TASK DEFINITION: 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.
PROBLEM: The recent outbreak of the human Zaire ebolavirus (EBOV) epidemic is spiraling out of control in West Africa. Human EBOV hemorrhagic fever has a case fatality rate of up to 90%. The EBOV is classified as a biosafety level 4 pathogen and is considered a category A agent of bioterrorism by Centers for Disease Control and Prevention, with no approved therapies and vaccines available for its treatment apart from supportive care. Although several promising therapeutic agents and vaccines against EBOV are undergoing the Phase I human trial, the current epidemic might be outpacing the speed at which drugs and vaccines can be produced. Like all viruses, the EBOV largely relies on host cell factors and physiological processes for its entry, replication, and egress. We have reviewed currently available therapeutic agents that have been shown to be effective in suppressing the proliferation of the EBOV in cell cultures or animal studies. Most of the therapeutic agents in this review are directed against non-mutable targets of the host, which is independent of viral mutation. These medications are approved by the Food and Drug Administration (FDA) for the treatment of other diseases. They are available and stockpileable for immediate use. They may also have a complementary role to those therapeutic agents under development that are directed against the mutable targets of the EBOV.

SOLUTION: Human Ebola virus infection in West Africa: a review of available therapeutic agents that target different steps of the life cycle of Ebola virus-mutable host cell therapeutic targets for Ebola virus, Cocktail therapeutic intervention for RNA virus Multilingual abstract

PROBLEM: 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.

SOLUTION: Host Gene Expression Profiling of Dengue Virus Infection in Cell Lines and Patients

PROBLEM: A survey of the available ultrastructural data on physiologically and pathologically occurring and virally-induced multinucleate giant cells (MNGCs) is presented. Emphasis is initially placed upon the bone osteoclast, the skeletal muscle myotube and the placental syncytiotrophoblast. The widespread occurrence of MNGCs in a range of pathological situations is discussed, with emphasis upon the broad involvement of the macrophage in inflammatory responses. Many viruses produce cell fusion in vivo and in vitro when cell cultures are infected. Several examples are given. A clear distinction is drawn between viral fusion from "without" and viral fusion from "within" the cell. The cytopathic effect (CPE) of the animal and human retroviruses is discussed in considerable detail. The in vivo and in vitro formation of lymphocytic and macrophage MNGCs by HIV-1 is given extensive coverage. The possible significance of the presence of brain MNGCs of macrophage/ microglial origin as a cellular feature of AIDS dementia is discussed. A new hypothesis is advanced relating to the possible role of endogenous C-type retrovirus in the physiological fusion of the invasive placental cytotrophoblasts to create the syncytiotrophoblast. The evolutionary and developmental significance of such an event in relation to the evolution of the placental mammals is discussed. The possible importance of MNGC formation in the depletion of the CD4 population of T-lymphocytes in vivo in the clinical progression of the AIDS-related complex and AIDS is related to the potent fusogenic effect of HIV-I when cell cultures are infected.

SOLUTION:
The Ultrastructure of Multinucleate Giant Cells