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: 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.

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

PROBLEM: We performed experiments to determine the effect of PKR activation on respiratory syncytial virus (RSV) replication. We first determined that RSV infection activates PKR which induces the phosphorylation of eIF2α, resulting in the formation of host stress granules. We used RNA interference to decrease endogenous PKR levels. RSV replication was not altered in cells deficient for PKR expression. However, RSV-mediated stress granule formation was significantly reduced in PKR-knockdown cells. As an alternative method to block PKR activation, we used treatment with the kinase inhibitor 2-aminopurine (2-AP). We observed that 2-AP treatment significantly reduced viral replication. We also treated PKR-knockdown cells with 2-AP and inoculated with RSV. Under these conditions, 2-AP treatment diminished viral replication in the absence of PKR expression. These results suggest that PKR activation has a minimal effect on RSV replication and that the antiviral effect of 2-AP during RSV infection likely occurs via a PKR-independent mechanism.

SOLUTION: Activation of protein kinase R is required for induction of stress granules by respiratory syncytial virus but dispensable for viral replication

PROBLEM: Ebola haemorrhagic fever causes deadly disease in humans and non-human primates resulting from infection with the Ebola virus (EBOV) genus of the family leaflet association remain poorly understood. This review describes the biological functions of EBOV proteins and their roles in the lifecycle, summarizes the factors related to EBOV proteins or RNA expression throughout the different phases, and reviews advances with regards to the molecular events and mechanisms of the EBOV lifecycle. Furthermore, the review outlines the aspects remain unclear that urgently need to be solved in future research. Comparison of the transcription and replication strategies of marburg virus and Ebola virus by using artificial replication systems.

SOLUTION:
The lifecycle of the Ebola virus in host cells