instruction:
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".
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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
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True


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Paragraph: The simian hemorrhagic fever virus (SHFV) genome differs from those of other members of the family Arteriviridae in encoding three papain-like one proteases (PLP1␣, PLP1␤ and PLP1␥) at the 5 end and two adjacent sets of four minor structural proteins at the 3 end. The catalytic Cys and His residues and cleavage sites for each of the SHFV PLP1s were predicted and their functionality was tested in in vitro transcription/translation reactions done with wildtype or mutant polyprotein constructs. Mass spectrometry analyses of selected autoproteolytic products confirmed cleavage site locations. The catalytic Cys of PLP1␣ is unusual in being adjacent to an Ala instead of a Typ. PLP1␥ cleaves at both downstream and upstream sites. Intermediate precursor and alternative cleavage products were detected in the in vitro transcription/translation reactions but only the three mature nsp1 proteins were detected in SHFV-infected MA104 cell lysates with SHFV nsp1 protein-specific antibodies. The duplicated sets of SHFV minor structural proteins were predicted to be functionally redundant. A stable, full-length, infectious SHFV-LVR cDNA clone was constructed and a set of mutant infectious clones was generated each with the start codon of one of the minor structural proteins mutated. All eight of the minor structural proteins were found to be required for production of infectious extracellular virus. SHFV causes a fatal hemorrhagic fever in macaques but asymptomatic, persistent infections in natural hosts such as baboons. SHFV infections were compared in macrophages and myeloid dendritic cells from baboons and macaques. Virus yields were higher from macaque cells than from baboon cells. Macrophage cultures from the two types of animals differed dramatically in the percentage of cells infected. In contrast, similar percentages of myeloid dendritic cells were infected but virus replication was efficient in the macaque cells but inefficient in the baboon cells. SHFV infection induced the production of pro-inflammatory cytokines, including IL-1␤, IL-6, IL-12/23(p40), TNF-␣ and MIP-1␣, in macaque cells but not baboon cells. (M.A. Brinton). capsid types (coronaviruses-helical and arteriviruses-spherical) and virion sizes. Arteriviruses infect macrophages (M s) and dendritic cells (DCs) and have restricted host ranges; EAV infects horses and donkeys, PRRSV infects pigs, LDV infects mice and SHFV infects nonhuman primates (NHPs) (Snijder and Meulenberg, 1998) . Disease symptoms associated with EAV and PRRSV infections include fever, respiratory disease, tissue necrosis and spontaneous abortions while LDV typically causes an asymptomatic, persistent infection (Snijder and Spaan, 2006) . The majority of research on arteriviruses has focused on EAV and PRRSV due to the significant agricultural impact of the diseases they cause. SHFV was first isolated in 1964 as the causative agent of hemorrhagic fever outbreaks associated with high mortality in macaque colonies in the United States and the USSR http://dx. 
 Title: Simian hemorrhagic fever virus: Recent advances
answer:
True


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Paragraph: Risk of COVID-19 infection in Wuhan has been estimated using imported case counts of international travelers, often under the assumption that all cases in travelers are ascertained. Recent work indicates variation among countries in detection capacity for imported cases. Singapore has historically had very strong epidemiological surveillance and contact-tracing capacity and has shown in the COVID-19 epidemic evidence of a high sensitivity of case detection. We therefore used a Bayesian modeling approach to estimate the relative imported case detection capacity for other countries compared to that of Singapore. We estimate that the global ability to detect imported cases is 38% (95% HPDI 22% -64%) of Singapore's capacity. Equivalently, an estimate of 2.8 (95% HPDI 1.5 -4.4) times the current number of imported cases, could have been detected, if all countries had had the same detection capacity as Singapore. Using the second component of the Global Health Security index to stratify likely case-detection capacities, we found that the ability to detect imported cases relative to Singapore among high surveillance locations is 40% (95% HPDI 22% -67%), among intermediate surveillance locations it is 37% (95% HPDI 18% -68%), and among low surveillance locations it is 11% (95% HPDI 0% -42%). Using a simple mathematical model, we further find that treating all travelers as if they were residents (rather than accounting for the brief stay of some of these travelers in Wuhan) can modestly contribute to underestimation of prevalence as well. We conclude that estimates of case counts in Wuhan based on assumptions of perfect detection in travelers . CC-BY-NC-ND 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. : medRxiv preprint term can be well approximated as We plot this approximation of V given doubling times . V ≈ 1 − e −(r+γ)d aligned with 4 , a range of durations of detectable infection and a range of lengths of stay 2 ( Figure 2 ). We estimate that the global ability to detect imported cases is 38% ( 95% HPDI 22% -64%) of Singapore's capacity. Equivalently, an estimate of 2.8 (95% HPDI 1.5 -4.4) times the current number of imported cases, could have been detected, if all countries had had the same detection capacity as Singapore, which leads to 1.8 (95% CI 0.5 -3.4) undetected cases per detected case. The ability to detect imported cases among high surveillance countries is 40% (95% HPDI 22% -67%), among intermediate surveillance countries it is 37% (95% HPDI 18% -68%), and among low surveillance countries it is 11% (95% HPDI 0% -42%). : medRxiv preprint 7 In this paper, we have aimed to test two assumptions underlying the estimation of incidence at the epicentre of the SARS-Cov2 outbreak. The first of these is that the capacity for detection of international imported cases is 100% sensitive and specific across locations. While we know of no reason to doubt specificity of detection, we tested the assumption of perfect sensitivity. Based on our previous estimates 5 we assumed Singapore has the highest capacity of surveillance with respect to COVID-19. We regressed the cumulative cases against Wuhan-to-location air travel volume considering Singapore to have the greatest detection capacity and estimating the relative underdetection compared to Singapore in the remaining 190 locations classified according to the GHS 2 index 9 . While it is unlikely that this index reflects the true ranking of countries for any specific epidemic, such as the current one of COVID-19, we assume that it captures different levels of surveillance capacity. We therefore grouped the remaining locations into three big classes high, medium, and low surveillance capacity instead of using exact ranking. We estimated that detection of exported cases from Wuhan worldwide is 38% (95% HPDI 22%-64%) as sensitive as it has been in Singapore. Put another way, this implies that the true number of cases in travelers is at least 2.8 (95% HPDI 1.5 -4.4) times the number that has been detected. Equivalently, for each detected case there are at least 1.8 (95% CI 0.5-3.4) undetected cases. If the model is correct, this is an upper bound on the detection frequency because (1) Singapore's detection is probably not 100% efficient. Singapore had as of 12 February 2020 eight 
 Title: Quantifying bias of COVID-19 prevalence and severity estimates in Wuhan, China that depend on reported cases in international travelers
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False