Natural selection acts on cellular organisms by ensuring the genes responsible for an advantageous phenotype consistently reap the phenotypic advantage. This is possible because reproductive cells of these organisms are almost always haploid, separating the beneficial gene from its rival allele at every generation. How natural selection acts on plus-strand RNA viruses is unclear because these viruses frequently load host cells with numerous genome copies and replicate thousands of progeny genomes in each cell. Recent studies suggest that these viruses encode the Bottleneck, Isolate, Amplify, Select (BIAS) mechanism that blocks all but a few viral genome copies from replication, thus creating the environment in which the bottleneck-escaping viral genome copies are isolated from each other, allowing natural selection to reward beneficial mutations and purge lethal errors. This BIAS mechanism also blocks the genomes of highly homologous superinfecting viruses, thus explaining cellular-level superinfection exclusion. Expected final online publication date for the Annual Review of Virology, Volume 9 is September 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.
Long noncoding RNAs (lncRNAs) of virus origin accumulate in cells infected by many positive strand (+) RNA viruses to bolster viral infectivity. Their biogenesis mostly utilizes exoribonucleases of host cells that degrade viral genomic or subgenomic RNAs in the 5’-to-3’ direction until being stalled by well-defined RNA structures. Here we report a viral lncRNA that is produced by a novel replication-dependent mechanism. This lncRNA corresponds to the last 283 nucleotides of the turnip crinkle virus (TCV) genome, hence is designated tiny TCV subgenomic RNA (ttsgR). ttsgR accumulated to high levels in TCV-infected Nicotiana benthamiana cells when the TCV-encoded RNA-dependent RNA polymerase (RdRp), also known as p88, was overexpressed. Both (+) and (-) strand forms of ttsgR were produced in a manner dependent on the RdRp functionality. Strikingly, templates as short as ttsgR itself were sufficient to program ttsgR amplification, as long as the TCV-encoded replication proteins, p28 and p88, were provided in trans . Consistent with its replicational origin, ttsgR accumulation required a 5’ terminal carmovirus consensus sequence (CCS), a sequence motif shared by genomic and subgenomic RNAs of many viruses phylogenetically related to TCV. More importantly, introducing a new CCS motif elsewhere in the TCV genome was alone sufficient to cause the emergence of another lncRNA. Finally, abolishing ttsgR by mutating its 5’ CCS gave rise to a TCV mutant that failed to compete with wildtype TCV in Arabidopsis. Collectively our results unveil a replication-dependent mechanism for the biogenesis of viral lncRNAs, thus suggesting that multiple mechanisms, individually or in combination, may be responsible for viral lncRNA production. Importance Many positive strand (+) RNA viruses produce long noncoding RNAs (lncRNAs) during the process of cellular infections, and mobilize these lncRNAs to counteract antiviral defenses, as well as coordinate the translation of viral proteins. Most viral lncRNAs arise from 5’-to-3’ degradation of longer viral RNAs being stalled at stable secondary structures. We report a viral lncRNA that is produced by the replication machinery of turnip crinkle virus (TCV). This lncRNA, designated ttsgR, shares the terminal characteristics with TCV genomic and subgenomic RNAs, and over-accumulates in the presence of moderately overexpressed TCV RNA-dependent RNA polymerase (RdRp). Furthermore, templates that are of similar sizes as ttsgR itself are readily replicated by TCV replication proteins (p28 and RdRp) provided from non-viral sources. In summary, this study establishes an approach for uncovering low abundance viral lncRNAs, and characterizes a replicating TCV lncRNA. Similar investigations on human-pathogenic (+) RNA viruses could yield novel therapeutic targets.
The impact of Gibberella ear rot (GER; caused by Fusarium graminearum) on deoxynivalenol contamination of grain (DON) and yield components in maize were investigated using data from 30 environments in Ohio (3 years x 10 locations). Fifteen hybrids, later classified as susceptible (SU), moderately susceptible (MS), or moderately resistant (MR), based on the magnitude of differences in mean arcsine square-root-transformed GER severity (arcSEV) and log-transformed DON (logDON) relative to a reference susceptible check, were planted in each environment, and 10 ears per hybrid were inoculated with a spore suspension of F. graminearum. Relationships between GER severity and DON were well described by a Kono-Sugino-type nonlinear equation. Estimated parameters representing height (A) and steepness (β) of the curves were significantly higher for SU than MS and MR hybrids, but A was not significantly different between MS and MR. Results from a surrogacy analysis showed that GER was a moderate trial- and individual-level surrogate for DON. Both grain weight per ear and ear diameter decreased with increasing arcSEV, but the regression slopes varied among resistance classes. The rates of reduction in both yield components per unit increase in arcSEV were significantly greater for SU than for MS and MR. An estimated 50% reduction in grain weight occurred at 62% GER severity for SU, compared to 77% severity for MS, and 83% for MR. These results show that GER severity can be used as a surrogate for early estimation of DON contamination and yield loss to help guide grain handling and marketing decisions.
Bacterial resistance is a sanitary issue explained by indiscriminate use of nonprescription drugs, and antimicrobial use in food production for growth promotion. Bothropstoxin-I (BthTx-I) is a phospholipase A2 (PLA2) from Bothrops jararacussu venom, which has a known antimicrobial effect. The goal of this study was the unprecedented evaluation of in vivo antimicrobial activity of BthTx-I in broilers. Microbiological, biochemical, and histological parameters were determined using 84 21-day old broilers that were kept in cages with four birds each at a density of 625 cm2/broiler. The experiment was randomized by three treatments with seven repetitions of four broilers each that lasted seven days. The treatments were: 1) bacitracin zinc diet; 2) PLA2-BthTx-I; 3) without additives. The data obtained from the studied variables was subjected to analysis of variance and an F-test at the 5% significance level. Averages of each variable in each treatment were compared by Tukey’s test. Broiler bacterial cloacal counts showed that BthTx-I decreased the microbial population without reducing body weight, intestinal morphology, or liver or kidney histopathological damage. The toxin showed in vivo activity, being an alternative for better performance in the production of broiler chickens, because it acted by decreasing the microbial load of potentially pathogenic bacteria in the intestinal microbiota of the birds and did not cause muscle, liver or kidney damage at the assessed dosage.
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