFN-␣/␤ receptor (IFNAR) in astrocytes using mGFAPcre IFNAR fl/fl mice resulted in severe encephalomyelitis and mortality, coincident with uncontrolled virus replication. Further, virus spread was not restricted to astrocytes but also affected microglia and neurons, despite increased and sustained Ifn␣/␤ and ISG mRNA levels within the CNS. IFN-␥, a crucial mediator for MHV control, was not impaired in infected mGFAPcre IFNAR fl/fl mice despite reduced T cell CNS infiltration. Unexpectedly however, poor induction of IFN-␥-dependent major histocompatibility complex (MHC) class II expression on microglia supported that defective IFN-␥ signaling contributes to uncontrolled virus replication. A link between sustained elevated IFN-␣/␤ and impaired responsiveness to IFN-␥ supports the novel concept that temporally limited early IFN-␣/␤ responses are critical for effective antiviral IFN-␥ function. Overall, our results imply that IFN-␣/␤ signaling in astrocytes is not only critical in limiting early CNS viral spread but also promotes protective antiviral IFN-␥ function.

A:
Alpha/Beta Interferon (IFN-␣/␤) Signaling in Astrocytes Mediates Protection against Viral Encephalomyelitis and Regulates IFN-␥-Dependent Responses
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