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.
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Question: Viral infection induces innate immunity and apoptosis. Apoptosis is an effective means to sacrifice virus-infected host cells and therefore restrict the spread of pathogens. However, the underlying mechanisms of this process are still poorly understood. Here, we show that the mitochondrial antiviral signaling protein (MAVS/VISA/Cardif/IPS-1) is critical for SeV (Sendai virus)-induced apoptosis. MAVS specifically activates c-Jun N-terminal kinase 2 (JNK2) but not other MAP kinases. Jnk22/2 cells, but not Jnk12/2 cells, are unable to initiate virus-induced apoptosis and SeV further fails to trigger apoptosis in MAPK kinase 7 (MKK7) knockout (Mkk72/2) cells. Mechanistically, MAVS recruits MKK7 onto mitochondria via its 3D domain, which subsequently phosphorylates JNK2 and thus activates the apoptosis pathway. Consistently, Jnk22/2 mice, but not Jnk12/2 mice, display marked inflammatory injury in lung and liver after viral challenge. Collectively, we have identified a novel signaling pathway, involving MAVS-MKK7-JNK2, which mediates virus-induced apoptosis and highlights the indispensable role of mitochondrial outer membrane in host defenses.

Answer: MAVS-MKK7-JNK2 Defines a Novel Apoptotic Signaling Pathway during Viral Infection


Question: With the emergence of highly pathogenic variant strains, porcine epidemic diarrhea virus (PEDV) has led to significant economic loss in the global swine industry. Many studies have described how coronaviruses enter cells, but information on PEDV invasion strategies remains insufficient. Given that the differences in gene sequences and pathogenicity between classical and mutant strains of PEDV may lead to diverse invasion mechanisms, this study focused on the cellular entry pathways and cellular transport of the PEDV GI and GII subtype strains in Vero cells and IPEC-J2 cells. We first characterized the kinetics of PEDV entry into cells and found that the highest invasion rate of PEDV was approximately 33% in the IPEC-J2 cells and approximately 100% in the Vero cells. To clarify the specific endocytic pathways, systematic research methods were used and showed that PEDV enters cells via the clathrin-and caveolae-mediated endocytosis pathways, in which dynamin II, clathrin heavy chain, Eps15, cholesterol, and caveolin-1 were indispensably involved. In addition, lipid raft extraction assay showed that PEDV can also enter cells through lipid raft-mediated endocytosis. To investigate the trafficking of internalized PEDV, we found that PEDV entry into cells relied on low pH and internalized virions reached lysosomes through the early endosome-late endosome-lysosome pathway. The results concretely revealed the entry mechanisms of PEDV and provided an insightful theoretical basis for the further understanding of PEDV pathogenesis and guidance for new targets of antiviral drugs. © The Author(s) 2020. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article' s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article'

Answer: PEDV enters cells through clathrin-, caveolae-, and lipid raft-mediated endocytosis and traffics via the endo-/lysosome pathway


Question: To the memory of Rossiter H. Crozier , an evolutionary biologist, who with his generosity and inquisitiveness inspired many students and scientists, in Australia and abroad. doi: bioRxiv preprint 2 Molecular phylogenetics plays a key role in comparative genomics and has an increasinglysignificant impacts on science, industry, government, public health, and society. We posit that the current phylogenetic protocol is missing two critical steps, and that their absence allows model misspecification and confirmation bias to unduly influence our phylogenetic estimates. Based on the potential offered by well-established but under-used procedures (e.g., assessment of phylogenetic assumptions and tests of goodness-of-fit), we introduce a new phylogenetic protocol that will reduce confirmation bias and increase the accuracy of phylogenetic estimates. doi: bioRxiv preprint CONFIRMATION BIAS IN PHYLOGENETICS Bayesian methods (77-82)), or using non-parametric phylogenetic methods (i.e., parsimony methods (66,68,70,71,(83)(84)(85)). In reality, many researchers analyze their data using a range of model-based phylogenetic methods, and reports that only use parsimony methods are increasingly rare. Depending on the chosen phylogenetic method, researchers may have to select a suitable model of sequence evolution (i.e., a model that combines the substitution model and the rates-across-sites model) to apply to the sub-MSA. This choice is often made by using model-selection methods (6,86-97). Having chosen a phylogenetic method and, in relevant cases, a suitable model of sequence evolution, the next step involves obtaining accurate estimates of the tree and evolutionary processes that led to the data. Phylogenetic methods are implemented in many programs (66-85) and, depending on the methods chosen, users often also obtain the nonparametric bootstrap probability (98) or clade credibility (99) to measure support for divergence events in the phylogeny.

Answer:
A new phylogenetic protocol: Dealing with model misspecification and confirmation bias in molecular phylogenetics