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: A randomized, double-blind, placebo-controlled clinical trial was conducted to evaluate the ability of Echinacea purpurea to prevent infection with rhinovirus type 39 (RV-39). Forty-eight previously healthy adults received echinacea or placebo, 2.5 mL 3 times per day, for 7 days before and 7 days after intranasal inoculation with RV-39. Symptoms were assessed to evaluate clinical illness. Viral culture and serologic studies were performed to evaluate the presence of rhinovirus infection. A total of 92% of echinacea recipients and 95% of placebo recipients were infected. Colds developed in 58% of echinacea recipients and 82% of placebo recipients ( , by Fisher's exact test). Administration of echinacea before and after exposure to rhinovirus did not P p .114 decrease the rate of infection; however, because of the small sample size, statistical hypothesis testing had relatively poor power to detect statistically significant differences in the frequency and severity of illness. Colds are the most common acute infectious illnesses in humans. Prevention of the common cold with immunization is not practical because of the antigenic diversity of the many viruses causing colds. For example, rhinoviruses, which account for ∼40% of adult colds, have 1100 antigenic serotypes. Viruses of different and distinct families, such as coronavirus, parainfluenza virus, respiratory syncytial virus, influenza virus, adenovirus, and metapneumovirus, also cause colds. Products derived from Echinacea purpurea, the purple coneflower, are among the most popular herbal remedies in the United States. It is estimated that Americans spend more than $300 million/year on these products [1], which are commonly self-administered for the prevention and treatment of the common cold. The 3

SOLUTION: Echinacea purpurea for Prevention of Experimental Rhinovirus Colds

PROBLEM: doi: bioRxiv preprint 65 required for the antiviral activity of both IFITM3 and IFITM1 [9]. The subcellular localization of 66 IFITMs is a key determinant of their antiviral profile. When expressed singly, IFITM3 and IFITM2 67 preferentially localize to early and late endosomes and lysosomes, and restrict viruses that enter via 68 these endo-lysosomal compartments. In contrast, IFITM1 primarily localizes at the cell surface and 69 can restrict viruses that enter through the plasma membrane [11-14]. Indeed, mutants of IFITM3 70 that lack an N-terminal endocytic sorting motif 20 YEML 23 localize to the plasma membrane and lose 71 their ability to inhibit influenza A virus (IAV), alphavirus and coronavirus infection by endosomal 72 routes [14-18]. 73 74 Studies focusing on IFITM3 restriction of IAV and Semliki Forest Virus (SFV) indicate that virus 75 internalization is unaffected by IFITM3 expression and, for SFV at least, the viral envelope 76 . CC-BY-NC-ND 4.0 International license author/funder. It is made available under a The copyright holder for this preprint (which was not peer-reviewed) is the . https://doi.org/10.1101/737841 doi: bioRxiv preprint 109 knockout mice show enhanced morbidity after infection with IAV, alphaviruses and flaviviruses [33-110 .

SOLUTION: Comparative analysis reveals adaptive evolution of bat IFITMs and a novel 1 antiviral determinant

PROBLEM: Graphical Abstract Highlights d Temporal proteomic analysis quantifies host and viral dynamics during vaccinia infection d Host protein families are proteasomally degraded over the course of vaccinia infection d Vaccinia protein C6 targets HDAC5 for proteasomal degradation d HDAC5 is a host antiviral factor that restricts different families of DNA viruses SUMMARY Vaccinia virus (VACV) has numerous immune evasion strategies, including multiple mechanisms of inhibition of interferon regulatory factor 3 (IRF-3), nuclear factor kB (NF-kB), and type I interferon (IFN) signaling. Here, we use highly multiplexed proteomics to quantify $9,000 cellular proteins and $80% of viral proteins at seven time points throughout VACV infection. A total of 265 cellular proteins are downregulated >2-fold by VACV, including putative natural killer cell ligands and IFN-stimulated genes. Two-thirds of these viral targets, including class II histone deacetylase 5 (HDAC5), are degraded proteolytically during infection. In follow-up analysis, we demonstrate that HDAC5 restricts replication of both VACV and herpes simplex virus type 1. By generating a proteinbased temporal classification of VACV gene expression, we identify protein C6, a multifunctional IFN antagonist, as being necessary and sufficient for proteasomal degradation of HDAC5. Our approach thus identifies both a host antiviral factor and a viral mechanism of innate immune evasion.

SOLUTION:
Quantitative Temporal Proteomic Analysis of Vaccinia Virus Infection Reveals Regulation of Histone Deacetylases by an Interferon Antagonist