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.

Ex Input:
The presence of immunoglobulin oligoclonal bands in the cerebrospinal fluid of Multiple Sclerosis (MS) patients supports the hypothesis of an infectious etiology, although the antigenic targets remain elusive. Neurotropic mouse hepatitis virus (MHV) infection in mice provides a useful tool for studying mechanisms of demyelination in a virus-induced experimental model of MS. This study uses Affymetrix microarray analysis to compare differential spinal cord mRNA levels between mice infected with demyelinating and non-demyelinating strains of MHV to identify host immune genes expressed in this demyelinating disease model. The study reveals that during the acute stage of infection, both strains induce inflammatory innate immune response genes, whereas upregulation of several immunoglobulin genes during chronic stage infection is unique to infection with the demyelinating strain. Results suggest that the demyelinating strain induced an innate-immune response during acute infection that may promote switching of Ig isotype genes during chronic infection, potentially playing a role in antibody-mediated progressive demyelination even after viral clearance.

Ex Output:
Demyelinating strain of mouse hepatitis virus infection bridging innate and adaptive immune response in the induction of demyelination

Ex Input:
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.

Ex Output:
Chapter 6. Protection of patients and staff during a pandemic

Ex Input:
Massive aggregations of macrophages are frequently detected in afflicted lungs of patients with severe acute respiratory syndrome-associated coronavirus (SARS-CoV) infection. In vitro, ectopic expression of transcription factors, in particular CCAAT/enhancer-binding protein alpha (C/EBP) and C/EBP, can convert B cells into functional macrophages. However, little is known about the specific ligands responsible for such phenotype conversion. Here, we investigated whether spike protein of SARS-CoV can act as a ligand to trigger the conversion of B cells to macrophages. We transduced SARS-CoV spike proteindisplayed recombinant baculovirus (SSDRB), vAtEpGS688, into peripheral B cells and B lymphoma cells. Cell surface expression of CD19 or Mac-1 (CD11b) was determined by flow cytometry. SSDRB-mediated changes in gene expression profiles of B lymphoma cells were analyzed by microarray. In this report, we showed that spike protein of SARS virus could induce phenotypic conversion of human B cells, either from peripheral blood or B lymphoma cells, to macrophage-like cells that were steadily losing the B-cell marker CD19 and in turn expressing the macrophage-specific marker Mac-1. Furthermore, we found that SSDRB enhanced the expression of CD86, hypoxia-inducible factor-1 (HIF1), suppressor of cytokine signaling (SOCS or STAT-induced STAT inhibitor)-3, C/EBP, insulin-like growth factor-binding protein 3 (IGFBP3), Krupple-like factor (KLF)-5, and CD54, without marked influence on C/EBP or PU.1 expression in transduced cells. Prolonged exposure to hypoxia could also induce macrophage-like conversion of B cells. These macrophage-like cells were defective in phagocytosis of red fluorescent beads. In conclusion, our results suggest that conversion of B cells to macrophage-like cells, similar to a pathophysiological response, could be mediated by a devastating viral ligand, in particular spike protein of SARS virus, or in combination with severe local hypoxia, which is a condition often observed in afflicted lungs of SARS patients.

Ex Output:
SARS spike protein induces phenotypic conversion of human B cells to macrophage-like cells