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".

Input: Consider Input: Paragraph: was first discovered in 2012. MERS-CoV can infect multiple host species and cause severe diseases in human. We conducted a series of phylogenetic and bioinformatic analyses to study the evolution dynamics of MERS-CoV among different host species with genomic data. Our analyses show: 1) 28 potential recombinant sequences were detected and they can be classified into seven potential recombinant types; 2) The spike (S) protein of MERS-CoV was under strong positive selection when Middle East Respiratory Syndrome coronavirus (MERS-CoV) is a novel beta-coronavirus with high pathogenicity, which imposes a serious threat to human health 1 . Substantial evidence has showed that MERS-CoVs have existed in central and east Africa for decades 2,3 , and have many natural hosts including two species of bats (Neoromicia capensis and Vespertilio superans), dromedary camel (Camelus dromedarius), and European hedgehog (Erinaceus europaeus) 4-7 . Yet it seemed that human MERS-CoV first isolated in Saudi Arabian in 2012, and then spread among humans worldwide 8 . Studies of prototype human MERS-CoV also suggested that the tMRCA (the time of most recent common ancestor) of human MERS-CoV can be traced back to about 2011 9 . Because the genome sequence of bat MERS-CoV is highly identical to that of human MERS-CoV, it has been indicated that human MERS-CoV might have a bat origin 10 , while there is also some evidence of camel-to-human MERS-CoV transmission 11,12 . Together, these studies proposed that zoonotic event may play a nontrivial part in MERS-CoV evolution and transmission. Previous studies showed that recombination was common among the members of beta-coronavirus 13,14 . By joining the previously unlinked DNA, recombination event can create new viral strains which may be capable of infecting new hosts and evading host's immuno-responses. The phylogenetic analysis showed that there were two main MERS-CoV clades-clade A and B, and clade B can be further divided into five phylogenetic groups 15 . There is evidence that recombination event had happened between group III and group V 15 . However, whether there was potential recombination event happened between the other groups or among multiple phylogenetic groups remains unclear. The genome of MERS-CoV is over 30,000 nucleotides (nt) in length, which contains seven predicted open reading frames (ORFs) and four structural genes-spike (S), envelope (E), membrane (M), and nucleocapsid (N) 16 (supplementary Fig. 1c ). The surface located spike (S) protein of beta-coronaviruses is one of the major determinants in their cross-species transmission because it mediates the virus-receptor recognition and thereby activates viral infection process 17 . Additionally, the receptor binding domain (RBD) on S protein's N-terminal is the key element for beta-coronavirus entering into host cells and the mutations in coronavirus's RBD affects its infection and cross-species capability 18, 19 . For example, the study of the spike protein from severe acute respiratory syndrome coronavirus (SARS-CoV), another beta-coronavirus with high pathogenicity, revealed four amino 
 Title: Evolutionary Dynamics of MERS- CoV: Potential Recombination, Positive Selection and Transmission OPEN

Output: False


Input: Consider Input: Paragraph: The severe acute respiratory syndrome (SARS) pandemic revealed that zoonotic transmission of animal coronaviruses (CoV) to humans poses a significant threat to public health and warrants surveillance and the development of countermeasures. The activity of host cell proteases, which cleave and activate the SARS-CoV spike (S) protein, is essential for viral infectivity and constitutes a target for intervention. However, the identities of the proteases involved have been unclear. Pioneer studies identified cathepsins and type II transmembrane serine proteases as cellular activators of SARS-CoV and demonstrated that several emerging viruses might exploit these enzymes to promote their spread. Here, we will review the proteolytic systems hijacked by SARS-CoV for S protein activation, we will discuss their contribution to viral spread in the host and we will outline antiviral strategies targeting these enzymes. This paper forms part of a series of invited articles in Antiviral Research on ''From SARS to MERS: 10 years of research on highly pathogenic human coronaviruses.'' Ó 
 Title: Proteolytic activation of the SARS-coronavirus spike protein: Cutting enzymes at the cutting edge of antiviral research

Output: False


Input: Consider Input: Paragraph: Vero E6 African green monkey kidney cells are highly susceptible to infection with the newly emerging severe acute respiratory syndrome coronavirus (SARS-CoV), and they are permissive for rapid viral replication, with resultant cytopathic effects. We employed cDNA microarray analysis to characterize the cellular transcriptional responses of homologous human genes at 12 h post-infection. Seventy mRNA transcripts belonging to various functional classes exhibited significant alterations in gene expression. There was considerable induction of heat shock proteins that are crucial to the immune response mechanism. Modified levels of several transcripts involved in pro-inflammatory and anti-inflammatory processes exemplified the balance between opposing forces during SARS pathogenesis. Other genes displaying altered transcription included those associated with host translation, cellular metabolism, cell cycle, signal transduction, transcriptional regulation, protein trafficking, protein modulators, and cytoskeletal proteins. Alterations in the levels of several novel transcripts encoding hypothetical proteins and expressed sequence tags were also identified. In addition, transcription of apoptosis-related genes DENN and hIAP1 was upregulated in contrast to FAIM. Elevated Mx1 expression signified a strong host response to mediate antiviral resistance. Also expressed in infected cells was the C-terminal alternative splice variant of the p53 tumor suppressor gene encoding a modified truncated protein that can influence the activity of wild-type p53. We observed the interplay between various mechanisms to favor virus multiplication before full-blown apoptosis and the triggering of several pathways in host cells in an attempt to eliminate the pathogen. Microarray analysis identifies the critical hostpathogen interactions during SARS-CoV infection and provides new insights into the pathophysiology of SARS. 
 Title: Microarray and real-time RT-PCR analyses of differential human gene expression patterns induced by severe acute respiratory syndrome (SARS) coronavirus infection of Vero cells


Output: True