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: Using sequence data to infer population dynamics is playing an increasing role in the analysis of outbreaks. The most common methods in use, based on coalescent inference, have been widely used but not extensively tested against simulated epidemics. Here, we use simulated data to test the ability of both parametric and non-parametric methods for inference of effective population size (coded in the popular BEAST package) to reconstruct epidemic dynamics. We consider a range of simulations centred on scenarios considered plausible for pandemic influenza, but our conclusions are generic for any exponentially growing epidemic. We highlight systematic biases in non-parametric effective population size estimation. The most prominent such bias leads to the false inference of slowing of epidemic spread in the recent past even when the real epidemic is growing exponentially. We suggest some sampling strategies that could reduce (but not eliminate) some of the biases. Parametric methods can correct for these biases if the infected population size is large. We also explore how some poor sampling strategies (e.g. that over-represent epidemiologically linked clusters of cases) could dramatically exacerbate bias in an uncontrolled manner. Finally, we present a simple diagnostic indicator, based on coalescent density and which can easily be applied to reconstructed phylogenies, that identifies time-periods for which effective population size estimates are less likely to be biased. We illustrate this with an application to the 2009 H1N1 pandemic. Pandemic growth rates from sequences E. de Silva et al. 1799 Pandemic growth rates from sequences E. de Silva et al. 1807
Title: Inferring pandemic growth rates from sequence data
[A]: True

[Q]: Paragraph: The structure and function of cells are critically dependent on membranes, which not only separate the interior of the cell from its environment but also define the internal compartments. It is therefore not surprising that the major steps of the life cycle of viruses of animals and plants also depend on cellular membranes. Indeed, interactions of viral proteins with host cell membranes are important for viruses to enter into host cells, replicate their genome, and produce progeny particles. To replicate its genome, a virus first needs to cross the plasma membrane. Some viruses can also modify intracellular membranes of host cells to create a compartment in which genome replication will take place. Finally, some viruses acquire an envelope, which is derived either from the plasma membrane or an internal membrane of the host cell. This paper reviews recent findings on the interactions of viral proteins with host cell membranes during the viral life cycle.
Title: Interactions Between Virus Proteins and Host Cell Membranes During the Viral Life Cycle
[A]: False

[Q]: Paragraph: Although mosquitoes serve as vectors of many pathogens of public health importance, their response to viral infection is poorly understood. It also remains to be investigated whether viruses deploy some mechanism to be able to overcome this immune response. Here, we have used an RNA-Seq approach to identify differentially regulated genes in Culex quinquefasciatus cells following West Nile virus (WNV) infection, identifying 265 transcripts from various cellular pathways that were either upregulated or downregulated. Ubiquitin-proteasomal pathway genes, comprising 12% of total differentially regulated genes, were selected for further validation by real time RT-qPCR and functional analysis. It was found that treatment of infected cells with proteasomal inhibitor, MG-132, decreased WNV titers, indicating importance of this pathway during infection process. In infection models, the Culex ortholog of mammalian Cul4A/B (cullin RING ubiquitin ligase) was found to be upregulated in vitro as well as in vivo, especially in midguts of mosquitoes. Gene knockdown using dsRNA and overexpression studies indicated that Culex Cul4 acts as a pro-viral protein by degradation of CxSTAT via ubiquitin-proteasomal pathway. We also show that gene knockdown of Culex Cul4 leads to activation of the Jak-STAT pathway in mosquitoes leading to decrease viral replication in the body as well as saliva. Our results suggest a novel mechanism adopted by WNV to overcome mosquito immune response and increase viral replication. PLOS Pathogens |
Title: Cullin4 Is Pro-Viral during West Nile Virus Infection of Culex Mosquitoes
[A]:
False