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.

[EX Q]: 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
[EX A]: Echinacea purpurea for Prevention of Experimental Rhinovirus Colds

[EX Q]: We determined the interferon-␥ (IFN-␥) cDNA sequence from three porcine breeds, Duroc, Landrance/Duroc hybrid, and Landrance breeds. Five single nucleotide polymorphisms (SNPs) of porcine IFN-␥ (PoIFN-␥) were identified, respectively, at positions 269 (A/G), 376 (C/T), 426 (T/C), and 465 (T/C) of the coding sequence in Landrance/Duroc hybrid, and at position 251 (A/G) in Landrance breed. Among them, A269G and A251G polymorphisms resulted in Q67R and K61R replacements in the mature protein. PoIFN-␥ cDNAs of Duroc breed (PoIFN-␥-W) and Landrance/Duroc hybrid (PoIFN-␥-M), which, respectively, encoded Q67 and R67, were introduced into a prokaryotic expression vector pET32 to express recombinant PoIFN-␥-W (rPoIFN-␥-W) and rPoIFN-␥-M protein variants in Escherichia coli. The identity of both protein variants was further confirmed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS). We then compared bioactivities of these two recombinant proteins. Although both recombinant protein variants exhibited comparable activities in antiproliferation of PK-15 cells and in nitric oxide (NO) induction of porcine peripheral monocytes, antiviral activity of rPoIFN-␥-W protein was significantly higher (P < 0.001) than that of rPoIFN-␥-M protein in a plaque inhibition assay using pseudorabies virus (PRV). IC50 values of rPoIFN-␥-W and rPoIFN-␥-M protein in anti-PRV assay were determined as 5.3 ± 1.3 and 9.3 ± 4.3 nM, respectively. In conclusion, we have identified five novel SNPs in PoIFN-␥ cDNA, including two missense polymorphisms that result in Q67R and K61R replacements. Our results further demonstrate that Q67R can markedly reduce antiviral activity of the PoIFN-␥ protein. This is the first report that shows the functional SNP in the coding region of IFN-␥. In the future, it is imperative to determine whether Q67R replacement in IFN-␥ may have disease association.
[EX A]: A missense polymorphism in porcine interferon-␥ cDNA affects antiviral activity of the protein variant

[EX Q]: Graphical Abstract Highlights d IFN-gamma inhibits murine norovirus replication complexes via the LC3 conjugation system d Degradative autophagy is not required to affect LC3mediated RC restriction d LC3 and IFN-inducible GTPases are targeted to the RC membrane d IFN-inducible GTPases are required to inhibit MNV replication in mice and humans SUMMARY All viruses with positive-sense RNA genomes replicate on membranous structures in the cytoplasm called replication complexes (RCs). RCs provide an advantageous microenvironment for viral replication, but it is unknown how the host immune system counteracts these structures. Here we show that interferon-gamma (IFNG) disrupts the RC of murine norovirus (MNV) via evolutionarily conserved autophagy proteins and the induction of IFN-inducible GTPases, which are known to destroy the membrane of vacuoles containing bacteria, protists, or fungi. The MNV RC was marked by the microtubule-associatedprotein-1-light-chain-3 (LC3) conjugation system of autophagy and then targeted by immunity-related GTPases (IRGs) and guanylate-binding proteins (GBPs) upon their induction by IFNG. Further, the LC3 conjugation system and the IFN-inducible GTPases were necessary to inhibit MNV replication in mice and human cells. These data suggest that viral RCs can be marked and antagonized by a universal immune defense mechanism targeting diverse pathogens replicating in cytosolic membrane structures.
[EX A]:
Viral Replication Complexes Are Targeted by LC3- Guided Interferon-Inducible GTPases Article Viral Replication Complexes Are Targeted by LC3-Guided Interferon-Inducible GTPases