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.
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Question: Human coronaviruses (HCoVs) are known respiratory pathogens associated with a range of respiratory outcomes. In the past 14 years, the onset of severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV) have thrust HCoVs into spotlight of the research community due to their high pathogenicity in humans. The study of HCoV-host interactions has contributed extensively to our understanding of HCoV pathogenesis. In this review, we discuss some of the recent findings of host cell factors that might be exploited by HCoVs to facilitate their own replication cycle. We also discuss various cellular processes, such as apoptosis, innate immunity, ER stress response, mitogen-activated protein kinase (MAPK) pathway and nuclear factor kappa B (NF-B) pathway that may be modulated by HCoVs. Diseases 2016, 4, 26 2 of 28 but with a much higher mortality rate of about 35% [17] . Unlike SARS-CoV, which exhibits super-spreader events, transmission of MERS-CoV is geographically limited [12] . In fact, reported cases of MERS-CoV often stem from outbreaks within the Middle Eastern countries or recent travel to the region [18, 19] . CoVs are a group of large enveloped RNA viruses under the Coronaviridae family. Together with Artierivirdae and Roniviridae, Coronaviridae is classified under the Nidovirale order [20] . As proposed by the International Committee for Taxonomy of Viruses, CoVs are further categorized into four main genera, Alpha-, Beta-, Gammaand Deltacoronaviruses based on sequence comparisons of entire viral genomes [21, 22] . These CoVs can infect a wide variety of hosts, including avian, swine and humans. HCoVs are identified to be either in the Alphaor Betacoronavirus genera, including Alphacoronaviruses, HCoV-229E and HCoV-NL63, and Betacoronaviruses, HCoV-HKU1, SARS-CoV, MERS-CoV and HCoV-OC43 (Table 1) . Under the electron microscope, the CoV virions appear to be roughly spherical or moderately pleomorphic, with distinct "club-like" projections formed by the spike (S) protein [23, 24] . Within the virion interior lies a helically symmetrical nucleocapsid that encloses a single-stranded and positive sense RNA viral genome of an extraordinarily large size of about 26 to 32 kilobases [20] . The positive sense viral genomic RNA acts as a messenger RNA (mRNA), comprising a 5 1 terminal cap structure and a 3 1 poly A tail. This genomic RNA acts in three capacities during the viral life cycle: (1) as an initial RNA of the infectious cycle; (2) as a template for replication and transcription; and (3) as a substrate for packaging into the progeny virus. The replicase-transcriptase is the only protein translated from the genome, while the viral products of all downstream open reading frames are derived from subgenomic mRNAs. In all CoVs, the replicase gene makes up approximately 5 1 two-thirds of the genome and is comprised of two overlapping open reading frames (ORFs), ORF1a and ORF1b, which encodes 16 non-structural proteins. The final one-third of the CoV genomic RNA encodes CoV canonical set of four structural protein genes, in the order of spike (S), envelope (E), membrane (M) and nucleocapsid (N). In addition, several accessory ORFs are also interspersed along the structural protein genes and the number and location varies among CoV species [25] (Figure 1). Diseases 2016, 4, 26 2 of 27 SARS-CoV but with a much higher mortality rate of about 35% [17]. Unlike SARS-CoV, which exhibits super-spreader events, transmission of MERS-CoV is geographically limited [12]. In fact, reported cases of MERS-CoV often stem from outbreaks within the Middle Eastern countries or recent travel to the region [18,19]. CoVs are a group of large enveloped RNA viruses under the Coronaviridae family. Together with Artierivirdae and Roniviridae, Coronaviridae is classified under the Nidovirale order [20] . As proposed by the International Committee for Taxonomy of Viruses, CoVs are further categorized into four main genera, Alpha-, Beta-, Gamma-and Deltacoronaviruses based on sequence comparisons of entire viral genomes [21, 22] . These CoVs can infect a wide variety of hosts, including avian, swine and humans. HCoVs are identified to be either in the Alpha-or Betacoronavirus genera, including Alphacoronaviruses, HCoV-229E and HCoV-NL63, and Betacoronaviruses, HCoV-HKU1, SARS-CoV, MERS-CoV and HCoV-OC43 (Table 1) . Under the electron microscope, the CoV virions appear to be roughly spherical or moderately pleomorphic, with distinct "club-like" projections formed by the spike (S) protein [23, 24] . Within the virion interior lies a helically symmetrical nucleocapsid that encloses a single-stranded and positive sense RNA viral genome of an extraordinarily large size of about 26 to 32 kilobases [20] . The positive sense viral genomic RNA acts as a messenger RNA (mRNA), comprising a 5 terminal cap structure and a 3 poly A tail. This genomic RNA acts in three capacities during the viral life cycle: (1) as an initial RNA of the infectious cycle; (2) as a template for replication and transcription; and (3) as a substrate for packaging into the progeny virus. The replicase-transcriptase is the only protein translated from the genome, while the viral products of all downstream open reading frames are derived from subgenomic mRNAs. In all CoVs, the replicase gene makes up approximately 5 twothirds of the genome and is comprised of two overlapping open reading frames (ORFs), ORF1a and ORF1b, which encodes 16 non-structural proteins. The final one-third of the CoV genomic RNA encodes CoV canonical set of four structural protein genes, in the order of spike (S), envelope (E), membrane (M) and nucleocapsid (N). In addition, several accessory ORFs are also interspersed along the structural protein genes and the number and location varies among CoV species [25] (Figure 1 ).

Answer: Human Coronaviruses: A Review of Virus-Host Interactions

Question: ('filoviruses') that cause severe hemorrhagic fever with human case fatality rates of up to 90%. Filovirus infection requires fusion of the host cell and virus membranes, a process that is mediated by the envelope glycoprotein (GP). GP contains two subunits, the surface subunit (GP1), which is responsible for cell attachment, and the transmembrane subunit (GP2), which catalyzes membrane fusion. The GP2 ectodomain contains two heptad repeat regions, N-terminal and C-terminal (NHR and CHR, respectively) that adopt a six-helix bundle during the fusion process. The refolding of this six-helix bundle provides the thermodynamic driving force to overcome barriers associated with membrane fusion. Here we report the crystal structure of the MARV GP2 core domain in its post-fusion (six-helix bundle) conformation at 1.9 A resolution. The MARV GP2 core domain backbone conformation is virtually identical to that of EBOV GP2 (reported previously), and consists of a central NHR core trimeric coiled-coil packed against peripheral CHR -helices and an intervening loop/helix-turn-helix segment. We previously reported that the stability of the MARV GP2 post-fusion structure is highly pH-dependent, with increasing stability at lower pH [Harrison, J.S.; Koellhoffer, J. K.; Chandran, K.; and Lai, J. R. Biochemistry, 2012Biochemistry, , 51, 2515Biochemistry, -2525. We hypothesized that this pH-dependent stability provides a mechanism for conformational control such that the post-fusion six helix bundle is promoted in the environments of appropriately matured endosomes. In this report, a structural rationale for this pH-dependent stability is described, and involves a high-density array of core and surface acidic side chains at the midsection of the structure, termed the 'anion stripe.' In addition, many surface-exposed salt bridges likely contribute to stabilizing the post-fusion structure at low pH. These results provide structural insights into the mechanism of MARV GP2-mediated membrane fusion.

Answer: Crystal Structure of the Marburg Virus GP2 Core Domain in its Post-Fusion Conformation

Question: Existing and emerging infectious diseases are among the most pressing global threats to biodiversity, food safety and human health. The complex interplay between host, pathogen and environment creates a challenge for conserving species, communities and ecosystem functions, while mediating the many known ecological and socio-economic negative effects of disease. Despite the clear ecological and evolutionary contexts of host-pathogen dynamics, approaches to managing wildlife disease remain predominantly reactionary, focusing on surveillance and some attempts at eradication. A few exceptional studies have heeded recent calls for better integration of ecological concepts in the study and management of wildlife disease; however, evolutionary concepts remain underused. Applied evolution consists of four principles: evolutionary history, genetic and phenotypic variation, selection and eco-evolutionary dynamics. In this article, we first update a classical framework for understanding wildlife disease to integrate better these principles. Within this framework, we explore the evolutionary implications of environment-disease interactions. Subsequently, we synthesize areas where applied evolution can be employed in wildlife disease management. Finally, we discuss some future directions and challenges. Here, we underscore that despite some evolutionary principles currently playing an important role in our understanding of disease in wild animals, considerable opportunities remain for fostering the practice of evolutionarily enlightened wildlife disease management.

Answer:
Applying evolutionary concepts to wildlife disease ecology and management