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: Recent results have provided increasing evidence for the existence of an intermediate membrane compartment between the rough endoplasmic reticulum and the Golgi complex which seems to function in protein sorting and the regulation of membrane traffic in the early part of the exocytic pathway . Localization of resident marker proteins has shown that this compartment consists of both peripheral and central elements . The aim of the present review is to combine the data on the pre-Golgi compartment with previous ideas of membrane traffic at the ER-Golgi interface . We propose a model which describes how mobile, endosome-like elements of the pre-Golgi compartment function in the generation of the compositional andfunctional boundary between the widely distributed ER and the more central4 located Golgi stacks . 
 Title: Pathways of protein sorting and membrane traffic between the rough endoplasmic reticulum and the Golgi complex jaakko Saraste *t and Esa Kuismanent
True

Paragraph: Graphical Abstract Highlights d DENV NS4B induces mitochondria elongation during viral infection d Elongated mitochondria and virus-induced convoluted membranes are physically linked d NS4B inhibits activation of the mitochondrial fission factor DRP1 d Mitochondria elongation alleviates DENV-induced RIG-Idependent innate immunity SUMMARY With no antiviral drugs or widely available vaccines, Dengue virus (DENV) constitutes a public health concern. DENV replicates at ER-derived cytoplasmic structures that include substructures called convoluted membranes (CMs); however, the purpose of these membrane alterations remains unclear. We determine that DENV nonstructural protein (NS)4B, a promising drug target with unknown function, associates with mitochondrial proteins and alters mitochondria morphology to promote infection. During infection, NS4B induces elongation of mitochondria, which physically contact CMs. This restructuring compromises the integrity of mitochondria-associated membranes, sites of ER-mitochondria interface critical for innate immune signaling. The spatio-temporal parameters of CM biogenesis and mitochondria elongation are linked to loss of activation of the fission factor Dynamin-Related Protein-1. Mitochondria elongation promotes DENV replication and alleviates RIG-I-dependent activation of interferon responses. As Zika virus infection induces similar mitochondria elongation, this perturbation may protect DENV and related viruses from innate immunity and create a favorable replicative environment. 
 Title: Dengue Virus Perturbs Mitochondrial Morphodynamics to Dampen Innate Immune Responses Article Dengue Virus Perturbs Mitochondrial Morphodynamics to Dampen Innate Immune Responses
True

Paragraph: Background: During respiratory viral infections host injury occurs due in part to inappropriate host responses. In this study we sought to uncover the host transcriptional responses underlying differences between high-and lowpathogenic infections. Results: From a compendium of 12 studies that included responses to influenza A subtype H5N1, reconstructed 1918 influenza A virus, and SARS coronavirus, we used meta-analysis to derive multiple gene expression signatures. We compared these signatures by their capacity to segregate biological conditions by pathogenicity and predict pathogenicity in a test data set. The highest-performing signature was expressed as a continuum in low-, medium-, and high-pathogenicity samples, suggesting a direct, analog relationship between expression and pathogenicity. This signature comprised 57 genes including a subnetwork of chemokines, implicating dysregulated cell recruitment in injury. Conclusions: Highly pathogenic viruses elicit expression of many of the same key genes as lower pathogenic viruses but to a higher degree. This increased degree of expression may result in the uncontrolled co-localization of inflammatory cell types and lead to irreversible host damage. 
 Title: A chemokine gene expression signature derived from meta-analysis predicts the pathogenicity of viral respiratory infections

False

