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]: The emergence of the severe acute respiratory syndrome coronavirus (SARS-CoV) has led to a renewed interest in studying the role of accessory proteins in regulating coronavirus infections in the natural host. A significant body of evidence has accumulated in the area of SARS-CoV and host interactions that indicate that the accessory proteins might play an important role in modulating the host response to virus infection and thereby, contribute to pathogenesis. In this review, we have compiled the current knowledge about SARS-CoV accessory proteins, obtained from studies in cell culture systems, reverse genetics and animal models, to shed some light into the possible role of these proteins in the propagation and virulence of SARS-CoV in its natural host. We conclude by providing some questions for future studies that will greatly advance our knowledge about the biological significance and contributions of the accessory proteins in the development of SARS in humans.
[A]: SARS coronavirus accessory proteins

[Q]: We utilized one-step multiplex reverse transcription-PCR (RT-PCR) and Luminex xMAP technology to develop a respiratory multiplex liquid-chip assay (rMLA) for China, Middle East Respiratory Syndrome coronavirus (MERS-CoV). Performance of rMLA was evaluated by comparing with real-time RT-PCR. Detection data from clinical specimens showed that the rMLA had diagnostic sensitivities of 97.10% for FluA, 94.59% for FluB, 98.68% for PIV-3, 94.87% for RSV and 95.92% for MPV (No Data for MERS-CoV due to the lack of positive specimens). Data of analytical sensitivities showed that the detection limits of the rMLA assay were 5-25 viral RNA copies per l for FluA, FluB, PIV-3 and MERS-CoV, approximate to the real-time RT-PCR assay; while the values were 8 and 22copies/l for MPV and RSV, lower than the real-time RT-PCR(78 and 114 copies/l respectively). The results indicated that the rMLA is a sensitive, specific detection tool and comparable to real-time RT-PCR, especially suitable for high-throughput detection of respiratory specimens.
[A]: A multiplex liquid-chip assay based on Luminex xMAP technology for simultaneous detection of six common respiratory viruses

[Q]: Swine influenza is an acute respiratory disease in pigs caused by swine influenza virus (SIV). Highly virulent SIV strains cause mortality of up to 10%. Importantly, pigs have long been considered ''mixing vessels'' that generate novel influenza viruses with pandemic potential, a constant threat to public health. Since its emergence in 2009 and subsequent pandemic spread, the pandemic (H1N1) 2009 (H1N1pdm) has been detected in pig farms, creating the risk of generating new reassortants and their possible infection of humans. Pathogenesis in SIV or H1N1pdm-infected pigs remains poorly characterized. Proinflammatory and antiviral cytokine responses are considered correlated with the intensity of clinical signs, and swine macrophages are found to be indispensible in effective clearance of SIV from pig lungs. In this study, we report a unique pattern of cytokine responses in swine macrophages infected with H1N1pdm. The roles of mitogen-activated protein (MAP) kinases in the regulation of the host responses were examined. We found that proinflammatory cytokines IL-6, IL-8, IL-10, and TNF-a were significantly induced and their induction was ERK1/2-dependent. IFN-b and IFN-inducible antiviral Mx and 2959-OAS were sharply induced, but the inductions were effectively abolished when ERK1/2 was inhibited. Induction of CCL5 (RANTES) was completely inhibited by inhibitors of ERK1/2 and JNK1/2, which appeared also to regulate FasL and TNF-a, critical for apoptosis in pig macrophages. We found that NFkB was activated in H1N1pdm-infected cells, but the activation was suppressed when ERK1/2 was inhibited, indicating there is cross-talk between MAP kinase and NFkB responses in pig macrophages. Our data suggest that MAP kinase may activate NFkB through the induction of RIG-1, which leads to the induction of IFN-b in swine macrophages. Understanding host responses and their underlying mechanisms may help identify venues for effective control of SIV and assist in prevention of future influenza pandemics.
[A]:
Distinct Regulation of Host Responses by ERK and JNK MAP Kinases in Swine Macrophages Infected with Pandemic (H1N1) 2009 Influenza Virus