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".

Example Input: Paragraph: Avian infectious bronchitis virus (IBV) is a coronavirus which infects chickens (Gallus gallus) of all ages and causes significant economic losses to the poultry industry worldwide. The present study aims to analyze the miRNAs related to pathogenicity of nephropathogenic IBVs. It was found that four miRNAs (miR-1454, miR-3538, miR-146a-5p and miR-215-5p) were related to the infection of virulent nephropathogenic IBV with transcript per million (TPM) > 500 and more than a 2-fold alteration. In vitro study results showed that the alterations of these four miRNAs were consistent with in vivo data. In vitro, we found that high levels of miR-146a-5p could enhance the replication of IBV at the early stage of infection, and its down regulated level could slow down the replication of IBV. Finally, high levels of exogenous miR-146a-5p in HD11 cells led to down regulation of IL-1 receptor associated kinase-2 (IRAK2) and Tumor necrosis factor receptor superfamily member 18 (TNFRSF18) genes. Luciferase reporter assays revealed that miR-146a-5p could bind to the 3-UTRs of IRAK2 and TNFRSF18. This is the first study demonstrating that IBV induced miR-146a-5p is related to virus pathogenesis by down regulating IRAK2 and TNFRSF18, which may serve as a therapeutic strategy for the prevention of IBV infections. * Corresponding author. Tel./fax: +86 028 8547 1599.
Title: miR-146a-5p promotes replication of infectious bronchitis virus by targeting IRAK2 and TNFRSF18
Example Output: True

Example Input: Paragraph: There is an urgent need to project how transmission of the novel betacoronavirus SARS-CoV-2 will unfold in coming years. These dynamics will depend on seasonality, the duration of immunity, and the strength of cross-immunity to/from the other human coronaviruses. Using data from the United States, we measured how these factors affect transmission of human betacoronaviruses HCoV-OC43 and HCoV-HKU1. We then built a mathematical model to simulate transmission of SARS-CoV-2 through the year 2025. We project that recurrent wintertime outbreaks of SARS-CoV-2 will probably occur after an initial pandemic wave. We summarize the full range of plausible transmission scenarios and identify key data still needed to distinguish between them, most importantly longitudinal serological studies to determine the duration of immunity to SARS-CoV-2. Main text. The ongoing SARS-CoV-2 epidemic has caused nearly 80,000 detected cases of COVID-19 illness and claimed over 2,500 lives as of 24 Feb 2020 (1). With sustained transmission reported in China, Japan, Iran, Italy, and South Korea (1), the outbreak is on the verge of becoming a pandemic. The required intensity, duration, and urgency of public health responses will depend on how the initial pandemic wave unfolds and on the subsequent transmission dynamics of SARS-CoV-2. One possibility is that SARS-CoV-2 will follow its closest genetic relative, SARS-CoV, and be eradicated by intensive public health measures after causing a brief but intense epidemic (2). Increasingly, public health authorities consider this scenario unlikely (3). Alternatively, the transmission of SARS-CoV-2 could resemble that of pandemic influenza by circulating seasonally after causing an initial global wave of infection (4). Such a scenario could reflect the previous emergence of known human coronaviruses from zoonotic origins e.g. human coronavirus (HCoV) OC43 (5). This paper identifies viral, environmental, and immunologic factors which in combination will determine which scenarios in fact play out, and identifies key data needed to distinguish between them. The transmission dynamics of the SARS-CoV-2 epidemic will depend on factors including the degree of seasonal variation in transmission strength, the duration of immunity, and the degree of cross-immunity between SARS-CoV-2 and other coronaviruses. SARS-CoV-2 belongs to the betacoronavirus genus, which includes the SARS coronavirus, MERS coronavirus, and two other human coronaviruses, HCoV-OC43 and HCoV-HKU1. The SARS and MERS coronaviruses cause severe illness with case fatality rates of 9 and 36% respectively, but the transmission of both has remained limited (6). HCoV-OC43 and HCoV-HKU1 infections may be asymptomatic or associated with mild to moderate upper respiratory tract illness; these HCoVs are considered the second most common cause of the common cold (6). While investigations into the spectrum of illness caused by SARS-CoV-2 are ongoing, recent evidence indicates the majority of cases experience mild illness with more limited occurrence of severe lower respiratory infection (7). Current COVID-19 case fatality rates in China are estimated at 2.9% within Hubei province, and 0.4% outside (8), suggesting lower severity than SARS and MERS but higher severity than HCoV-OC43 and HCoV-HKU1. In terms of transmission, the ability of SARS-CoV-2 to cause widespread infection is more reflective of HCoV-OC43 and HCoV-HKU1 than of its more clinically severe relatives. HCoV-OC43 and HCoV-HKU1 cause annual wintertime outbreaks of respiratory illness in temperate regions (9, 10), suggesting that wintertime climate and host behaviors may facilitate transmission, as is true for influenza (11) (12) (13) . Immunity to HCoV-OC43 and HCoV-HKU1 appears to wane appreciably within one year (14), while SARS infection can induce longer-lasting immunity (15). The . CC-BY-NC-ND 4.0 International license It is made available under a author/funder, who has granted medRxiv a license to display the preprint in perpetuity. is the (which was not peer-reviewed) The copyright holder for this preprint .
Title: Projecting the transmission dynamics of SARS-CoV-2 through the post-pandemic period
Example Output: False

Example Input: Paragraph: Interferon lambda 4 (IFN4) has been recently known and studied for its role in hepatitis C virus (HCV) infection, but its clinical potential is significantly hampered due to its poor expression in vitro. Our study reports the successful production of IFN4 from a mammalian cell line through a glycoengineering and structure-based approach. We introduced de novo N-glycosylation of IFN4, guided by structural analysis, and produced IFN4 variants in Expi293F that displayed improved expression and potency. To preserve the structure and functionality of IFN4, the model structure of the IFN4 signaling complex was analyzed and the N-glycosylation candidate sites were selected. The receptor binding activity of engineered IFN4 variants and their receptormediated signaling pathway were similar to the E. coli version of IFN4 (eIFN4), while the antiviral activity and induction levels of interferon-stimulated gene (ISG) were all more robust in our variants. Our engineered IFN4 variants may be further developed for clinical applications and utilized in basic research to decipher the immunological roles of IFN4. Previously, the transient expression of wild-type IFN4 in mammalian cells failed to produce significant amounts of recombinant
Title: Structure-based glycoengineering of interferon lambda 4 enhances its productivity and anti-viral potency
Example Output:
True