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: C57 strain mice were inoculated intraperitoneally with denatured mouse hepatitis virus strain 3 particles and virus surface projection, membrane and ribonucleoprotein subeomponents, obtained from detergent treated purified virus preparations. All immunised animals developed high levels of serum antibody directed against the respective antigens, detectable by enzyme-linked immunosorbent assay. Mice that had been immunised with denatured virus particles or surface projections were protected against infection with mouse hepatitis virus strain 3, whereas immunisation with virus membrane or ribonucleoprotein subcomponents failed to protect mice against virus challenge.

Answer: Archives of Virology Antigenieity of Mouse Hepatitis Virus Strain 3 Subeomponents in C57 Strain Miee


Question: Tacaribe virus (TCRV) is a mammalian arenavirus that was first isolated from artibeus bats in the 1950s. Subsequent experimental infection of Jamaican fruit bats (Artibeus jamaicensis) caused a disease similar to that of naturally infected bats. Although substantial attention has focused on bats as reservoir hosts of viruses that cause human disease, little is known about the interactions between bats and their pathogens. We performed a transcriptome-wide study to illuminate the response of Jamaican fruit bats experimentally infected with TCRV. Differential gene expression analysis of multiple tissues revealed global and organ-specific responses associated with innate antiviral responses, including interferon alpha/beta and Toll-like receptor signaling, activation of complement cascades, and cytokine signaling, among others. Genes encoding proteins involved in adaptive immune responses, such as gamma interferon signaling and costimulation of T cells by the CD28 family, were also altered in response to TCRV infection. Immunoglobulin gene expression was also elevated in the spleens of infected bats, including IgG, IgA, and IgE isotypes. These results indicate an active innate and adaptive immune response to TCRV infection occurred but did not prevent fatal disease. This de novo assembly provides a highthroughput data set of the Jamaican fruit bat and its host response to TCRV infection, which remains a valuable tool to understand the molecular signatures involved in antiviral responses in bats.

Answer: Transcriptomic Signatures of Tacaribe Virus-Infected Jamaican Fruit Bats


Question: Recent cases of emergent diseases have renewed interest in the evolutionary and ecological mechanisms that promote parasite adaptation to novel hosts [1] [2] [3] [4] [5] [6] . Crucial to adaptation is the degree of mixing of original, susceptible hosts, and novel hosts. An increase in the frequency of the original host has two opposing effects on adaptation: an increase in the supply of mutant pathogens with improved performance on the novel host [7-9]; and reduced selection to infect novel hosts, caused by fitness costs commonly observed to be associated with host switching [10] [11] [12] [13] [14] [15] [16] [17] . The probability of disease emergence will therefore peak at intermediate frequencies of the original host. We tested these predictions by following the evolution of a virus grown under a range of different frequencies of susceptible (original) and resistant (novel) host bacteria. Viruses that evolved to infect resistant hosts were only detected when susceptible hosts were at frequencies between 0.1% and 1%. Subsequent experiments supported the predictions that there was reduced selection and mutation supply at higher and lower frequencies, respectively. These results suggest that adaptation to novel hosts can occur only under very specific ecological conditions, and that small changes in contact rates between host species might help to mitigate disease emergence.

Answer:
Report Host Mixing and Disease Emergence