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.

Background: A novel strain of influenza A (H1N1) was identified in April 2009 and developed into a pandemic by June 2009. This rapid and unexpected event had enormous implications for infection preventionists (IP) internationally. Lessons learned from this event should guide future pandemic planning efforts. Methods: Focus groups were conducted at the Association for Professionals in Infection Control and Epidemiology, Inc, (APIC) 2009 conference to evaluate IPs' experience with the novel H1N1 influenza pandemic and assess their perceived needs related to novel H1N1 topics and products required for future education and reference materials. Results: Forty IPs (37 from the United States and 3 international) participated in the focus groups. Needed reference materials identified by attendees included infection prevention guidance for nonacute care settings; occupational health polices; and brief, multilanguage patient/family educational materials. Educational topics on which IPs need to be trained include isolation precautions/ personal protective equipment recommendations for novel H1N1 patients, coordination between hospitals and community response agencies, and surge management. The rapidly changing and conflicting recommendations related to patient management made responding to this event challenging. IPs require synthesized infection prevention guidelines developed in a concise, real-time format. Conclusion: IPs must continue to partner with public health and other response agencies to address gaps in pandemic planning.
Infection preventionists' experience during the first months of the 2009 novel H1N1 influenza A pandemic

Pentraxin 3 (PTX3) is a soluble pattern recognition receptor which is classified as a long-pentraxin in the pentraxin family. It is known to play an important role in innate immunity, inflammatory regulation, and female fertility. PTX3 is synthesized by specific cells, primarily in response to inflammatory signals. Among these various cells, neutrophils have a unique PTX3 production system. Neutrophils store PTX3 in neutrophil-specific granules and then the stored PTX3 is released and localizes in neutrophil extracellular traps (NETs). Although certain NET components have been identified, such as histones and anti-microbial proteins, the detailed mechanisms by which NETs localize, as well as capture and kill microbes, have not been fully elucidated. PTX3 is a candidate diagnostic marker of infection and vascular damage. In severe infectious diseases such as sepsis, the circulating PTX3 concentration increases greatly (up to 100 ng/mL, i.e., up to 100-fold of the normal level). Even though it is clearly implied that PTX3 plays a protective role in sepsis and certain other disorders, the detailed mechanisms by which it does so remain unclear. A proteomic study of PTX3 ligands in septic patients revealed that PTX3 forms a complex with certain NET component proteins. This suggests a role for PTX3 in which it facilitates the efficiency of anti-microbial protein pathogen clearance by interacting with both pathogens and anti-microbial proteins. We discuss the possible relationships between PTX3 and NET component proteins in the host protection afforded by the innate immune response. The PTX3 complex has the potential to be a highly useful diagnostic marker of sepsis and other inflammatory diseases.
Host-protective effect of circulating pentraxin 3 (PTX3) and complex formation with neutrophil extracellular traps

Replication of plus-strand RNA viruses depends on recruited host factors that aid several critical steps during replication. In this paper, we show that an essential translation factor, Ded1p DEAD-box RNA helicase of yeast, directly affects replication of Tomato bushy stunt virus (TBSV). To separate the role of Ded1p in viral protein translation from its putative replication function, we utilized a cell-free TBSV replication assay and recombinant Ded1p. The in vitro data show that Ded1p plays a role in enhancing plus-strand synthesis by the viral replicase. We also find that Ded1p is a component of the tombusvirus replicase complex and Ded1p binds to the 39-end of the viral minus-stranded RNA. The data obtained with wt and ATPase deficient Ded1p mutants support the model that Ded1p unwinds local structures at the 39-end of the TBSV (2)RNA, rendering the RNA compatible for initiation of (+)-strand synthesis. Interestingly, we find that Ded1p and glyceraldehyde-3phosphate dehydrogenase (GAPDH), which is another host factor for TBSV, play non-overlapping functions to enhance (+)strand synthesis. Altogether, the two host factors enhance TBSV replication synergistically by interacting with the viral (2)RNA and the replication proteins. In addition, we have developed an in vitro assay for Flock house virus (FHV), a small RNA virus of insects, that also demonstrated positive effect on FHV replicase activity by the added Ded1p helicase. Thus, two small RNA viruses, which do not code for their own helicases, seems to recruit a host RNA helicase to aid their replication in infected cells.

A Co-Opted DEAD-Box RNA Helicase Enhances Tombusvirus Plus-Strand Synthesis