TASK DEFINITION: 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.
PROBLEM: Severe acute respiratory syndrome coronavirus (SARS-CoV) encodes eight accessory proteins, the functions of which are not yet fully understood. SARS-CoV protein 6 (P6) is one of the previously studied accessory proteins that have been documented to enhance viral replication and suppress host interferon (IFN) signaling pathways. Through yeast two-hybrid screening, we identified eight potential cellular P6-interacting proteins from a human spleen cDNA library. KEYWORDS severe acute respiratory syndrome coronavirus (SARS-CoV); P6; N-Myc (and STAT) interactor (Nmi); interferon (IFN) signaling pathway; ubiquitination; proteosomal degradation

SOLUTION: Severe acute respiratory syndrome coronavirus protein 6 mediates ubiquitin-dependent proteosomal degradation of N-Myc (and STAT) interactor

PROBLEM: Synthetic decapeptides (N 206) covering the entire sequence of mouse liver fumarylacetoacetate hydrolase (FAH) were used to analyze the specificities of the autoantibodies (autoAb) elicited towards this enzyme in mice infected with mouse hepatitis virus (MHV). These autoAb bound mainly to N-and C-terminal FAH peptides, the most reactive sequences being 1e50 and 390e420, respectively. Surprisingly, although FAH sequence 1e50 shares a high degree of homology with various MHV proteins, the C-terminal portion does not. Moreover, whereas the autoAb reacted with homologous peptides surrounding residues 70, 160 and 360, non-similar sequences around residues 130, 210, 240, 250, and 300 were also recognized, indicating that autoAb were not restricted to epitopes with sequence homologies. There was also a lack of correlation between the amount of anti-MHV or anti-FAH antibodies produced and the reactivity towards the peptides. Moreover, the spectrum of peptides recognized by the autoAb of a given mouse did not change significantly with time, which suggests that the MHV-elicited autoimmune response does not induce an epitope recognition spreading. Finally, anti-FAH Ab produced after immunization with rat liver FAH recognized essentially the same mouse FAH regions than autoAb from MHV-infected mice. Results indicated that the induction of the autoAb is not only related to molecular or structural mimicry, but rather supports the Danger model, in which any aggression, in this case the MHV infection, is susceptible to trigger the production of autoAb.

SOLUTION: The peptide specificities of the autoantibodies elicited by mouse hepatitis virus A59

PROBLEM: Follicular CXCR5 + CD8 + T cells have antiviral effects in chronic virus infection, but the roles of these cells during dengue virus 2 (DENV2) infection remain poorly understood. Objective: This study was conducted to analyzed in detail the dynamic changes and functional properties of circulating follicular CXCR5 + CD8 + T cells to explore their effects on DENV2 infection. Methods: Circulating follicular CXCR5 + CD8 + T cells and cytokines were analyzed by flow cytometry in DENV2 patients at difference days after DENV2 infection. CD8 + T cells were isolated and purified from DENV2 patients, then were stimulated with NS1 peptides and TCR stimulant. After cultivation, multiple parameters were tested. Results: (1) CXCR5 + CD8 + T cells emerged after DENV2 infection, with high PD-1 expression, and were correlated with the reduction in DENV2 RNA viral loads. (2) PD-1 + CXCR5 + CD8 + T cells were negatively associated with disease progression. (3) Serum IFN-g, IL-6 and IL-10 levels were increased late in the course of DENV2 infection. (4) CXCR5 + CD8 + T cells from DENV2 patients exhibited increased cytotoxicity and IFN-g and IL-10 secretion. Conclusion: CXCR5 + CD8 + T cells could play a protective role in dengue pathogenesis and may be a novel strategy for controlling DENV2 infection and vaccine development.

SOLUTION:
Protective role of follicular CXCR5 + CD8 + T cells against dengue virus 2 infection