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: Interactions between the immune system and the central nervous system (CNS) constitute the most complex and interactive regulatory network in mammals. The high degree of specialization of cell types that comprise the CNS, and their intricate communication, controls both cognitive and vital functions. Disruption of the communication network and poor CNS regenerative properties make this organ vulnerable to microbial as well as physical injury. Although it is known that host responses must be strictly regulated to preserve CNS function and to minimize the incidence of autoimmunity, the factors regulating CNS immune and repair responses are not well understood. In addition to the absence of a dedicated lymphatic drainage system, CNS cells express few, if any, molecules encoded by the major histocompatibility complex (MHC) 1-3 . Therefore, in the quiescent CNS there is little endogenous antigen presentation or potential to activate T cells. Although the underlying basis for this limited immunological activity is not completely understood, interactions between both neurons and the glial population represented by microglia, astrocytes and oligodendrocytes (BOX 1), as well as constitutive secretion of neurotrophins and transforming growth factor-β, might contribute to this quiescent resting state 1,4-7 . The limited expression of adhesion molecules by endothelial cells of the blood-brain barrier (BBB) and the presence of tight junctions between these cells also limit or prevent large molecules, such as antibodies, and T cells from entering the CNS 2,8 . Despite this, a few activated/memory CD4 + and CD8 + T cells randomly patrol the CNS in the absence of 'danger' signals, and either exit or die in situ in the absence of antigen recognition 2,8 . Abstract | Several viruses infect the mammalian central nervous system (CNS), some with devastating consequences, others resulting in chronic or persistent infections associated with little or no overt pathology. Coronavirus infection of the murine CNS illustrates the contributions of both the innate immune response and specific host effector mechanisms that control virus replication in distinct CNS cell types. Despite T-cell-mediated control of acute virus infection, host regulatory mechanisms, probably designed to protect CNS integrity, contribute to the failure to eliminate virus. Distinct from cytolytic effector mechanisms expressed during acute infection, non-lytic humoral immunity prevails in suppressing infectious virus during persistence. 
 Title: Neurotrophins Coronavirus infection of the central nervous system: host-virus stand-off

Output: False


Input: Consider Input: Paragraph: Cox, E., Pensaert, M.B., Callebaut, P. and van Deun, K., 1990. Intestinal replication of a porcine respiratory coronavirus closely related antigenically to transmissible gastroenteritis virus. Vet. Microbiol., One-week-old piglets were inoculated with the porcine respiratory coronavirus (PRCV) either intravenously or directly into the lumen of the gastrointestinal tract. Both inoculation routes resulted in the isolation of virus from the caudal small intestine. Viral replication, however, was only observed upon inoculation into the digestive tract in quantities of > 10 3 TCIDso. Replication remained limited to a few unidentified cells located in or underneath the epithelial layer at villus-or crypt-sites. Virus was excreted in the faeces for several days but infection of the respiratory tract occurred rarely in the same pigs. The results of this study indicate that small changes in molecular structure between PRCV and transmissible gastroenteritis virus have resulted in important changes in host cell tropism. 
 Title: Intestinal replication of a porcine respiratory coronavirus closely related antigenically to the enteric transmissible gastroenteritis virus

Output: False


Input: Consider Input: Paragraph: Background: Members of the Baculoviridae encode two types of proteins that mediate virus:cell membrane fusion and penetration into the host cell. Alignments of primary amino acid sequences indicate that baculovirus fusion proteins of group I nucleopolyhedroviruses (NPV) form the GP64 superfamily. The structure of these viral penetrenes has not been determined. The GP64 superfamily includes the glycoprotein (GP) encoded by members of the Thogotovirus genus of the Orthomyxoviridae. The entry proteins of other baculoviruses, group II NPV and granuloviruses, are class I penetrenes. Results: Class III penetrenes encoded by members of the Rhabdoviridae and Herpesviridae have an internal fusion domain comprised of beta sheets, other beta sheet domains, an extended alpha helical domain, a membrane proximal stem domain and a carboxyl terminal anchor. Similar sequences and structural/functional motifs that characterize class III penetrenes are located collinearly in GP64 of group I baculoviruses and related glycoproteins encoded by thogotoviruses. Structural models based on a prototypic class III penetrene, vesicular stomatitis virus glycoprotein (VSV G), were established for Thogoto virus (THOV) GP and Autographa california multiple NPV (AcMNPV) GP64 demonstrating feasible cysteine linkages. Glycosylation sites in THOV GP and AcMNPV GP64 appear in similar model locations to the two glycosylation sites of VSV G. These results suggest that proteins in the GP64 superfamily are class III penetrenes. 
 Title: Virology Journal Proteomics computational analyses suggest that baculovirus GP64 superfamily proteins are class III penetrenes


Output: False