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:
Synthetic decapeptides (N ¼ 206) covering the entire sequence of mouse liver fumarylacetoacetate hydrolase (FAH) were used to analyze the specificities of the autoantibodies (autoAb) elicited towards this enzyme in mice infected with mouse hepatitis virus (MHV). These autoAb bound mainly to N-and C-terminal FAH peptides, the most reactive sequences being 1e50 and 390e420, respectively. Surprisingly, although FAH sequence 1e50 shares a high degree of homology with various MHV proteins, the C-terminal portion does not. Moreover, whereas the autoAb reacted with homologous peptides surrounding residues 70, 160 and 360, non-similar sequences around residues 130, 210, 240, 250, and 300 were also recognized, indicating that autoAb were not restricted to epitopes with sequence homologies. There was also a lack of correlation between the amount of anti-MHV or anti-FAH antibodies produced and the reactivity towards the peptides. Moreover, the spectrum of peptides recognized by the autoAb of a given mouse did not change significantly with time, which suggests that the MHV-elicited autoimmune response does not induce an epitope recognition spreading. Finally, anti-FAH Ab produced after immunization with rat liver FAH recognized essentially the same mouse FAH regions than autoAb from MHV-infected mice. Results indicated that the induction of the autoAb is not only related to molecular or structural mimicry, but rather supports the Danger model, in which any aggression, in this case the MHV infection, is susceptible to trigger the production of autoAb.

Ex Output:
The peptide specificities of the autoantibodies elicited by mouse hepatitis virus A59


Ex Input:
The objectives were to determine the median infective dose (ID 50 ) of Cryptosporidium parvum and to describe the dose-response relationship including associated clinical illness in experimentally challenged dairy calves. Within the first 24 h of life, 27 test calves were experimentally challenged with C. parvum oocysts and 3 control calves were sham dosed. Test calves received 1 of 8 possible doses (25, 50, 100, 500, 1 × 10 3 , 1 × 10 4 , 1 × 10 5 , and 1 × 10 6 oocysts). All 27 test calves developed diarrhea. Fecal oocyst shedding occurred in 25 (92.6%) test calves and in 0 control calves. The 2 non-shedding test calves both received 25 oocysts. There was an inverse relationship between dose and time to onset of fecal oocyst shedding (P = 0.005). There was no relationship found between dose and duration (P = 0.2) or cessation (P = 0.3) of fecal oocyst shedding. In addition, there was not a significant relationship between log-dose and the log-peak oocysts (P = 0.2) or log-total oocysts (P = 0.5) counted/g of feces across the dose groups. There was a positive dose-response relationship between log-dose and diarrhea (P = 0.01). However, when controlling for other factors, such as onset and cessation of fecal oocyst shedding, dose was not a significant predictor of diarrhea (P = 0.5). Onset and cessation of fecal oocyst shedding were found to be the best predictors of diarrhea (P = 0.0006 and P = 0.04, respectively). The ID 50 for fecal oocyst shedding was 5.8 oocysts, for diarrhea was 9.7 oocysts, and for fecal oocyst shedding with diarrhea was 16.6 oocysts. Given that the ID 50 of C. parvum is far less than would be excreted into the environment by a naturally infected calf, prevention and control of cryptosporidiosis is a formidable challenge.

Ex Output:
Cryptosporidium parvum: Determination of ID 50 and the dose-response relationship in experimentally challenged dairy calves


Ex Input:
The CPK cells derived from swine kidney were infected with the attenuated TO-163 strain of transmissible gastroenteritis (TGE) virus, and fused with uninfected Vero cells in the presence of polyethylene glycol. Repeated cocultivafion of the fused cells with uninfected Vero cells rendered the virus to grow in Vero cells. The Vero cell-adapted virus acquired the ability to infect and produce cytopathic effects in several other non-permissive cell lines of nonporcine origin. No major differences in viral polypeptides were shown between the Vero cell-adapted TO-163 strain and its parent strain by indirect immunofluorescence and Western blotting using monoclonal and polyclonal antibodies to TGE virus. Transmissible gastroenteritis (TGE) virus is a coronavirus with an envelope and positive strand RNA genome. The virion contains 3 structural proteins, i.e., peplomer (S or E 2), transmembrane (M or E 1), and nucleocapsid (N) [4] . The virus replicates predominantly in villous epithelial cells of the small intestines, and results in diarrhea in infected pigs [11, 17] . Although clinical symptoms are not clearly demonstrated, the respiratory tract and the tonsils are also susceptible to infection [3, 8, 15] . The host range of TGE virus is restricted like the other coronaviruses [16], and for the propagation of the virus, swine cell cultures are commonly used, although canine [12] and feline [6] cell cultures are less often used. An attempt was made to adapt TGE virus to Vero cells non-permissive to TGE virus infection. The CPK cells derived from swine kidney [10] were inoculated with the avirulent TO-163 strain of TGE virus [5], at a multiplicity of infection of 10, and incubated at 37 °C for 18 h. The infected cells were fused

Ex Output:

Adaptation of transmissible gastroenteritis virus to growth in non-permissive Vero cells Brief Report