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".

Input: Consider Input: Paragraph: The pathology of 2 zoonotic human viral infections that recently emerged, severe acute respiratory syndrome (SARS) due to coronavirus (SARS-CoV) and avian influenza A subtype H5N1, is reviewed and compared based on the literature and the cases examined by the authors. Pneumocytes are the primary target of infection resulting in diffuse alveolar damage. Systemic cytokine activation results in hemophagocytic syndrome, lymphoid depletion, and skeletal muscle fiber necrosis. Severe acute respiratory syndrome induces a more fibrocellular intra-alveolar organization with a bbronchiolitis obliterans organizing pneumoniaQ-like pattern and presence of multinucleated histiocytes and pneumocytes. H5N1 causes a more fulminant and necrotizing diffuse alveolar damage with patchy and interstitial paucicellular fibrosis. Severe acute respiratory syndrome associated coronavirus persists in the lung up to the second month, whereas H5N1 persists in the lung up to the third week. Severe acute respiratory syndrome associated coronavirus disseminates to blood, urine, feces, gastrointestinal tract, and liver. There is recent report of possible cerebral involvement by H5N1 and its isolation in the blood, gastrointestinal tract, and cerebrospinal fluid. More pathologic studies are urgently needed. D
Title: The comparative pathology of severe acute respiratory syndrome and avian influenza A subtype H5N1-a review

Output: True

Input: Consider Input: 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

Output: True

Input: Consider Input: Paragraph: Only a few years ago, viral diagnosis was largely an exercise for academic researchers and public health practitioners with focus on epidemiologic analyses and outbreak prevention, detection, and control. Opportunities for therapeutic intervention were limited to only a few applications such as herpesvirus infections, infl uenza, and HIV/AIDS; hence, once a bacterial or fungal infection was excluded, clinicians were limited to providing supportive care for what was presumed to be a viral syndrome. Public health organizations tracked the incidence of viral infections and the development of resistance to the few antiviral drugs in use and provided input to governments and the pharmaceutical industry regarding selection of vaccine targets. More recently, interest in viral diagnostics has burgeoned with the advent of new tools for detection and discovery, global recognition of pandemic risk, high-throughput drug screening, rational drug design, and immunotherapeutics. An additional impetus has been the implication of viruses in chronic illnesses not previously attributed to infection. The objective of this chapter is to review the factors responsible for the rise in awareness of viral infections, methods for diagnosis and monitoring viral infections, and future prospects for improvements in discovery, detection, and response to the challenges of clinical virology.
Title: Diagnosis, Discovery and Dissection of Viral Diseases
Output: False