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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Question: Background: The influenza A virus subtypes H1N1, H1N2 and H3N2 are the most prevalent subtypes in swine. In 2003, a reassorted H1N2 swine influenza virus (SIV) subtype appeared and became prevalent in Denmark. In the present study, the reassortant H1N2 subtype was characterised genetically and the infection dynamics compared to an "avian-like" H1N1 virus by an experimental infection study. Methods: Sequence analyses were performed of the H1N2 virus. Two groups of pigs were inoculated with the reassortant H1N2 virus and an "avian-like" H1N1 virus, respectively, followed by inoculation with the opposite subtype four weeks later. Measurements of HI antibodies and acute phase proteins were performed. Nasal virus excretion and virus load in lungs were determined by real-time RT-PCR. The phylogenetic analysis revealed that the reassorted H1N2 virus contained a European "avian-like" H1-gene and a European "swine-like" N2-gene, thus being genetically distinct from most H1N2 viruses circulating in Europe, but similar to viruses reported in 2009/2010 in Sweden and Italy. Sequence analyses of the internal genes revealed that the reassortment probably arose between circulating Danish "avian-like" H1N1 and H3N2 SIVs. Infected pigs developed cross-reactive antibodies, and increased levels of acute phase proteins after inoculations. Pigs inoculated with H1N2 exhibited nasal virus excretion for seven days, peaking day 1 after inoculation two days earlier than H1N1 infected pigs and at a six times higher level. The difference, however, was not statistically significant. Pigs euthanized on day 4 after inoculation, had a high virus load in all lung lobes. After the second inoculation, the nasal virus excretion was minimal. There were no clinical sign except elevated body temperature under the experimental conditions. The "avian-like" H1N2 subtype, which has been established in the Danish pig population at least since 2003, is a reassortant between circulating swine "avian-like" H1N1 and H3N2. The Danish H1N2 has an "avian-like" H1 and differs from most other reported H1N2 viruses in Europe and North America/Asia, which have H1-genes of human or "classical-swine" origin, respectively. The variant seems, however, also to be circulating in countries like Sweden and Italy. The infection dynamics of the reassorted "avian-like" H1N2 is similar to the older "avian-like" H1N1 subtype.

Answer: Genetic and biological characterisation of an avian-like H1N2 swine influenza virus generated by reassortment of circulating avian-like H1N1 and H3N2 subtypes in Denmark

Question: Overlapping genes represent a fascinating evolutionary puzzle, since they encode two functionally unrelated proteins from the same DNA sequence. They originate by a mechanism of overprinting, in which point mutations in an existing frame allow the expression (the "birth") of a completely new protein from a second frame. In viruses, in which overlapping genes are abundant, these new proteins often play a critical role in infection, yet they are frequently overlooked during genome annotation. This results in erroneous interpretation of mutational studies and in a significant waste of resources. Therefore, overlapping genes need to be correctly detected, especially since they are now thought to be abundant also in eukaryotes. Developing better detection methods and conducting systematic evolutionary studies require a large, reliable benchmark dataset of known cases. We thus assembled a highquality dataset of 80 viral overlapping genes whose expression is experimentally proven. Many of them were not present in databases. We found that overall, overlapping genes differ significantly from non-overlapping genes in their nucleotide and amino acid composition. In particular, the proteins they encode are enriched in high-degeneracy amino acids and depleted in low-degeneracy ones, which may alleviate the evolutionary constraints acting on overlapping genes. Principal component analysis revealed that the vast majority of overlapping genes follow a similar composition bias, despite their heterogeneity in length and function. Six proven mammalian overlapping genes also followed this bias. We propose that this apparently near-universal composition bias may either favour the birth of overlapping genes, or/and result from selection pressure acting on them.

Answer: Overlapping genes and the proteins they encode differ significantly in their sequence composition from non-overlapping genes

Question: We live in a hostile environment, surrounded by microbial pathogens and subject to a range of physical and chemical insults. To survive in this environment, vertebrates have evolved complex immune systems. A key element of this defence is the deployment of rapid response elements at the most probable sites of attack, which are the epithelial-cell boundaries between the body and the environment in the skin, gut and lungs. As the body's largest and most exposed interface with the environment, the skin has a central role in host defence. Before the relatively recent discovery of the immunological defences of skin, the cutaneous interface was viewed as a passive barrier between the host and the hostile environment. In the past few decades, however, it has become apparent that the mechanical aspects of epidermal defence are reinforced by a versatile and robust system of immune surveillance 1 (FIG. 1) . The crucial role of immune surveillance in maintaining homeostasis is evident from the marked increase in the frequency and severity of cutaneous malignancies and infections when immune function is limited, for example in patients with genetic and acquired immunodeficiency disorders and in those receiving immunosuppressive therapy after organ transplantation 2,3 . The regulation of skin defence mechanisms is also crucial, as inappropriate or misdirected immune activity is implicated in the pathogenesis of a large variety of acquired inflammatory skin disorders, including psoriasis, atopic and allergic contact dermatitis, lichen planus, alopecia areata and vitiligo 4-10 . The role of immune dysfunction in these conditions is emphasized by their response to immunosuppressive therapeutic interventions [11] [12] [13] [14] . Understanding the mechanisms of immune surveillance in the skin and tissue-specific immune responses also has important implications for the rational design of vaccines. To promote protective immunity, an immunization protocol must elicit not only an antigenspecific immune response, but also an effective memory response that will provide long-lived protection at the most probable sites of invasion. This applies equally to immunization against infectious organisms, which in most cases invade through the skin or the epithelia of the gastrointestinal or respiratory systems, and to the elicitation of immune responses against tumours. As we discuss, the route and means of adjuvant stimulation that is used can affect the effectiveness and utility of specific vaccine strategies. In this review, we discuss these issues in the context of recent advances in our understanding of cutaneous immune mechanisms, highlighting the interaction of The skin, as the primary interface between the body and the environment, provides the first line of defence against a broad array of microbial pathogens and trauma. In addition to its properties as a physical barrier, the skin has many active defence mechanisms. In this review, we discuss the interaction between the innate and adaptive immune systems in the skin as a model for immune function at epithelial-cell interfaces with the environment. How these mechanisms account for the robust nature of cutaneous immune surveillance and how their dysregulation drives the pathogenesis of inflammatory skin disorders and skin-based tumours are the subjects of this review.

Answer:
IMMUNE SURVEILLANCE IN THE SKIN: MECHANISMS AND CLINICAL CONSEQUENCES