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.

[EX Q]: Since the first imported case of Middle East respiratory syndrome coronavirus (MERS-CoV) infection was reported on May 20, 2015 in Korea, there have been 186 laboratoryconfirmed cases of MERS-CoV infection with 36 fatalities. Ninety-seven percent (181/186) of the cases had exposure to the health care facilities. We are reporting a superspreading event that transmitted MERS-CoV to 81 persons at a hospital emergency room (ER) during the Korean outbreak in 2015. The index case was a 35-yr-old man who had vigorous coughing while staying at the ER for 58 hr. As in severe acute respiratory syndrome outbreaks, superspreading events can cause a large outbreak of MERS in healthcare facilities with severe consequences. All healthcare facilities should establish and implement infection prevention and control measure as well as triage policies and procedures for early detection and isolation of suspected MERS-CoV cases.
[EX A]: Middle East Respiratory Syndrome Coronavirus Superspreading Event Involving 81 Persons, Korea 2015

[EX Q]: Early innate and cell-intrinsic responses are essential to protect host cells against pathogens. In turn, viruses have developed sophisticated mechanisms to establish productive infections, counteracting the host innate immune responses. Increasing evidence indicates that these antiviral factors may have a dual role by directly inhibiting viral replication, as well as by sensing and transmitting signals to induce antiviral cytokines. Recent studies have pointed at new, unappreciated mechanisms of viral evasion of host innate protective responses including manipulating the host ubiquitin system. Viral inhibition of antiviral factors by ubiquitin-dependent degradation is emerging as critical evasion mechanism of the antiviral response. In addition, recent studies have uncovered new mechanisms by which viral encoded proteins inhibit ubiquitin and ubiquitin-like modification of host proteins involved innate immune signaling pathways. Here we discuss recent findings and novel strategies that viruses have developed to counteract these early innate antiviral defenses. Early events in viral infection include attachment to the host cell membrane and entry, release of the viral RNA, DNA, and protein complexes into the cytoplasm of the cell and early recognition by the host innate immune system. At each of these steps, host cells have developed mechanisms to limit virus infection. In turn, viruses have rapidly evolved to counteract host defenses by different mechanisms. Many recent studies have pointed at the importance of cell type and host specific expression of antiviral factors as critical for
[EX A]: Viral evasion mechanisms of early antiviral responses involving regulation of ubiquitin pathways NIH Public Access

[EX Q]: Infectious bursal disease virus (IBDV) is the etiological agent of a highly contagious disease in chickens. In a recent report, proteasome inhibitor MG132 has been shown to completely inhibit IBDV-induced apoptosis. This raises the possibility that the ubiquitin-proteasome pathway may be used by the virus to promote viral replication. In this study, we examined the interplay between IBDV replication and the ubiquitin-proteasome pathway in cultured cells. Treatment of DF-1 cells with the proteasome inhibitors MG132 or lactacystin significantly decreased virus release in the supernatant and prevented virus-induced cytopathic effect. Inhibition of the ubiquitin-proteasome pathway did reduce markedly viral RNA transcription and protein translation but not affect virus internalization. We also demonstrated that IBDV activates caspase pathway via triggering the efflux of cytochrome c in mitochondria into cytosol of infected cells. This activity was dose-dependently reduced by proteasome inhibitor treatment. Taken together, our data suggest that proteasome inhibitor reduces IBDV replication through inhibition of viral RNA transcription and protein synthesis, and thus preventing IBDV-induced apoptosis.
[EX A]:
Reduction of infectious bursal disease virus replication in cultured cells by proteasome inhibitors