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.

Example Input: Foot-and-mouth disease GIS OpenFOAM Livestock infectious diseases, such as foot-and-mouth disease (FMD), cause substantial economic damage to livestock farms and their related industries. Among various causes of disease spread, airborne dispersion has previously been considered to be an important factor that could not be controlled by preventive measures to stop the spread of disease that focus on direct and indirect contact. Forecasting and predicting airborne virus spread are important to make time for developing strategies and to minimise the damage of the disease. To predict the airborne spread of the disease a modelling approach is important since field experiments using sensors are ineffective because of the rarefied concentrations of virus in the air. The simulation of airborne spread during past outbreaks required improvement both for farmers and for policy decision makers. In this study a free license computational fluid dynamics (CFD) code was used to simulate airborne virus spread. Forecasting data from the Korea Meteorological Administration (KMA) was directly connected in the developed model for real-time forecasting for 48 h in three-hourly intervals. To reduce computation time, scalar transport for airborne virus spread was simulated based on a database for the CFD computed airflow in the investigated area using representative wind conditions. The simulation results, and the weather data were then used to make a database for a web-based forecasting system that could be accessible to users. ScienceDirect jo urnal homepage: www .e lsev ie r.com/ locate/issn/153 75110 b i o s y s t e m s e n g i n e e r i n g 1 2 9 ( 2 0 1 5 ) 1 6 9 e1 8 4 http://dx.
Example Output: Web-based forecasting system for the airborne spread of livestock infectious disease using computational fluid dynamics

Example Input: Objective: Human Bocavirus (HBoV) was first identified in 2005 and has been shown to be a common cause of respiratory infections and gastroenteritis in children. In a recent study, we found that 10.7% of children with acute respiratory infections (ARI) were infected by HBoV. Genetic characterization of this virus remains unknown in Central Africa, particularly in Cameroon Leeding us to evaluate the molecular characteristics of HBoV strains in Cameroonian children with ARI. Results: Phylogenetic analysis of partial HBoV VP1/2 sequences showed a low level of nucleotide variation and the circulation of HBoV genotype 1 (HBoV-1) only. Three clades were obtained, two clustering with each of the reference strains ST1 and ST2, and a third group consisting of only Cameroon strains. By comparing with the Swedish reference sequences, ST1 and ST2, Cameroon sequences showed nucleotide and amino acid similarities of respectively 97.36-100% and 98.35-100%. These results could help improve strategies for monitoring and control of respiratory infections in Cameroon.
Example Output: Phylogenic analysis of human bocavirus detected in children with acute respiratory infection in Yaounde, Cameroon

Example Input: The genetic dissection of various human infectious diseases has led to the definition of inborn errors of human STAT1 immunity of four types, including (i) autosomal recessive (AR) complete STAT1 deficiency, (ii) AR partial STAT1 deficiency, (iii) autosomal dominant (AD) STAT1 deficiency, and (iv) AD gain of STAT1 activity. The two types of AR STAT1 defect give rise to a broad infectious phenotype with susceptibility to intramacrophagic bacteria (mostly mycobacteria) and viruses (herpes viruses at least), due principally to the impairment of IFN-γ-mediated and IFN-α/β-mediated immunity, respectively. Clinical outcome depends on the extent to which the STAT1 defect decreases responsiveness to these cytokines. AD STAT1 deficiency selectively predisposes individuals to mycobacterial disease, owing to the impairment of IFN-γ-mediated immunity, as IFN-α/β-mediated immunity is maintained. Finally, AD gain of STAT1 activity is associated with autoimmunity, probably owing to an enhancement of IFN-α/β-mediated immunity. More surprisingly, it is also associated with chronic mucocutaneous candidiasis, through as yet undetermined mechanisms involving an inhibition of the development of IL-17producing T cells. Thus, germline mutations in human STAT1 define four distinct clinical disorders. Various combinations of viral, mycobacterial and fungal infections are therefore allelic at the human STAT1 locus. These experiments of Nature neatly highlight the clinical and immunological impact of the human genetic dissection of infectious phenotypes.
Example Output:
Inborn errors of human STAT1: allelic heterogeneity governs the diversity of immunological and infectious phenotypes