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In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.
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Recent years have seen several advances in our understanding of immunity to virus infection of the lower respiratory tract, including to influenza virus infection. Here, we review the cellular targets of viruses and the features of the host immune response that are unique to the lungs. We describe the interplay between innate and adaptive immune cells in the induction, expression and control of antiviral immunity, and discuss the impact of the infected lung milieu on moulding the response of antiviral effector T cells. Recent findings on the mechanisms that underlie the increased frequency of severe pulmonary bacterial infections following respiratory virus infection are also discussed. Viruses are highly evolved and ubiquitous pathogens. Although infection with many viruses results in a mild, self-limited disease, other viruses can produce severe and frequently fatal infections. The respiratory tract is a major portal through which viruses enter to initiate infection. Whereas some viruses can initiate infection in the respiratory tract and then disseminate to other sites in the body, other viruses typically remain localized to the respiratory tract, where they replicate and induce tissue injury (see Supplementary information S1 (table)). Various defence mechanisms have evolved in the respiratory tract to prevent and control infection by viruses and other pathogens. The respiratory tract can be divided anatomically into the upper respiratory tract (including the nose, mouth and pharynx) and the lower respiratory tract (which consists of the trachea, bronchi and lungs), with the lymphoid tissue of Waldeyer's ring (including the pharyngeal and palatine tonsils) representing the line of demarcation. Because of the crucial role of the lower respiratory tract in respiration, we limit the focus of this Review to recent advances in our understanding of the host immune response to virus infection at this site.
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Regulating the adaptive immune response to respiratory virus infection NIH Public Access


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lord mayor and aldermen of the city of London put into place a set of orders "concerning the infection of the plague," which was then sweeping through the population. He intended that these actions would be "very expedient for preventing and avoiding of infection of sickness" (1). At that time, London faced a public health crisis, with an inadequate scientific base in that the role of rats and their fleas in disease transmission was unknown. Nonetheless, this crisis was faced with good intentions by the top medical and political figures of the community. Daniel Defoe made an observation that could apply to many public health interventions then and today, "This shutting up of houses was at first counted a very cruel and unchristian method… but it was a public good that justified a private mischief" (1). Then, just as today, a complex relationship existed between the science of public health and the practice of public health and politics. We address the relationship between science, public health, and politics, with a particular emphasis on infectious diseases. Science, public health, and politics are not only compatible, but all three are necessary to improve the public's health. The progress of each area of public health is related to the strength of the other areas. The effect of politics in public health becomes dangerous when policy is dictated by ideology. Policy is also threatened when it is solely determined by science, devoid of considerations of social condition, culture, economics, and public will. When using the word "politics," we refer not simply to partisan politics but to the broader set of policies and sys-tems. Although ideology is used in many different ways, in this case, it refers to individual systems of belief that may color a person's attitudes and actions and that are not necessarily based on scientific evidence (2).
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Plagues, Public Health, and Politics 1


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One sentence summary: Understanding factors that shape Escherichia coli shedding by cattle promises to advance prophylactic and therapeutic interventions and has critical medical and public health implications. Editor: Wolfgang Kneifel ABSTRACT Several early models describing host-pathogen interaction have assumed that each individual host has approximately the same likelihood of becoming infected or of infecting others. More recently, a concept that has been increasingly emphasized in many studies is that for many infectious diseases, transmission is not homogeneous but highly skewed at the level of populations. In what became known as the '20/80 rule', about 20% of the hosts in a population were found to contribute to about 80% of the transmission potential. These heterogeneities have been described for the interaction between many microorganisms and their human or animal hosts. Several epidemiological studies have reported transmission heterogeneities for Escherichia coli by cattle, a phenomenon with far-reaching agricultural, medical and public health implications. Focusing on E. coli as a case study, this paper will describe super-spreading and super-shedding by cattle, review the main factors that shape these transmission heterogeneities and examine the interface with human health. Escherichia coli super-shedding and super-spreading by cattle are shaped by microorganism-specific, cattle-specific and environmental factors. Understanding the factors that shape heterogeneities in E. coli dispersion by cattle and the implications for human health represent key components that are critical for targeted infection control initiatives.
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Escherichia coli, cattle and the propagation of disease