TASK DEFINITION: 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".
PROBLEM: Paragraph: Determining the fitness of viral genotypes has become a standard practice in virology as it is essential to evaluate their evolutionary potential. Darwinian fitness, defined as the advantage of a given genotype with respect to a reference one, is a complex property that captures, in a single figure, differences in performance at every stage of viral infection. To what extent does viral fitness result from specific molecular interactions with host factors and regulatory networks during infection? Can we identify host genes in functional classes whose expression depends on viral fitness? Here, we compared the transcriptomes of tobacco plants infected with seven genotypes of tobacco etch potyvirus that differ in fitness. We found that the larger the fitness differences among genotypes, the more dissimilar the transcriptomic profiles are. Consistently, two different mutations, one in the viral RNA polymerase and another in the viral suppressor of RNA silencing, resulted in significantly similar gene expression profiles. Moreover, we identified host genes whose expression showed a significant correlation, positive or negative, with the virus' fitness. Differentially expressed genes which were positively correlated with viral fitness activate hormone-and RNA silencing-mediated pathways of plant defense. In contrast, those that were negatively correlated with fitness affect metabolism, reducing growth, and development. Overall, these results reveal the high information content of viral fitness and suggest its potential use to predict differences in genomic profiles of infected hosts. 
 Title: Viral Fitness Correlates with the Magnitude and Direction of the Perturbation Induced in the Host's Transcriptome: The Tobacco Etch Potyvirus-Tobacco Case Study

SOLUTION: False

PROBLEM: Paragraph: Ever since the discovery of SARS-CoV in the year 2003, numerous researchers around the world have been working relentlessly to understand the biology of this virus. As in other coronaviruses, nucleocapsid (N) is one of the most crucial structural components of the SARS-CoV. Hence major attention has been focused on characterization of this protein. Independent studies conducted by several laboratories have elucidated significant insight into the primary function of this protein, which is to encapsidate the viral genome. In addition, many reports also suggest that this protein interferes with different cellular pathways, thus implying it to be a key regulatory component of the virus too. In the first part of this review, we will discuss these different properties of the N-protein in a consolidated manner. Further, this protein has also been proposed to be an efficient diagnostic tool and a candidate vaccine against the SARS-CoV. Hence, towards the end of this article, we will discuss some recent progress regarding the possible clinically relevant use of the N-protein. # 
 Title: The SARS-CoV nucleocapsid protein: A protein with multifarious activities

SOLUTION: True

PROBLEM: Paragraph: cally active but which do not bind antibody 259 have been prepared recently; cells transformed by such mutants were not altered morphologically, nor did they show greatly inhibited thymidine incorporation, after injection of antibody 259 26 • It is assumed that while viral oncogenes function without normal control, their mechanism of action is similar to that of related cellular genes. Here we have presented evidence to support this idea in the case of growth factor receptor-like molecules and related oncogenes. It is therefore possible that these data might aid in understanding the way in which cellular genes interact in the control of normal proliferation. Our results indicate that some receptor-like oncogenes depend on ras proteins while some cytoplasmic oncogenes do not. There are, of course, numerous oncogenes which we have not yet tested which might behave differently from those described here. With this limitation in mind and on the basis of our present data, we propose that an important class of proliferative signals are received at the cell surface by receptor molecules such as growth factor receptors, and the c-ras proteins are essential in the transfer of these signals to cytoplasmic effectors having serine kinase activity; the effectors then modify target molecules which are directly involved in initiating a proliferative cycle. Accordingly, if the cytoplasmic effector were mutated such that it functioned without activation, proliferation would continue independently of c-ras proteins. Receptor molecules, on the other hand, would always require c-ras to stimulate proliferation. While our data are consistent with the above scheme, they do not exclude many other possibilities involving multiple metabolic pathways and more complex interactions. For example, we have not reported results with nuclear oncogenes owing to their difficulty in transforming NIH 3T3 cells. The proposed scheme is primarily attractive because of its similarity to the carefully studied mechanism of signal transduction involving cyclic AMP. While it is unlikely that cyclic AMP itself regulates proliferation 27 , G-regulatory proteins with enzymatic similarities to c-ras proteins are involved. These regulatory proteins control signal transduction from cell-surface receptors to cytoplasmic serine kinase effector molecules by regulating adenyl cyclase activity28. While the present study has examined only one aspect of what is likely to be a highly complex system for regulating proliferation, it does provide a means of functionally comparing separate viral oncogenes. Injection of antibody has been used in other studies to characterize the types of molecules responsible for tumour cell proliferation. Like NIH 3T3 cells transformed by mos or raj genes, many tumour cells show no inhibition of proliferation when injected with anti-ras antibody. In this way their proliferation is distinct from that of the normal cell types studied, each of which was efficiently inhibited by the injected antibodyl6. 
 Title: Viral particles induce Ia antigen expression on astrocytes

SOLUTION:
False