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.

Background: Avian leukosis virus (ALV) is a major infectious disease that impacts the poultry industry worldwide. Despite intensive efforts, no effective vaccine has been developed against ALV because of mutations that lead to resistant forms. Therefore, there is a dire need to develop antiviral agents for the treatment of ALV infections and RNA interference (RNAi) is considered an effective antiviral strategy. Results: In this study, the avian leukosis virus subgroup J (ALV-J) proviral genome, including the gag genes, were treated as targets for RNAi. Four pairs of miRNA sequences were designed and synthesized that targeted different regions of the gag gene. The screened target (i.e., the gag genes) was shown to effectively suppress the replication of ALV-J by 19.0-77.3%. To avoid the generation of escape variants during virus infection, expression vectors of multi-target miRNAs were constructed using the multi-target serial strategy (against different regions of the gag, pol, and env genes). Multi-target miRNAs were shown to play a synergistic role in the inhibition of ALV-J replication, with an inhibition efficiency of viral replication ranging from 85.0-91.2%. Conclusion: The strategy of multi-target miRNAs might be an effective method for inhibiting ALV replication and the acquisition of resistant mutations.
Enhanced inhibition of Avian leukosis virus subgroup J replication by multi-target miRNAs

One word can be used to best describe the theme of each day that has transpired since the onset of the COVID-19 pandemic: uncertainty. Urologic surgical residents around the nation are faced with the unknown when they walk through the doors of the hospital each day. While experience has taught us navigational strategies to handle these circumstances, the COVID-19 pandemic has undoubtedly brought new meaning to this concept. Priorities have quickly transitioned from closely following our previously developed academic curriculum and enhancing our surgical skills, to limiting physician-patient encounters and ensuring the safety and health of our team. Normalcy within our professional and personal lives is completely lost. Yet, as health care providers, we must and will forge on. We review the techniques and guidelines that our institution has implemented in order to allow us to do just that. We believe that our leadership, both at an enterprise and program level, has taken the necessary and early measures to prepare our residency cohort for the uncertain future and challenges posed by COVID-19. This plan emphasizes social and professional distancing, allows residents and faculty to stay current on academic topics, and provides reasonable opportunities for personal wellness, all while emphasizing safety and rationalization. Most importantly, however, we have continued to provide our patients with exceptional urologic care at 2 adult hospitals and 1 children's hospital in the Greater Akron, Ohio area. While we understand each residency program has a unique curriculum with a different number of residents that cover a range of different hospitals, we hope to provide insight into our personal experience. We believe that this method of organization allows a residency program to continue to grow professionally, socially, academically, and personally during the uncertainty that is COVID-19. This framework could serve as an immediate action plan for future pandemics and natural disasters, especially for residency programs that cover multiple hospitals and health care settings.
Editorial Cleveland Clinic Akron General Urology Residency Program's COVID-19 Experience

Viral 2=,5=-phosphodiesterases (2=,5=-PDEs) help disparate RNA viruses evade the antiviral activity of interferon (IFN) by degrading 2=,5=-oligoadenylate (2-5A) activators of RNase L. A kinase anchoring proteins (AKAPs) bind the regulatory subunits of protein kinase A (PKA) to localize and organize cyclic AMP (cAMP) signaling during diverse physiological processes. Among more than 43 AKAP isoforms, AKAP7 appears to be unique in its homology to viral 2=,5=-PDEs. Here we show that mouse AKAP7 rapidly degrades 2-5A with kinetics similar to that of murine coronavirus (mouse hepatitis virus [MHV]) strain A59 ns2 and human rotavirus strain WA VP3 proteins. To determine whether AKAP7 could substitute for a viral 2=,5=-PDE, we inserted AKAP7 cDNA into an MHV genome with an inactivated ns2 gene. The AKAP7 PDE domain or N-terminally truncated AKAP7 (both lacking a nuclear localization motif), but not full-length AKAP7 or a mutant, AKAP7 H185R , PDE domain restored the infectivity of ns2 mutant MHV in bone marrow macrophages and in livers of infected mice. Interestingly, the AKAP7 PDE domain and N-terminally deleted AKAP7 were present in the cytoplasm (the site of MHV replication), whereas full-length AKAP7 was observed only in nuclei. We suggest the possibility that viral acquisition of the host AKAP7 PDE domain might have occurred during evolution, allowing diverse RNA viruses to antagonize the RNase L pathway. We also reported that the rotavirus VP3 C-terminal domain (VP3-CTD) cleaves 2-5A and that it may rescue ns2 mutant MHV. Here we report that a cellular protein, AKAP7, has an analogous 2=,5=-phosphodiesterase (2=,5=-PDE) domain that is able to restore the growth of chimeric MHV expressing inactive ns2. The proviral effect requires cytoplasmic localization of the AKAP7 PDE domain. We speculate that AKAP7 is the ancestral precursor of viral proteins, such as ns2 and VP3, that degrade 2-5A to evade the antiviral activity of RNase L. RH. 2014 . Murine AKAP7 has a 2=,5=-phosphodiesterase domain that can complement an inactive murine coronavirus ns2 gene. mBio 5(4):e01312-14.

Murine AKAP7 Has a 2=,5=-Phosphodiesterase Domain That Can Complement an Inactive Murine Coronavirus ns2 Gene