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 presentation of viral peptide epitopes to host cytotoxic T lymphocytes (CTLs) is crucial for adaptive cellular immunity to clear the virus infection, especially for some chronic viral infections. Indeed, hosts have developed effective strategies to achieve this goal. The ideal scenario would be that the peptide epitopes stimulate a broad spectrum of CTL responses with diversified T-cell receptor (TCR) usage (the TCR repertoire). It is believed that a diversified TCR repertoire requires a "featured" peptide to be presented by the host major histocompatibility complex (MHC). A featured peptide can be processed and presented in a number of ways. Here, using the X-ray diffraction method, the crystal structures of an antigenic peptide derived from rinderpest virus presented by bovine MHC class I N*01801 (BoLA-A11) have been solved, and two distinct conformations of the presented peptide are clearly displayed. A detailed analysis of the structure and comparative sequences revealed that the polymorphic amino acid isoleucine 73 (Ile73) is extremely flexible, allowing the MHC groove to adopt different conformations to accommodate the rinderpest virus peptide. This makes the peptide more featured by exposing different amino acids for T-cell recognition. The crystal structures also demonstrated that the N*01801 molecule has an unusually large A pocket, resulting in the special conformation of the P1 residue at the N terminus of the peptide. We propose that this strategy of host peptide presentation might be beneficial for creating a diversified TCR repertoire, which is important for a moreeffective CTL response. Viral diseases and other infections caused by intracellular pathogens of cattle result in large global economic losses every year. In the past several decades, rinderpest virus (RPV) (23, 40), foot-and-mouth disease virus (FMDV) (7), and bovine tuberculosis infection (62) have brought disastrous consequences, including social panic and even a threat to human health. Nearly 6 decades ago, most countries were committed to developing more-effective vaccines (46), and remarkable achievements were made in controlling threatening bovine viral infectious diseases and other zoonoses (23, 46). In the 1960s, British virologist Walter Plowright developed a live attenuated vaccine against rinderpest virus, which was widely used in rinderpest eradication efforts (40). However, it still remains extremely challenging for humans to completely eradicate a virus. The questions of how the bovine attenuated vaccine induces immune responses and how the viral peptides are presented and recognized by host immune molecules are still largely unanswered. Therefore, studies on bovine immunity against the rinderpest virus may provide clues for our battle against other viral infections. Generally speaking, effective vaccines have common characteristics: they are rich in T-cell and B-cell epitopes and can induce the immune system to generate protective immune responses (3, 36, 54) . During this process, major histocompatibility complex (MHC) molecules play a pivotal role in the host. MHC class I (MHC I) molecules form a heterotrimer complex composed of the heavy chain of MHC, the antigenic peptide, and ␤ 2 -microglobulin (␤ 2 m). Generally, MHC I loads endogenous peptides, including the virus-derived peptides. Briefly, at the initial stage of virus infection, antigenic proteins are processed in a proteasome-dependent or -independent manner. The resultant short peptides are then transported to the endoplasmic reticulum and are loaded onto the peptidebinding grooves of MHC I molecules. Consequently, the peptide-loading MHC I complexes are translocated to the cell surface and are recognized by cytotoxic T lymphocytes (CTLs) with specific T-cell receptors (TCRs) (49, 63). This immune recognition induces an MHC-restricted CD8 ϩ T-cell response that is characterized by the killing and elimination of the infected cells by effector T cells. The majority of virus-derived peptides are processed and presented through this pathway
[A]: Two Distinct Conformations of a Rinderpest Virus Epitope Presented by Bovine Major Histocompatibility Complex Class I N*01801: a Host Strategy To Present Featured Peptides ᰔ †


[Q]: Early growth response gene-1 (EGR1) is a multifunctional transcription factor that is implicated in viral infection. In this study, we observed that foot-and-mouth disease virus (FMDV) infection significantly triggered EGR1 expression. Overexpression of EGR1 suppressed FMDV replication in porcine cells, and knockdown of EGR1 considerably promoted FMDV replication. A previously reported FMDV mutant virus (with two amino acids mutations in SAP domain) that displays a strong type I interferon (IFN) induction activity was used in this study. We found that SAP mutant FMDV infection induced a higher expression of EGR1 than wildtype FMDV infection, and also triggered higher IFNβ and IFN-stimulated genes (ISGs) expression than wildtype FMDV infection. This implied a link between EGR1 and type I IFN signaling. Further study showed that overexpression of EGR1 resulted in Sendai virus (SeV)-induced IFN-stimulated response element (ISRE) and NF-κB promoter activation. In addition, the SeV-induced ISGs expression was impaired in EGR1 knockdown cells. EGR1 upregulation promoted type I IFN signaling activation and suppressed FMDV and Seneca Valley virus replication. Suppression of the transcriptional activity of EGR1 did not affect its antiviral effect against FMDV. This study reveals a new mechanism evolved by EGR1 to enhance type I IFN signaling and suppress FMDV replication.
[A]: Citation: Early Growth Response Gene-1 Suppresses Foot-and-Mouth Disease Virus Replication by Enhancing Type I Interferon Pathway Signal Transduction


[Q]: Susceptible BALB/c mice, after experimental infection with mouse hepatitis virus 3 (MHV3), revealed virus titres in the liver that increased gradually to a peak of 8 x 10 5 PFU/g of tissue after 3 days' infection, when the mice died of acute hepatitis. BALB/c mice were infected with MHV3, subsequently labelled in vivo with 3SS-methionine, and then the liver preparations from both infected and non-infected animals were subjected to two-dimensional gel electrophoresis. Comparisons of the patterns by computer image analysis revealed 17 gene products which increased, and 8 gene products which decreased, upon virus infection in their two-dimensional gel spot intensity. We conclude that during MHV3 infection of a susceptible strain of mice, a major modification in protein synthesis occurs. The pattern alterations were not related to the virus gene products but were mostly endogenous mouse proteins. Whether these proteins are a result of a defance attempt by the animal, or are dictated by the virus in order to prevent a protective response from happening, remains to be shown.
[A]:
The pattern of proteins synthesized in the liver is profoundly modified upon infection of susceptible mice with mouse hepatitis virus 3