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".

Paragraph: Contact patterns among hosts are considered as one of the most critical factors contributing to unequal pathogen transmission. Consequently, networks have been widely applied in infectious disease modeling. However most studies assume static network structure due to lack of accurate observation and appropriate analytic tools. In this study we used high temporal and spatial resolution animal position data to construct a high-resolution contact network relevant to infectious disease transmission. The animal contact network aggregated at hourly level was highly variable and dynamic within and between days, for both network structure (network degree distribution) and individual rank of degree distribution in the network (degree order). We integrated network degree distribution and degree order heterogeneities with a commonly used contact-based, directly transmitted disease model to quantify the effect of these two sources of heterogeneity on the infectious disease dynamics. Four conditions were simulated based on the combination of these two heterogeneities. Simulation results indicated that disease dynamics and individual contribution to new infections varied substantially among these four conditions under both parameter settings. Changes in the contact network had a greater effect on disease dynamics for pathogens with smaller basic reproduction number (i.e. R 0 , 2). 
 Title: Highly dynamic animal contact network and implications on disease transmission
True

Paragraph: Human rhinovirus 3C protease (HRV 3C pro ) is known to be a promising target for development of therapeutic agents against the common cold because of the importance of the protease in viral replication as well as its expression in a large number of serotypes. To explore non-peptidic inhibitors of HRV 3C pro , a series of novel heteroaromatic esters was synthesized and evaluated for inhibitory activity against HRV 3C pro , to determine the structure-activity relationships. The most potent inhibitor, 7, with a 5-bromopyridinyl group, had an IC 50 value of 80 nM. In addition, the binding mode of a novel analog, 19, with the 4hydroxyquinolinone moiety, was explored by molecular docking, suggesting a new interaction in the S1 pocket. Ó 2009 Elsevier Ltd. All rights reserved. Picornaviruses include important human pathogens such as human rhinovirus (HRV), enterovirus (EV), coxsackievirus (CV), poliovirus (PV), and hepatitis A virus (HAV). HRVs are the single major cause of the common cold in populations of all ages. 1,2 Although rhinovirus infection is self-limiting, complications still occur in patients with asthma, congestive heart failure, bronchiectasis, and cystic fibrosis. 1 To date, no agent has been approved by the FDA for treatment of rhinovirus infection. In addition, the large number (>100) of known HRV serotypes makes vaccine development difficult. 3 Clinical treatments are directed toward relief of the most prominent symptoms of each clinical syndrome. Previous work on anti-rhinoviral therapeutic agents focused principally on capsid-binding anti-picornaviral compounds 4 and HRV 3C protease (3C pro ) inhibitors. 5, 6 HRV 3C pro is essential for virus replication, specifically catalyzing the cleavage of glutamine-glycine peptide bonds in a 230 kDa viral polyprotein produced by cellular translation of the viral RNA genome. HRV 3C pro belongs to the cysteine protease family, showing structural similarity to trypsin proteases, but sharing minimal homology with common mammalian enzymes. 7,8 Because of the importance of the enzyme in viral replication, and the high conservation of enzyme active site components in all known HRV serotypes, potent and selective HRV 3C pro inhibitors could be potential broad-spectrum anti-rhinoviral therapeutic agents. [9] [10] [11] As part of an effort to develop HRV 3C pro inhibitors, peptidomimetic approaches have been widely employed based on active site structure and cleavage specificity. To date, one peptidomimetic analog, rupintrivir (AG7088) (1), shown in Figure 1 , is the only HRV 3C Pro inhibitor that has advanced to the stage of human clinical trials. Phase II clinical trials of rupintrivir showed that intranasal delivery reduced the mean total daily symptom score by 33%. 12 Recently, several efforts to develop orally bioavailable anti-rhinoviral agents have been reported; these include a rupintrivir analog, 2, 13 with an improved pharmacokinetic profile, and the non-peptidic inhibitors 3 and 4. 14-16 The crystal structure of severe acute respiratory syndrome (SARS) coronavirus 3C-like protease (3CL pro ) 17 revealed a high similarity of active site architecture to that of HRV 3C pro , suggesting that picornavirus 3C pro and SARS 3CL pro inhibitors should cross-react. In fact, SARS 3CL pro inhibitors were developed by modifying rupintrivir 18 and common inhibitors with IC 50 values in the micromolar range were recently identified for both picornavirus 3C pro and coronavirus 3CL pro using high-throughput screening. 19,20 The pyridinyl thiophene ester 5 was discovered by screening a small molecule library (50,000 molecules) and has significant inhibitory activity against both HAV 3C pro and SARS 3CL pro (IC 50 = 0.5 lM). 19, 21 Further work on a series of heteroaromatic esters resulted in the discovery of the most potent ester 6, inhibiting SARS 3CL pro with an IC 50 of 30 nM and an antiviral activity (EC 50 value) of 6.9 lM. 22 Another analog, 7, also showed potent inhibition of HAV 3C pro with an IC 50 of 53 nM. 23 Studies on the inhibitory and molecular docking mechanisms of heteroaromatic esters have shown that the 5-halopyridine moiety is crucial in binding to the S1 pocket, because both 3C pro and 3CL pro show high specificity for Gln as the P1 residue. 23 0960-894X/$ -see front matter Ó 
 Title: Structure-activity relationships of heteroaromatic esters as human rhinovirus 3C protease inhibitors
True

Paragraph: The presence of immunoglobulin oligoclonal bands in the cerebrospinal fluid of Multiple Sclerosis (MS) patients supports the hypothesis of an infectious etiology, although the antigenic targets remain elusive. Neurotropic mouse hepatitis virus (MHV) infection in mice provides a useful tool for studying mechanisms of demyelination in a virus-induced experimental model of MS. This study uses Affymetrix microarray analysis to compare differential spinal cord mRNA levels between mice infected with demyelinating and non-demyelinating strains of MHV to identify host immune genes expressed in this demyelinating disease model. The study reveals that during the acute stage of infection, both strains induce inflammatory innate immune response genes, whereas upregulation of several immunoglobulin genes during chronic stage infection is unique to infection with the demyelinating strain. Results suggest that the demyelinating strain induced an innate-immune response during acute infection that may promote switching of Ig isotype genes during chronic infection, potentially playing a role in antibody-mediated progressive demyelination even after viral clearance. 
 Title: Demyelinating strain of mouse hepatitis virus infection bridging innate and adaptive immune response in the induction of demyelination

True