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:
The spread of infectious disease epidemics is mediated by human travel. Yet human mobility patterns vary substantially between countries and regions. Quantifying the frequency of travel and length of journeys in well-defined population is therefore critical for predicting the likely speed and pattern of spread of emerging infectious diseases, such as a new influenza pandemic. Here we present the results of a large population survey undertaken in 2007 in two areas of China: Shenzhen city in Guangdong province, and Huangshan city in Anhui province. In each area, 10,000 randomly selected individuals were interviewed, and data on regular and occasional journeys collected. Travel behaviour was examined as a function of age, sex, economic status and home location. Women and children were generally found to travel shorter distances than men. Travel patterns in the economically developed Shenzhen region are shown to resemble those in developed and economically advanced middle income countries with a significant fraction of the population commuting over distances in excess of 50 km. Conversely, in the less developed rural region of Anhui, travel was much more local, with very few journeys over 30 km. Travel patterns in both populations were well-fitted by a gravity model with a lognormal kernel function. The results provide the first quantitative information on human travel patterns in modern China, and suggest that a pandemic emerging in a less developed area of rural China might spread geographically sufficiently slowly for containment to be feasible, while spatial spread in the more economically developed areas might be expected to be much more rapid, making containment more difficult.

Ex Output:
Travel Patterns in China


Ex Input:
Hepatitis C virus (HCV) is thought to be involved in the pathogenesis of autoimmune hepatitis (AIH) type 2, which is defined by the presence of type I antiliver kidney microsome autoantibodies directed mainly against cytochrome P450 (CYP)2D6 and by autoreactive liver infiltrating T cells. Virus-specific CD8 ϩ cytotoxic T lymphocytes (CTLs) that recognize infected cells and contribute to viral clearance and tissue injury during HCV infection could be involved in the induction of AIH. To explore whether the antiviral cellular immunity may turn against self-antigens, we characterized the primary CTL response against an HLA-A * 0201-restricted HCV-derived epitope, i.e., HCV core 178-187, which shows sequence homology with human CYP2A6 and CYP2A7 8-17. To determine the relevance of these homologies for the pathogenesis of HCV-associated AIH, we used synthetic peptides to induce primary CTL responses in peripheral blood mononuclear cells of healthy blood donors and patients with chronic HCV infection. We found that the naive CTL repertoire of both groups contains cross-reactive CTLs inducible by the HCV peptide recognizing both CYP2A6 and CYP2A7 peptides as well as endogenously processed CYP2A6 protein. Importantly, we failed to induce CTLs with the CYPderived peptides that showed a lower capacity to form stable complexes with the HLA-A2 molecule. These findings demonstrate the potential of HCV to induce autoreactive CD8 ϩ CTLs by molecular mimicry, possibly contributing to virus-associated autoimmunity.

Ex Output:
Molecular Mimicry of Human Cytochrome P450 by Hepatitis C Virus at the Level of Cytotoxic T Cell Recognition


Ex Input:
Background: SARS-Cov is the etiologic agent of severe acute respiratory syndrome. An understanding of the antibody responses to the viral components is very important for diagnosis and vaccine development. Objective: The spectrum of SARS-specific antibody profiles in SARS patients was investigated from 7 to 210 days after the onset of the symptoms. Study design: Serial serum samples from 14 SARS patients were isolated from 7 to 210 days after the onset of the symptoms, and were tested for anti-viral IgG and IgM by indirect immunofluorescence tests (IFA), anti-nucleocaspid antibody by ELISA tests and viral neutralization. Results: Anti-viral (IgG) and anti-nucleocaspid antibodies were observed in 13 of 14 patients at 14 days after the onset of symptoms, and in all 14 patients at 30-210 days thereafter. Anti-viral antibody (IgM) was detected maximally at 30 days, later than that for the IgG class. IgM antibody declined and became undetectable between 60 to 180 days after the onset of the symptoms. Neutralizing viral antibodies were demonstrated in the sera from all of the patients with SARS symptoms. Conclusions: Anti-viral IgG, IgM, and anti-nucleocaspid antibodies were detected 7-30 days in patients after the onset of SARS symptoms. Anti-viral IgM antibodies disappeared earlier than IgG. Viral neutralization was demonstrated in the sera from the convalescent patients.

Ex Output:

Antibody responses against SARS-coronavirus and its nucleocaspid in SARS patients