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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Question: Paragraph: Human cytomegalovirus (HCMV) is a ubiquitous betaherpesvirus that frequently causes morbidity and mortality in individuals with insufficient immunity, such as transplant recipients, AIDS patients, and congenitally infected newborns. Several antiviral drugs are approved to treat HCMV infections. However, resistant HCMV mutants can arise in patients receiving long-term therapy. Additionally, side effects and the risk to cause birth defects limit the use of currently approved antivirals against HCMV. Therefore, the identification of new drug targets is of clinical relevance. Recent work identified DNA-damage binding protein 1 (DDB1) and the family of the cellular cullin (Cul) RING ubiquitin (Ub) ligases (CRLs) as host-derived factors that are relevant for the replication of human and mouse cytomegaloviruses. The first-in-class CRL inhibitory compound Pevonedistat (also called MLN4924) is currently under investigation as an anti-tumor drug in several clinical trials. Cytomegaloviruses exploit CRLs to regulate the abundance of viral proteins, and to induce the proteasomal degradation of host restriction factors involved in innate and intrinsic immunity. Accordingly, pharmacological blockade of CRL activity diminishes viral replication in cell culture. In this review, we summarize the current knowledge concerning the relevance of DDB1 and CRLs during cytomegalovirus replication and discuss chances and drawbacks of CRL inhibitory drugs as potential antiviral treatment against HCMV.
Title: Molecular Sciences Cellular Cullin RING Ubiquitin Ligases: Druggable Host Dependency Factors of Cytomegaloviruses

Answer: True

Question: Paragraph: To ensure the safety of wastewater reuse for irrigation of food crops and drinking water pathogenic viruses must be reduced to levels that pose no significant risk. To achieve this goal minimum reduction of viruses by treatment trains have been suggested. For use of edible crops a 6-log reduction and for production of potable drinking water a 12-log reduction has been suggested. These reductions were based on assuming infective virus concentrations of 10 5 to 10 6 per liter. Recent application of molecular methods suggests that some pathogenic viruses may be occurring in concentrations of 10 7 to 10 9 per liter. Factors influencing these levels include the development of molecular methods for virus detection, emergence of newly recognized viruses, decrease in per capita water use due to conservation measures, and outbreaks. Since neither cell culture nor molecular methods can assess all the potentially infectious virus in wastewater conservative estimates should be used to assess the virus load in untreated wastewater. This review indicates that an additional 2-to 3-log reduction of viruses above current recommendations may be needed to ensure the safety of recycled water. Information is needed on peak loading of viruses. In addition, more virus groups need to be quantified using better methods of virus quantification, including more accurate methods for measuring viral infectivity in order to better quantify risks from viruses in recycled water.
Title: How much reduction of virus is needed for recycled water: A continuous changing need for assessment?

Answer: False

Question: Paragraph: The mammalian reoviruses and rotaviruses have evolved specifi c mechanisms to evade the Type I interferon (IFN) antiviral response. Rotavirus likely represses the IFN response by at least 4 mechanisms. First, the rotavirus protein NSP1, most likely functioning as an E3 ligase, can induce proteasome-dependent degradation of the transcription factors IRF3, IRF5, and IRF7 to prevent their induction of IFN. Second, NSP1 can induce proteasome-dependent degradation of the ubiquitin ligase complex protein -TrCP, resulting in stabilization of IB and concomitant failure of virus to activate NF-B for induction of IFN. Third, rotavirus may sequester NF-B in viroplasms. And fourth, rotavirus can prevent STAT1 and STAT2 nuclear translocation. The predominant mechanism for rotavirus inhibition of the IFN response is likely both rotavirus strain-specifi c and cell type-specifi c. The mammalian reoviruses also display strain-specifi c differences in their modulation of the IFN response. Reovirus activates RIG-I and IPS-1 for phosphorylation of IRF3. Reovirus-induced activation of MDA5 also participates in induction if IFN-, perhaps through activation of NF-B. Reovirus likely inhibits the IFN response by at least 3 virus strain-specifi c mechanisms. First, the reovirus 2 protein can induce an unusual nuclear accumulation of IRF9 and repress IFN-stimulated gene (ISG) expression, most likely by disrupting IRF9 function as part of the heterotrimeric transcription factor complex, ISGF3. Second, the reovirus 3 protein can bind dsRNA and prevent activation of the latent antiviral effector protein PKR. And third, genetic approaches have identifi ed the reovirus 2 and 2 proteins in virus strain-specifi c modulation of the IFN response, but the signifi cance remains unclear. In sum, members of the family Reoviridae have evolved a variety of mechanisms to subvert the host's innate protective response. Yue Z, Shatkin AJ. 1997. Double-stranded RNA-dependent protein kinase (PKR) is regulated by reovirus structural proteins. Virology 234(2):364-371. Zurney J, Howard KE, Sherry B. 2007. Basal expression levels of IFNAR and Jak-STAT components are determinants of celltype-specifi c differences in cardiac antiviral responses. J Virol 81(24):13668-13680. Zurney J, Kobayashi T, Holm GH, Dermody TS, Sherry B. 2009. Reovirus mu2 protein inhibits interferon signaling through a novel mechanism involving nuclear accumulation of interferon regulatory factor 9. J Virol 83 (5):2178-2187.
Title: Rotavirus and Reovirus Modulation of the Interferon Response

Answer:
True