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.

Q: Ten years after the severe acute respiratory syndrome epidemic, a second coronavirus, the Middle East respiratory syndrome coronavirus (MERS-CoV), has been identified as the cause of a highly lethal pneumonia in patients in the Middle East and in travelers from this region. Over the past 9 months, since the virus was first isolated, much has been learned about the biology of the virus. It is now clear that MERS-CoV is transmissible from person to person, and its close relationship with several bat coronaviruses suggests that these animals may be the ultimate source of the infection. However, many key issues need to be addressed, including identification of the proximate, presumably zoonotic, source of the infection, the prevalence of the infection in human populations, details regarding clinical and pathological features of the human infection, the establishment of a small rodent model for the infection, and the virological and immune basis for the severe disease observed in most patients. Most importantly, we do not know whether a MERS-CoV epidemic is likely or not. Infection with the virus has so far resulted in only 91 cases and 46 deaths (as of 29 July 2013), but it is nonetheless setting off alarm bells among public health officials, including Margaret Chan, Director-General of the World Health Organization, who called MERS-CoV "a threat to the entire world." This article reviews some of the progress that has been made and discusses some of the questions that need to be answered. Citation Perlman S. 2013. The Middle East respiratory syndrome-how worried should we be? mBio 4(4):e00531-13.

A: The Middle East Respiratory Syndrome-How Worried Should We Be? A NOVEL VIRUS IS IDENTIFIED IN SAUDI ARABIA
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Q: Feline infectious peritonitis virus (FIPV) (Coronaviridae) causes the most lethal viral infection in cats: FIP. The related feline enteric coronavirus (FECV) causes mild enteritis. Why these feline coronaviruses manifest so differently in vivo is not known. In this study, infection kinetics (titres and antigen expression) of FIPV 79-1146, and FECV 79-1683, were determined in peripheral blood monocytes from 3 donor cats and compared to those in Crandell feline kidney (CrFK) cells. The infection kinetics in monocytes were host dependent. Monocytes from 1 cat were resistant to both FIPV-and FECV-infection. Monocytes from the other 2 cats could initially be infected by both FIPV and FECV but FIPV infection was sustained in monocytes of only one cat. FECV-infection was never sustained and viral production was up to 100 times lower than in FIPVinfected monocytes. In CrFK cells, FIPV and FECV infection kinetics did not differ. In monocytes of a larger cat population (n = 19) the 3 infection patterns were also found. Considering all 22 investigated cats, 3/22 were not susceptible for FIPV and FECV. The rest could be infected with FECV and FIPV but 10/22 cats had monocytes that only sustained FIPV infection and 9/22 sustained neither FIPV nor FECV infection. * Both authors contributed equally.

A: Replication of feline coronaviruses in peripheral blood monocytes
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Q: Hepatitis C virus (HCV) causes chronic hepatitis, which often results in the development of liver cirrhosis and hepatocellular carcinoma (HCC) worldwide. In this study, we demonstrated that the non-structural protein NS3 of HCV enhances cyclooxygenase-2 (COX-2) gene promoter activity, COX-2 mRNA expression, COX-2 protein production, and prostaglandin E2 (PGE2) release in HepG2 cells in a concentration-dependent fashion. We also showed that transcription factor NF-B is required for the activation of COX-2 regulated by NS3. In addition, multiple signaling pathways are involved cooperatively in the expression of COX-2 activated by the viral protein in a calcium-independent manner, which requires signaling components including JNK, ERK, and PKD2. A thorough investigation of mechanism involved in the activation of COX-2 regulated by HCV would provide insights into our understanding the processes of liver inflammatory response and hepatocellular carcinoma development caused by the viral infection and also into the development of novel therapeutics against HCV infection.

A:
NS3 protein of hepatitis C virus regulates cyclooxygenase-2 expression through multiple signaling pathways
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