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".

[EX Q]: Paragraph: Human cytomegalovirus (HCMV) is a ubiquitous betaherpesvirus that frequently causes morbidity and mortality in individuals with insufficient immunity, such as transplant recipients, AIDS patients, and congenitally infected newborns. Several antiviral drugs are approved to treat HCMV infections. However, resistant HCMV mutants can arise in patients receiving long-term therapy. Additionally, side effects and the risk to cause birth defects limit the use of currently approved antivirals against HCMV. Therefore, the identification of new drug targets is of clinical relevance. Recent work identified DNA-damage binding protein 1 (DDB1) and the family of the cellular cullin (Cul) RING ubiquitin (Ub) ligases (CRLs) as host-derived factors that are relevant for the replication of human and mouse cytomegaloviruses. The first-in-class CRL inhibitory compound Pevonedistat (also called MLN4924) is currently under investigation as an anti-tumor drug in several clinical trials. Cytomegaloviruses exploit CRLs to regulate the abundance of viral proteins, and to induce the proteasomal degradation of host restriction factors involved in innate and intrinsic immunity. Accordingly, pharmacological blockade of CRL activity diminishes viral replication in cell culture. In this review, we summarize the current knowledge concerning the relevance of DDB1 and CRLs during cytomegalovirus replication and discuss chances and drawbacks of CRL inhibitory drugs as potential antiviral treatment against HCMV. 
 Title: Molecular Sciences Cellular Cullin RING Ubiquitin Ligases: Druggable Host Dependency Factors of Cytomegaloviruses
[EX A]: True

[EX Q]: Paragraph: Hepatitis C Virus (HCV) infects 2% of the world's population and is the leading cause of liver disease and liver transplantation. It poses a serious and growing worldwide public health problem that will only be partially addressed with the introduction of new antiviral therapies. However, these treatments will not prevent re-infection particularly in high risk populations. The introduction of a HCV vaccine has been predicted, using simulation models in a high risk population, to have a significant effect on reducing the incidence of HCV. A vaccine with 50 to 80% efficacy targeted to high-risk intravenous drug users could dramatically reduce HCV incidence in this population. Virus like particles (VLPs) are composed of viral structural proteins which self-assemble into non-infectious particles that lack genetic material and resemble native viruses. Thus, VLPs represent a safe and highly immunogenic vaccine delivery platform able to induce potent adaptive immune responses. Currently, many VLP-based vaccines have entered clinical trials, while licensed VLP vaccines for hepatitis B virus (HBV) and human papilloma virus (HPV) have been in use for many years. The HCV core, E1 and E2 proteins can self-assemble into immunogenic VLPs while inclusion of HCV antigens into heterogenous (chimeric) VLPs is also a promising approach. These VLPs are produced using different expression systems such as bacterial, yeast, mammalian, plant, or insect cells. Here, this paper will review HCV VLP-based vaccines and their immunogenicity in animal models as well as the different expression systems used in their production. 
 Title: Preclinical Development and Production of Virus-Like Particles As Vaccine Candidates for Hepatitis C
[EX A]: True

[EX Q]: Paragraph: Multiple sclerosis (MS) is an inflammatory, demyelinating, central nervous system disease mediated by myelin-specific T cells. Environmental triggers that cause a breakdown of myelinspecific T cell tolerance are unknown. We found that CD8 + myelin basic protein (MBP)-specific T cell tolerance can be broken and autoimmunity induced by infection with a virus that does not express MBP cross-reactive epitopes and does not depend on bystander activation. Instead, the virus activated dual T cell receptor (TCR)-expressing T cells capable of recognizing both MBP and viral antigens. These results demonstrate the importance of dual TCR T cells in autoimmunity and suggest a mechanism by which a ubiquitous viral infection could trigger autoimmunity in a subset of infected individuals, as hypothesized in the etiology of MS. Multiple sclerosis (MS) is an inflammatory, demyelinating disease of the central nervous system (CNS) that affects more than one million people worldwide. It is believed to be an autoimmune disease in which exposure of genetically predisposed individuals to environmental factors triggers a breakdown in T cell tolerance to myelin antigens. The specific types of myelin-specific T cells that contribute to the pathogenesis of MS are not known. Most studies have focused on the pathogenic role of myelin-specific CD4 + T cells because of the relatively strong association of MS susceptibility with major histocompatibility complex (MHC) class II alleles. In addition, CD4 + T cells are the primary effector T cells in experimental autoimmune encephalomyelitis (EAE), a widely used animal model of MS. However, there has been increasing recognition of the potential importance of CD8 + T cells in the pathogenesis of MS. CD8 + T cells typically outnumber CD4 + T cells in acute and chronic lesions in MS patients, and the CD8 + T cell subset exhibits more evidence of antigen-driven activation compared to CD4 + T cells in the CNS and blood of MS patients1, 2. The frequency of CNS antigen-specific CD8 + , but not CD4 + , using Power SYBR Green PCR Master Mix (Applied Biosystems). Tcra V α gene primers and a C α primer have been previously described50. Reactions were run in duplicate, and samples were normalized to the internal β actin control. All P values were calculated with a two-tailed Student's t-test. 
 Title: Viral Infection Triggers Central Nervous System Autoimmunity Via Activation of Dual TCR-Expressing CD8 + T Cells HHS Public Access Author manuscript
[EX A]:
False