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".

[Q]: Paragraph: Ageing individuals are immunologically characterized by loss of immunological protection and responsiveness, and autoimmunity occurs with increased incidence. Here we review studies on specific age-related changes in B cell generation, activation, and maintenance as well as characteristics of B cell responses and antibody levels during ageing in relation to other cells and factors that are interwoven with B cell biological processes. In the elderly, fewer new B cells are generated, B cell responsiveness to antigens is impaired, and smaller and fewer germinal centers are formed within an immune response with participation of less potent T cells and follicular dendritic cells, leading to the production of reduced, often insufficient plasma cell numbers. Recall responses in the elderly appear to be limited by the cells' proliferative capacity. Hence, vaccine responsiveness is often insufficient and autoantibody production emerges in the elderly. In total, B cells appear to be less affected by age as compared with T cells. Recently, new concepts have been developed to counteract immunosenescence beyond active vaccination, comprising the generation of specific monoclonal antibodies for passive vaccination, immune rejuvenation by immunoablation followed by autologous stem cell transplantation, and modulation of lifestyle. 
 Title: Characteristics of B Cells and B Cell Responses in Aged Individuals
[A]: True


[Q]: Paragraph: As simple organisms with a parasite nature, viruses have become masters in manipulating and subvert cellular components, including host proteins and organelles, to improve viral replication. Therefore, the understanding of viral strategies to manipulate cell function disrupting plant defenses and enhancing viral infection cycles is fundamental to the production of virus-resistant plant lines. After invading susceptible plants, viruses create conditions that favor local and systemic infections by suppressing multiple layers of innate host defenses while use cellular machinery to own benefit. Viral interference in interlinked essential cellular functions results in phenotypic changes and disease symptoms, which debilitates plants favoring infection establishment. Herein in this review, the novelty it will be the discussion about the strategies used by (+) single strand RNA viruses to affect cellular processes and components to improve viral replication, in parallel to overcome plant defenses, favoring disease establishment by applying in one action using the same viral protein to coordinate viral replication and breaking down plant defense. This focus on plant-virus interaction was never done before, and this knowledge has the potential to help in the development of new strategies to produce resistant plants. 
 Title: Killing two birds with one stone: How do Plant Viruses Break Down Plant Defenses and Manipulate Cellular Processes to Replicate Themselves?
[A]: True


[Q]: Paragraph: Vesiculoviruses enter cells by membrane fusion, driven by a large, low-pH-induced, conformational change in the fusion glycoprotein (G) that involves transition from a trimeric pre-fusion to a trimeric post-fusion state. G is the model of class III fusion glycoproteins which also includes the fusion glycoproteins of herpesviruses (gB) and baculoviruses (gp64). Class III fusion proteins combine features of the previously characterized class I and class II fusion proteins. In this review, we first present and discuss the data that indicate that the Vesiculovirus G structural transition proceeds through monomeric intermediates. Then, we focus on a recently determined crystal structure of the Chandipura virus G ectodomain that contained two monomeric intermediate conformations of the glycoprotein, revealing the chronological order of the structural changes in the protein and offering a detailed pathway for the conformational change, in agreement with electron microscopy data. In the crystal, the intermediates were associated through their fusion domain in an antiparallel manner to form an intermolecular β-sheet. Mutagenesis indicated that this interface is functionally relevant. All those structural data challenge the current model proposed for viral membrane fusion. Therefore, we wonder if this mode of operating is specific to Vesiculovirus G and discuss data indicating that class II fusion glycoproteins are monomeric when they interact with the target membrane but also crystal structures suggesting the existence of non-trimeric intermediates for influenza hemagglutinin which is the prototype of class I fusion proteins. 
 Title: Monomeric Intermediates Formed by Vesiculovirus Glycoprotein during Its Low-pH-induced Structural Transition
[A]:
False