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.

Input: Consider Input: The circRNA is a newly defined noncoding RNA and characterized by its unique splicing reactions to form circles. However, the function of circRNAs during viral infection remains largely unknown. In this study, the circRNA expression profile during porcine endemic diarrhea virus (PEDV) infection in IPEC-J2 cell line was investigated using the next-generation sequencing technology. A total of 26670 circRNA candidates were identified. The functional annotation analysis revealed that the parent genes of differentially expressed circRNAs might be associated with host response to PEDV infection. Further analysis verified the existence of eight selected circRNAs and confirmed that PEDV infection alerted the expression patterns of circRNAs and their linear parent genes in IPEC-J2 cell line. The circRNA-miRNA interaction network was also constructed to elucidate their potential targets. Our results provided not only the first large-scale profile analysis of circRNAs associated with PEDV infection but also a novel direction to elucidate host-PEDV interactions.

Output: Profile analysis of circRNAs induced by porcine endemic diarrhea virus infection in porcine intestinal epithelial cells


Input: Consider Input: Despite flaviviruses remaining the leading cause of systemic human infections worldwide, ocular manifestations of these mosquito-transmitted viruses are considered relatively uncommon in part due to under-reporting. However, recent outbreaks of Zika virus (ZIKV) implicated in causing multiple ocular abnormalities, such as conjunctivitis, retinal hemorrhages, chorioretinal atrophy, posterior uveitis, optic neuritis, and maculopathies, has rejuvenated a significant interest in understanding the pathogenesis of flaviviruses, including ZIKV, in the eye. In this review, first, we summarize the current knowledge of the major flaviviruses (Dengue, West Nile, Yellow Fever, and Japanese Encephalitis) reported to cause ocular manifestations in humans with emphasis on recent ZIKV outbreaks. Second, being an immune privilege organ, the eye is protected from systemic infections by the presence of blood-retinal barriers (BRB). Hence, we discuss how flaviviruses modulate retinal innate response and breach the protective BRB to cause ocular or retinal pathology. Finally, we describe recently identified infection signatures of ZIKV and discuss whether these system biology-predicted genes or signaling pathways (e.g., cellular metabolism) could contribute to the pathogenesis of ocular manifestations and assist in the development of ocular antiviral therapies against ZIKV and other flaviviruses.

Output: Ocular Manifestations of Emerging Flaviviruses and the Blood-Retinal Barrier


Input: Consider Input: Zika virus (ZIKV), a member of the Flaviviridae family, is the most recent emerging arbovirus with pandemic potential. During infection, viruses trigger the host cell stress response, leading to changes in RNA translation and the assembly of large aggregates of stalled translation preinitiation complexes, termed stress granules (SGs). Several reports demonstrate that flaviviruses modulate the assembly of stress granules (SG). As an emerging pathogen, little is known however about how ZIKV modulates the host cell stress response. In this work, we investigate how ZIKV modulates SG assembly. We demonstrate that ZIKV negatively impacts SG assembly under oxidative stress conditions induced by sodium arsenite (Ars), a treatment that leads to the phosphorylation of eIF2α. By contrast, no measurable difference in SG assembly was observed between mock and ZIKV-infected cells treated with sodium selenite (Se) or Pateamine A (PatA), compounds that trigger eIF2α-independent SG assembly. Interestingly, ZIKV infection markedly impaired the phosphorylation of eIF2α triggered in Ars-treated infected cells, and the abrogation of SG assembly in ZIKV-infected cells is, at least in part, dependent on eIF2α dephosphorylation. These data demonstrate that ZIKV elicits mechanisms to counteract host anti-viral stress responses to promote a cellular environment propitious for viral replication. Citation: Amorim R, Temzi A, Griffin BD, Mouland AJ (2017) Zika virus inhibits eIF2α-dependent stress granule assembly. PLoS Negl Trop Dis 11 (7): e0005775. https://doi.org/10.granules (SGs). We observed that ZIKV blocks SG assembly induced by sodium arsenite (Ars), but not by sodium selenite or Pateamine A. We demonstrate that this difference is related to the ability of ZIKV to modulate the dephosphorylation of eIF2α via its phosphatase. Our work demonstrates that ZIKV prevents a host stress response in order to maintain a cellular environment propitious for viral replication. Zika virus inhibits stress granule assembly PLOS Neglected Tropical Diseases | https://doi.


Output: Zika virus inhibits eIF2α-dependent stress granule assembly