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: 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: Daily oscillations of pulmonary function depend on the rhythmic activity of the circadian timing system. Environmental tobacco/cigarette smoke (CS) disrupts circadian clock leading to enhanced inflammatory responses. Infection with influenza A virus (IAV) increases hospitalization rates and death in susceptible individuals, including patients with Chronic Obstructive Pulmonary Disease (COPD). We hypothesized that molecular clock disruption is enhanced by IAV infection, altering cellular and lung function, leading to severity in airway disease phenotypes. C57BL/6J mice exposed to chronic CS, BMAL1 knockout (KO) mice and wild-type littermates were infected with IAV. Following infection, we measured diurnal rhythms of clock gene expression in the lung, locomotor activity, pulmonary function, inflammatory, pro-fibrotic and emphysematous responses. Chronic CS exposure combined with IAV infection altered the timing of clock gene expression and reduced locomotor activity in parallel with increased lung inflammation, disrupted rhythms of pulmonary function, and emphysema. BMAL1 KO mice infected with IAV showed pronounced detriments in behavior and survival, and increased lung inflammatory and pro-fibrotic responses. This suggests that remodeling of lung clock function following IAV infection alters clock-dependent gene expression and normal rhythms of lung function, enhanced emphysematous and injurious responses. This may have implications for the pathobiology of respiratory virus-induced airway disease severity and exacerbations. I nfluenza virus, rhinovirus, coronavirus, respiratory syncytial virus, parainfluenza, adenovirus and metapeumovirus are among the respiratory viruses known to cause exacerbations in Chronic Obstructive Pulmonary Disease (COPD) and asthma 1-4 . In fact, respiratory viral infections account for about 50-70% of acute exacerbations in patients with COPD 5 . COPD exacerbations are often followed by subsequent clinical pulmonary deterioration, including significant declines in forced expiratory volume at 1 second (FEV 1 ) and increased hospitalization or mortality 6 . This is associated with worsening of COPD phenotypes, such as cough, fever and mucus production; the timing of which depends on the activity of the biological clock. Circadian rhythms are biological oscillations that occur with a near-24-h period and are synchronized or entrained to environmental cues, such as the day-night cycle 7 . These rhythms are the manifestation of an autoregulatory molecular oscillator of interlocked positive and negative transcription factors collectively referred to as clock genes 8 . In mammals, the central pacemaker, localized to the suprachiasmatic nucleus (SCN) of the anterior hypothalamus, drives rhythms of physiology and behavior, and synchronizes internal timing with the external environment 7 . Apart from the central clock, peripheral tissues such as the liver, heart and the lung also contain autonomous circadian oscillators that coordinate tissue specific cellular functions and responses to environmental stimuli 7-12 . As an example, circadian rhythms in pulmonary function have been demonstrated in animal models and healthy individuals (highest at noon time and low during the early morning hours) [13] [14] [15] . The coordinated and synchronized activity of central and peripheral oscillators is referred to as the circadian timing system 9,12 . It has been shown that recruitment of leukocytes to tissues following infection is also regulated by the circadian timing system 16, 17 . For example, macrophages and mast cells exhibit robust rhythms of circadian clock and proinflammatory cytokine gene expression 18, 19 . The magnitude of immune and inflammatory parameters varies with time of day, and disruption of circadian rhythms (chronodisruption) has been implicated in cellular dysfunction, and in the pathogenesis of chronic metabolic disease, infection, and inflammatory diseases 20-22 .
Title: Influenza A virus-dependent remodeling of pulmonary clock function in a mouse model of COPD
Example Output: False

Example Input: Paragraph: Pandemic 2009 H1N1 is normally susceptible to oseltamivir, but variants harboring the H275Y (CAC TAC) mutation exhibit resistance. We describe the use of a combined reverse-transcription polymerase chain reaction (RT-PCR)/pyrosequencing approach to identify the H275 residue. A total of 223 specimens were tested with this method: 216 randomly selected clinical specimens positive for 2009 H1N1 and 7 cell-culture supernatants from the Centers for Disease Control and Prevention (CDC; 4 resistant, 3 susceptible 2009 H1N1 strains). The assay detected H275Y in 1 clinical respiratory sample (0.5%) and all 4 oseltamivir-resistant strains from the CDC; the remaining 215 clinical and 3 susceptible CDC specimens were wild-type. Sanger sequencing confirmed the results for 50 of 50 selected isolates. The RT-PCR/pyrosequencing method was highly specific, producing no amplicons or valid sequences from samples containing non-H1N1 viruses or bacteria. Our findings suggest that this method provides a rapid tool for H275Y detection, with high sensitivity and potential benefit for patient care.
Title: Reverse-transcription polymerase chain reaction/pyrosequencing to characterize neuraminidase H275 residue of influenza A 2009 H1N1 virus for rapid and specific detection of the viral oseltamivir resistance marker in a clinical laboratory
Example Output:
False