Part 1. Definition
In this task, you're given a paragraph and title from the research paper. Your task is to classify whether the given title is suitable or not for the research paper based on the given paragraph. Return "True" if title is proper according to paragraph else "False".
Part 2. Example
Paragraph: The severe acute respiratory syndrome (SARS) epidemic originating from China in 2002 was caused by a previously uncharacterized coronavirus that could be identified by specific RT-PCR amplification. Efforts to control future SARS outbreaks depend on the accurate and early identification of SARS-CoV infected patients. A real-time fluorogenic RT-PCR assay based on the 3 -noncoding region (3 -NCR) of SARS-CoV genome was developed as a quantitative SARS diagnostic tool. The ideal amplification efficiency of a sensitive SARS-CoV RT-PCR assay should yield an E value (PCR product concentration increase per amplification cycle) equal to 2.0. It was demonstrated that the 3 -NCR SARS-CoV based RT-PCR reactions could be formulated to reach excellent E values of 1.81, or 91% amplification efficacy. The SARS-CoV cDNA preparations derived from viral RNA extract and the cloned recombinant plasmid both exhibit the identical amplification characteristics, i.e. amplification efficacy using the same PCR formulation developed in this study. The viral genomic copy (or genomic equivalences, GE) per infectious unit (GE/pfu) of SARS-CoV used in this study was also established to be approximate 1200-1600:1. The assay's detection sensitivity could reach 0.005 pfu or 6-8 GE per assay. It was preliminarily demonstrated that the assay could efficiently detect SARS-CoV from clinical specimens of SARS probable and suspected patients identified in Taiwan. The 3 -NCR based SARS-CoV assay demonstrated 100% diagnostic specificity testing samples of patients with acute respiratory disease from a non-SARS epidemic region.
Title: Development and evaluation of an efficient 3 -noncoding region-based SARS coronavirus (SARS-CoV) RT-PCR assay for detection of SARS-CoV
Answer: True
Explanation: The answer is true because the title of the paragraph is correct where it described the development of 3 -noncoding region of SARS-CoV genome and assay efficiently detecting SARS-CoV from clinical specimens.
Part 3. Exercise
Paragraph: are lacking, the present study investigated these missing links during experimental infection of three SPF cats with FECV strain UCD. Two cats showed mild clinical signs, faecal shedding of infectious virus from 4 dpi, a cell-associated viraemia at inconsistent time points from 5 dpi, a highly neutralising antibody response from 9 dpi, and no major abnormalities in leukocyte numbers. Faecal shedding lasted for 28-56 days, but virus shed during this stage was less infectious in enterocyte cultures and affected by mutations. Remarkably, in the other cat neither clinical signs nor acute shedding were seen, but virus was detected in blood cells from 3 dpi, and shedding of non-enterotropic, mutated viruses suddenly occurred from 14 dpi onwards. Neutralising antibodies arose from 21 dpi. Leukocyte numbers were not different compared to the other cats, except for the CD8 + regulatory T cells. These data indicate that FECV can infect immune cells even in the absence of intestinal replication and raise the hypothesis that the gradual adaptation to these cells can allow non-enterotropic mutants to arise. Feline coronaviruses (FCoVs) occur as two pathotypes, associated with either enteric or systemic diseases in cats. Feline enteric coronavirus (FECV) is an enterotropic virus, ubiquitously present in the cat population 1,2 . The enteritis caused by the intestinal replication can manifest as a transient anorexia, weight loss and/or diarrhoea, but clinical signs are often too mild to be noticed 1,3,4 . Feline infectious peritonitis virus (FIPV) most likely arises from FECV by accumulation of mutations in individually infected cats [5] [6] [7] [8] [9] [10] [11] . These yet not fully characterized mutations abrogate the enterocyte tropism but provide the virus with tools to productively replicate in monocytes/macrophages, causing a highly fatal systemic disease, feline infectious peritonitis (FIP), which is characterised by a diffuse vasculitis, polyserositis and severe lymphopaenia 12-17 . To date, it remains unknown where, when, and how this pathotype switch is induced in FECV-infected cats. Due to its pathogenic behaviour, FIPV has received considerable attention, and clinical, virological, and immunological parameters during both natural and experimental FIPV infections have frequently been studied 14-16 . The last decade, comprehensive studies on the FIPV parent virus, FECV, have extensively contributed to our current understanding of the epizootiology and pathogenesis 4,18-20 , but many crucial virological and immunological data on the FECV-cat interactions are missing to fully understand the behaviour of this FIPV parent virus. Due to the lack of an FECV-susceptible cell line, there is so far no information on the infectivity (and its
Title: Experimental feline enteric coronavirus infection reveals an aberrant infection pattern and shedding of mutants with impaired infectivity in enterocyte cultures OPEN
Answer:
True