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: Purpose: To provide recommendations and standard operating procedures (SOPs) for intensive care unit (ICU) and hospital preparations for an influenza pandemic or mass disaster with a specific focus on protection of patients and staff. Methods: Based on a literature review and expert opinion, a Delphi process was used to define the essential topics including protection of patients and staff. Results: Key recommendations include: (1) prepare infection control and occupational health policies for clinical risks relating to potential disease transmission; (2) decrease clinical risks and provide adequate facilities through advanced planning to maximise capacity by increasing essential equipment, drugs, supplies and encouraging staff availability; (3) create robust systems to maintain staff confidence and safety by minimising non-clinical risks and maintaining or escalating essential services; (4) prepare formal reassurance plans for legal protection; (5) provide assistance to staff working outside their normal domains. Conclusions: Judicious planning and adoption of protocols for protection of patients and staff are necessary to optimise outcomes during a pandemic.

A: Chapter 6. Protection of patients and staff during a pandemic
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Q: Background: Despite the seriousness of dengue-related disease, with an estimated 50-100 million cases of dengue fever and 250,000-500,000 cases of dengue hemorrhagic fever/dengue shock syndrome each year, a clear understanding of dengue pathogenesis remains elusive. Because of the lack of a disease model in animals and the complex immune interaction in dengue infection, the study of host response and immunopathogenesis is difficult. The development of genomics technology, microarray and high throughput quantitative PCR have allowed researchers to study gene expression changes on a much broader scale. We therefore used this approach to investigate the host response in dengue virusinfected cell lines and in patients developing dengue fever. Methodology/Principal Findings: Using microarray and high throughput quantitative PCR method to monitor the host response to dengue viral replication in cell line infection models and in dengue patient blood samples, we identified differentially expressed genes along three major pathways; NF-kB initiated immune responses, type I interferon (IFN) and the ubiquitin proteasome pathway. Among the most highly upregulated genes were the chemokines IP-10 and I-TAC, both ligands of the CXCR3 receptor. Increased expression of IP-10 and I-TAC in the peripheral blood of ten patients at the early onset of fever was confirmed by ELISA. A highly upregulated gene in the IFN pathway, viperin, was overexpressed in A549 cells resulting in a significant reduction in viral replication. The upregulation of genes in the ubiquitin-proteasome pathway prompted the testing of proteasome inhibitors MG-132 and ALLN, both of which reduced viral replication. Conclusion/Significance: Unbiased gene expression analysis has identified new host genes associated with dengue infection, which we have validated in functional studies. We showed that some parts of the host response can be used as potential biomarkers for the disease while others can be used to control dengue viral replication, thus representing viable targets for drug therapy.

A: Host Gene Expression Profiling of Dengue Virus Infection in Cell Lines and Patients
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Q: A growing body of evidence suggests the non-protein coding human genome is of vital importance for human cell function. Besides small RNAs, the diverse class of long non-coding RNAs (lncRNAs) recently came into focus. however, their relevance for infection, a major evolutionary driving force, remains elusive. Using two commercially available microarray systems, namely Ncode™ and sureprint™ G3, we identified differential expression of 42 ncRNAs during influenza A virus (IAV) infection in human lung epithelial cells. This included several classes of lncRNAs, including large intergenic ncRNAs (lincRNAs). As analyzed by qRT-PcR, expression of one lincRNA, which we termed virus inducible lincRNA (VIN), is induced by several IAV strains (h1N1, h3N2, h7N7) as well as vesicular stomatitis virus. however, we did not observe an induction of VIN by influenza B virus, treatment with RNA mimics, or IFNβ. Thus, VIN expression seems to be a specific response to certain viral infections. RNA fractionation and RNA-FIsh experiments revealed that VIN is localized to the host cell nucleus. Most importantly, we show that abolition of VIN by RNA interference restricts IAV replication and viral protein synthesis, highlighting the relevance of this lincRNA for productive IAV infection. Our observations suggest that viral pathogens interfere with the non-coding portion of the human genome, thereby guaranteeing their successful propagation, and that the expression of VIN correlates with their virulence. consequently, our study provides a novel approach for understanding virus pathogenesis in greater detail, which will enable future design of new antiviral strategies targeting the host's non-protein coding genome.

A:
Evidence for a crucial role of a host non-coding RNA in influenza A virus replication
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