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: 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.

Output: Infection preventionists' experience during the first months of the 2009 novel H1N1 influenza A pandemic


Input: Consider Input: Current hemagglutinin (HA)-based seasonal influenza vaccines induce vaccine strain-specific neutralizing antibodies that usually fail to provide protection against mismatched circulating viruses. Inclusion in the vaccine of highly conserved internal proteins such as the nucleoprotein (NP) and the matrix protein 1 (M1) was shown previously to increase vaccine efficacy by eliciting cross-reactive T-cells. However, appropriate delivery systems are required for efficient priming of T-cell responses. In this study, we demonstrated that administration of novel self-amplifying mRNA (SAM 1 ) vectors expressing influenza NP (SAM (NP)), M1 (SAM(M1)), and NP and M1 (SAM(M1-NP)) delivered with lipid nanoparticles (LNP) induced robust polyfunctional CD4 T helper 1 cells, while NP-containing SAM also induced cytotoxic CD8 T cells. Robust expansions of central memory (T CM ) and effector memory (T EM ) CD4 and CD8 T cells were also measured. An enhanced recruitment of NPspecific cytotoxic CD8 T cells was observed in the lungs of SAM(NP)-immunized mice after influenza infection that paralleled with reduced lung viral titers and pathology, and increased survival after homologous and heterosubtypic influenza challenge. Finally, we demonstrated for the first time that the co-administration of RNA (SAM(M1-NP)) and protein (monovalent inactivated influenza vaccine (MIIV)) was feasible, induced simultaneously NP-, M1-and HA-specific T cells and HA-specific neutralizing antibodies, and enhanced MIIV efficacy against a heterologous challenge. In conclusion, systemic administration of SAM vectors expressing conserved internal influenza antigens induced protective immune responses in mice, supporting the SAM 1 platform as another promising strategy for the development of broad-spectrum universal influenza vaccines.

Output: Self-Amplifying mRNA Vaccines Expressing Multiple Conserved Influenza Antigens Confer Protection against Homologous and Heterosubtypic Viral Challenge


Input: Consider Input: Viral infection induces translocation of the nucleolar protein GLTSCR2 from the nucleus to the cytoplasm, resulting in attenuation of the type I interferon IFN-b. Addressing the role of GLTSCR2 in viral replication, we detect that knocking down GLTSCR2 by shRNAs results in significant suppression of viral replication in mammalian and chicken cells. Injection of chicken embryo with the GLTSCR2-specific shRNA-1370 simultaneously or 24 h prior to infection with Newcastle disease virus (NDV) substantially reduces viral replication in chicken embryo fibroblasts. Injection of shRNA-1370 into chicken embryo also reduces the replication of avian influenza virus (AIV). In contrast, GLTSCR2-derived protein G4-T, forming ahelical dimers, increases replication of seven various DNA and RNA viruses in cells. Our studies reveal that alteration of the function of cellular GLTSCR2 plays a role in supporting viral replication. GLTSCR2 should be seriously considered as a therapeutic target for developing broad spectrum antiviral agents to effectively control viral infection.


Output: Cellular protein GLTSCR2: A valuable target for the development of broad-spectrum antivirals