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: Single-stranded RNA (ssRNA) is the simplest form of genetic molecule and constitutes the genome in some viruses and presumably in primitive life-forms. However, an innate and unsolved problem regarding the ssRNA genome is formation of inactive doublestranded RNA (dsRNA) during replication. Here, we addressed this problem by focusing on the secondary structure. We systematically designed RNAs with various structures and observed dsRNA formation during replication using an RNA replicase (Q replicase). From the results, we extracted a simple rule regarding ssRNA genome replication with less dsRNA formation (less GC number in loops) and then designed an artificial RNA that encodes a domain of the -galactosidase gene based on this rule. We also obtained evidence that this rule governs the natural genomes of all bacterial and most fungal viruses presently known. This study revealed one of the structural design principles of an ssRNA genome that replicates continuously with less dsRNA formation.

Answer: A design principle for a single-stranded RNA genome that replicates with less double-strand formation

Question: In the last half century, significant attention has been given to animal diseases; however, our understanding of disease processes and how to manage them at the livestock-wildlife interface remains limited. In this study, we conduct a systematic review of the scientific literature to evaluate the status of diseases at the livestock-wildlife interface in the United States. Specifically, the goals of the literature review were three fold: first to evaluate domestic animal diseases currently found in the United States where wildlife may play a role; second to identify critical issues faced in managing these diseases at the livestock-wildlife interface; and third to identify potential technical and policy strategies for addressing these issues. We found that of the 86 avian, ruminant, swine, poultry, and lagomorph diseases that are reportable to the World Organization for Animal Health (OIE), 53 are present in the United States; 42 (79%) of these have a putative wildlife component associated with the transmission, maintenance, or life cycle of the pathogen; and 21 (40%) are known to be zoonotic. At least six of these reportable diseases-bovine tuberculosis, paratuberculosis, brucellosis, avian influenza, rabies, and cattle fever tick (vector control)-have a wildlife reservoir that is a recognized impediment to eradication in domestic populations. The complex nature of these systems highlights the need to understand the role of wildlife in the epidemiology, transmission, and maintenance of infectious diseases of livestock. Successful management or eradication of these diseases will require the development of cross-discipline and institutional collaborations. Despite social and policy challenges, there remain opportunities to develop new collaborations and new technologies to mitigate the risks posed at the livestock-wildlife interface. Published by Elsevier B.V.

Answer: Diseases at the livestock-wildlife interface: Status, challenges, and opportunities in the United States

Question: The early systemic production of interferon (IFN)-ab is an essential component of the antiviral host defense mechanisms, but is also thought to contribute to the toxic side effects accompanying gene therapy with adenoviral vectors. Here we investigated the IFN-ab response to human adenoviruses (Ads) in mice. By comparing the responses of normal, myeloid (m)DC-and plasmacytoid (p)DC-depleted mice and by measuring IFN-ab mRNA expression in different organs and cells types, we show that in vivo, Ads elicit strong and rapid IFN-ab production, almost exclusively in splenic mDCs. Using knockout mice, various strains of Ads (wild type, mutant and UV-inactivated) and MAP kinase inhibitors, we demonstrate that the Ad-induced IFN-ab response does not require Toll-like receptors (TLR), known cytosolic sensors of RNA (RIG-I/MDA-5) and DNA (DAI) recognition and interferon regulatory factor (IRF)-3, but is dependent on viral endosomal escape, signaling via the MAP kinase SAPK/JNK and IRF-7. Furthermore, we show that Ads induce IFN-ab and IL-6 in vivo by distinct pathways and confirm that IFN-ab positively regulates the IL-6 response. Finally, by measuring TNF-a responses to LPS in Ad-infected wild type and IFN-abR 2/2 mice, we show that IFN-ab is the key mediator of Ad-induced hypersensitivity to LPS. These findings indicate that, like endosomal TLR signaling in pDCs, TLR-independent virus recognition in splenic mDCs can also produce a robust early IFN-ab response, which is responsible for the bulk of IFN-ab production induced by adenovirus in vivo. The signaling requirements are different from known TLR-dependent or cytosolic IFN-ab induction mechanisms and suggest a novel cytosolic viral induction pathway. The hypersensitivity to components of the microbial flora and invading pathogens may in part explain the toxic side effects of adenoviral gene therapy and contribute to the pathogenesis of adenoviral disease.

Answer:
Key Role of Splenic Myeloid DCs in the IFN-ab Response to Adenoviruses In Vivo