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: Genetic and environmental factors will influence the growth of an RNA virus, but their relative contributions are challenging to resolve because standard culture methods mask how virus particles interact with individual host cells. Here, single particles of vesicular stomatitis virus, a prototype RNA virus, were used to infect individual BHK cells. Infected cells produced 50 to 8000 progeny virus particles, but these differences were lost upon subsequent culture, suggesting the diversity of yields reflected cell-to-cell differences rather than viral genetic variation. Cells infected at different phases of their cell cycle produced from 1400 (early S) to 8700 (G 2 M) infectious virus particles, coinciding with the middle-to-upper range of the observed distribution. Fluctuations in virus and cell compositions and noisy gene expression may also contribute to the broad distribution of virus yields. These findings take a step toward quantifying how environmental variation can impact the fitness distribution of an RNA virus.

Answer: Growth of an RNA virus in single cells reveals a broad fitness distribution

Question: Brome mosaic virus (BMV) protein 1a has multiple key roles in viral RNA replication. 1a localizes to perinuclear endoplasmic reticulum (ER) membranes as a peripheral membrane protein, induces ER membrane invaginations in which RNA replication complexes form, and recruits and stabilizes BMV 2a polymerase (2a Pol ) and RNA replication templates at these sites to establish active replication complexes. During replication, 1a provides RNA capping, NTPase and possibly RNA helicase functions. Here we identify in BMV 1a an amphipathic a-helix, helix A, and use NMR analysis to define its structure and propensity to insert in hydrophobic membrane-mimicking micelles. We show that helix A is essential for efficient 1a-ER membrane association and normal perinuclear ER localization, and that deletion or mutation of helix A abolishes RNA replication. Strikingly, mutations in helix A give rise to two dramatically opposite 1a function phenotypes, implying that helix A acts as a molecular switch regulating the intricate balance between separable 1a functions. One class of helix A deletions and amino acid substitutions markedly inhibits 1a-membrane association and abolishes ER membrane invagination, viral RNA template recruitment, and replication, but doubles the 1a-mediated increase in 2a Pol accumulation. The second class of helix A mutations not only maintains efficient 1a-membrane association but also amplifies the number of 1a-induced membrane invaginations 5-to 8-fold and enhances viral RNA template recruitment, while failing to stimulate 2a Pol accumulation. The results provide new insights into the pathways of RNA replication complex assembly and show that helix A is critical for assembly and function of the viral RNA replication complex, including its central role in targeting replication components and controlling modes of 1a action.

Answer: An Amphipathic a-Helix Controls Multiple Roles of Brome Mosaic Virus Protein 1a in RNA Replication Complex Assembly and Function

Question: Background: Enterovirus 71 (EV71) is a highly infectious agent that plays an etiological role in hand, foot, and mouth disease. It is associated with severe neurological complications and has caused significant mortalities in recent large-scale outbreaks. Currently, no effective vaccine or specific clinical therapy is available against EV71. Methods: Unmodified 21 nucleotide small interfering RNAs (siRNAs) and classic 2 0 -modified (2 0 -O-methylation or 2 0 -fluoro modification) siRNAs were designed to target highly conserved 5 0 untranslated region (UTR) of the EV71 genome and employed as anti-EV71 agents. Real-time TaqMan RT-PCR, western blot analysis and plaque assays were carried out to evaluate specific viral inhibition by the siRNAs. Results: Transfection of rhabdomyosarcoma (RD) cells with siRNAs targeting the EV71 genomic 5 0 UTR significantly delayed and alleviated the cytopathic effects of EV71 infection, increased cell viability in EV71-infected RD cells. The inhibitory effect on EV71 replication was sequence-specific and dosage-dependent, with significant corresponding decreases in viral RNA, VP1 protein and viral titer. Appropriate 2 0 -modified siRNAs exhibited similar RNA interference (RNAi) activity with dramatically increased serum stability in comparison with unmodified counterparts. Conclusion: Sequences were identified within the highly conserved 5 0 UTR that can be targeted to effectively inhibit EV71 replication through RNAi strategies. Appropriate 2 0 -modified siRNAs provide a promising approach to optimizing siRNAs to overcome barriers on RNAi-based antiviral therapies for broader administration.

Answer:
The highly conserved 5' untranslated region as an effective target towards the inhibition of Enterovirus 71 replication by unmodified and appropriate 2'-modified siRNAs