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".

[EX Q]: Paragraph: Virus infection often results in diverse outcomes. This variability of virus pathogenesis is not well understood. Here we revise theoretical arguments to further our understanding of factors controlling infection and its severity. We propose that variability in these factors results in different clinical outcomes, which ultimately ensure virus reproduction. A link between parasite virulence and its transmission efficiency is a paramount concept in modern epidemiology. The trade-off between these two pathogen's features has been studied and discussed for decades. 
 Title: Variability in viral pathogenesis: modeling the dynamic of acute and persistent infections Virulence versus transmission: a trade-off
[EX A]: False

[EX Q]: Paragraph: The next influenza pandemic may be imminent. Because antiviral agents and vaccines will be unavailable to people in most countries, we need to determine whether other agents could offer clinical benefits. Influenza is associated with an increase in acute cardiovascular diseases, and influenza viruses induce proinflammatory cytokines. Statins are cardioprotective and have anti-inflammatory and immunomodulatory effects, and they thus might benefit patients with influenza. This hypothesis should be evaluated by using administrative databases to search for reduced rates of hospitalization and death due to influenzarelated conditions among people taking statins. These studies should be followed by laboratory studies of statins in animal and cell-based models of influenza virus infection and, later, by clinical trials. Positive results from such studies would provide physicians in all countries with something to offer patients for treatment and prophylaxis of pandemic influenza. Generic statins will be widely distributed and inexpensive. They might be the only agents that could alter the course of a global pandemic. 
 Title: Pandemic Influenza: A Potential Role for Statins in Treatment and Prophylaxis
[EX A]: True

[EX Q]: 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
[EX A]:
False