TASK DEFINITION: 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.
PROBLEM: 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).

SOLUTION: Plagues, Public Health, and Politics 1

PROBLEM: Fowl adenovirus serotype 4 (FAdV-4) is the causative agent of hydropericardium syndrome. To clarify the effects of FAdV-4 on immune organs in birds, we conducted a detailed examination of dynamic morphology and damage mechanisms in chickens randomly divided into 4 groups (FAdV-4, vaccination, FAdV-4 plus vaccination, and control). FAdV-4 caused the depletion of lymphocytes and subsequent growth impairment in the thymus and bursa. Chickens infected with FAdV-4 and subjected to vaccination experienced greater inhibition of antibody responses to inactivated vaccines against Newcastle disease and avian influenza virus subtype H9 than uninfected and vaccinated chickens. The mechanisms underlying adenovirus-mediated lymphoid organ damage were further investigated via transferase-mediated dUTP nickend labeling and apoptotic genes transcription analyses. Notably, lymphocytes apoptosis in lymphoid organs and expression of specific gene transcripts was significantly upregulated after infection (P < 0.05). Furthermore, increased expression of interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-α mRNA was observed (P < 0.05), compared to the control group. Our collective findings suggested that FAdV-4 caused structural and functional damage of immune organs via apoptosis along with induction of a severe inflammatory response.

SOLUTION: Immunosuppressive potential of fowl adenovirus serotype 4

PROBLEM: The spike (S) glycoprotein of coronavirus is responsible for receptor binding and membrane fusion. A number of variants with deletions and mutations in the S protein have been isolated from naturally and persistently infected animals and tissue cultures. Here, we report the emergence and isolation of two temperature sensitive (ts) mutants and a revertant in the process of cold-adaptation of coronavirus infectious bronchitis virus (IBV) to a monkey kidney cell line. The complete sequences of wild type (wt) virus, two ts mutants, and the revertant were compared and variations linked to phenotypes were mapped. A single amino acid reversion (L 294 -to-Q) in the S protein is sufficient to abrogate the ts phenotype. Interestingly, unlike wt virus, the revertant grows well at and below 32 jC, the permissive temperature, as it carries other mutations in multiple genes that might be associated with the cold-adaptation phenotype. If the two ts mutants were allowed to enter cells at 32 jC, the S protein was synthesized, core-glycosylated and at least partially modified at 40 jC. However, compared with wt virus and the revertant, no infectious particles of these ts mutants were assembled and released from the ts mutant-infected cells at 40 jC. Evidence presented demonstrated that the Q 294 -to-L 294 mutation, located at a highly conserved domain of the S1 subunit, might hamper processing of the S protein to a matured 180-kDa, endo-glycosidase H-resistant glycoprotein and the translocation of the protein to the cell surface. Consequently, some essential functions of the S protein, including mediation of cell-to-cell fusion and its incorporation into virions, were completely abolished. D

SOLUTION:
A single amino acid mutation in the spike protein of coronavirus infectious bronchitis virus hampers its maturation and incorporation into virions at the nonpermissive temperature