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Little is known about the insect viruses in wheat sawfly, Dolerus tritici , which is an important agricultural insect feeding on wheat leaves. Here, we used RNA sequencing to identify a novel single positive-strand RNA virus from the larvae of wheat sawfly collected in northern China and then determined its complete genome sequence by rapid amplification of cDNA ends. The complete genome is 9,594 nt in length, including a polyA tail at its 3′ terminus, and it is predicted to encode a 326.3-kDa polyprotein. Phylogenetic analysis based on deduced amino acid sequences of the polyprotein revealed that this RNA virus clustered in a clade with deformed wing virus of the genus Iflavirus , family Iflaviridae. The full genome of this RNA virus shows 42.0–50.0% sequence identity with other iflaviruses. Comparisons of amino acid sequences showed that the coat protein of this RNA virus is most similar to that of slow bee paralysis virus, with 33.6% identity, suggesting that this virus is a new member in the genus Iflavirus . Thus, we have tentatively designated it as “Dolerus tritici iflavirus 1” (DtIV1). To our knowledge, this is the first report of an insect virus in wheat sawfly.

The globally distributed ectoparasite Varroa destructor is a vector for viral pathogens of the Western honeybee (Apis mellifera), in particular the Iflavirus Deformed Wing Virus (DWV). In the absence of Varroa low levels DWV occur, generally causing asymptomatic infections. Conversely, Varroa-infested colonies show markedly elevated virus levels, increased overwintering colony losses, with impairment of pupal development and symptomatic workers. To determine whether changes in the virus population were due Varroa amplifying and introducing virulent virus strains and/or suppressing the host immune responses, we exposed Varroa-naïve larvae to oral and Varroa-transmitted DWV. We monitored virus levels and diversity in developing pupae and associated Varroa, the resulting RNAi response and transcriptome changes in the host. Exposed pupae were stratified by Varroa association (presence/absence) and virus levels (low/high) into three groups. Varroa-free pupae all exhibited low levels of a highly diverse DWV population, with those exposed per os (group NV) exhibiting changes in the population composition. Varroa-associated pupae exhibited either low levels of a diverse DWV population (group VL) or high levels of a near-clonal virulent variant of DWV (group VH). These groups and unexposed controls (C) could be also discriminated by principal component analysis of the transcriptome changes observed, which included several genes involved in development and the immune response. All Varroa tested contained a diverse replicating DWV population implying the virulent variant present in group VH, and predominating in RNA-seq analysis of temporally and geographically separate Varroa-infested colonies, was selected upon transmission from Varroa, a conclusion supported by direct injection of pupae in vitro with mixed virus populations. Identification of a virulent variant of DWV, the role of Varroa in its transmission and the resulting host transcriptome changes furthers our understanding of this important viral pathogen of honeybees.

The association between the deformed wing virus and the parasitic mite Varroa destructor has been identified as a major cause of worldwide honeybee colony losses. The mite acts as a vector of the viral pathogen and can trigger its replication in infected bees. However, the mechanistic details underlying this tripartite interaction are still poorly defined, and, particularly, the causes of viral proliferation in mite-infested bees. Here, we develop and test a novel hypothesis that mite feeding destabilizes viral immune control through the removal of both virus and immune effectors, triggering uncontrolled viral replication. Our hypothesis is grounded on the predator–prey theory developed by Volterra, which predicts prey proliferation when both predators and preys are constantly removed from the system. Consistent with this hypothesis, we show that the experimental removal of increasing volumes of haemolymph from individual bees results in increasing viral densities. By contrast, we do not find consistent support for alternative proposed mechanisms of viral expansion via mite immune suppression or within-host viral evolution. Our results suggest that haemolymph removal plays an important role in the enhanced pathogen virulence observed in the presence of feeding Varroa mites. Overall, these results provide a new model for the mechanisms driving pathogen–parasite interactions in bees, which ultimately underpin honeybee health decline and colony losses.

Parasitoids alter host energy homeostasis to create a favorable environment for their own development. However, the mechanisms underlying this process remain largely unexplored, especially for gregarious parasitoids. Cotesia ruficrus , a gregarious endoparasitoid native to China, targets the invasive pest Spodoptera frugiperda (fall armyworm, FAW) and has been shown to effectively control FAW populations. This study investigates the role of the polydnavirus (PDV) produced by C. ruficrus in regulating lipid metabolism of FAW larvae. The results demonstrated that, following PDV injection for 5 days, both triglyceride concentrations and lipid droplet diameters in the fat bodies of FAW larvae significantly increased. RNA interference (RNAi) targeting the PDV gene CrBV3–31 led to a reduction in triglyceride concentrations and lipid droplet size, along with an upregulation of the LSD1 gene. Furthermore, silencing CrBV3–31 decreased triglyceride levels in C. ruficrus pupae and lowered its eclosion rate. These findings suggest that the PDV gene CrBV3–31 plays a crucial role in enhancing lipid accumulation in FAW larvae, thereby supporting the survival of C. ruficrus offspring. This study uncovers a novel mechanism by which gregarious endoparasitoids exploit symbiotic bracovirus genes to regulate host energy metabolism, increasing lipid levels to meet the developmental needs of their multiple offspring.

Human noroviruses (HuNoVs) are the most common cause of foodborne illness, with a societal cost of $60 billion and 219,000 deaths/year. The lack of robust small animal models has significantly hindered the understanding of norovirus biology and the development of effective therapeutics. Here we report that HuNoV GI and GII replicate to high titers in zebrafish (Danio rerio) larvae; replication peaks at day 2 post infection and is detectable for at least 6 days. The virus (HuNoV GII.4) could be passaged from larva to larva two consecutive times. HuNoV is detected in cells of the hematopoietic lineage and the intestine, supporting the notion of a dual tropism. Antiviral treatment reduces HuNoV replication by >2 log10, showing that this model is suited for antiviral studies. Zebrafish larvae constitute a simple and robust replication model that will largely facilitate studies of HuNoV biology and the development of antiviral strategies.

Many parasites modify their host behaviour to improve their own transmission and survival, but the proximate mechanisms remain poorly understood. An original model consists of the parasitoid Dinocampus coccinellae and its coccinellid host, Coleomegilla maculata; during the behaviour manipulation, the parasitoid is not in contact with its host anymore.We report herein the discovery and characterization of a new RNA virus of the parasitoid (D. coccinellae paralysis virus, DcPV). Using a combination of RT-qPCR and transmission electron microscopy, we demonstrate that DcPV is stored in the oviduct of parasitoid females, replicates in parasitoid larvae and is transmitted to the host during larval development. Next, DcPV replication in the host’s nervous tissue induces a severe neuropathy and antiviral immune response that correlate with the paralytic symptoms characterizing the behaviour manipulation. Remarkably, virus clearance correlates with recovery of normal coccinellid behaviour. These results provide evidence that changes in ladybeetle behaviour most likely result from DcPV replication in the cerebral ganglia rather than by manipulation by the parasitoid. This offers stimulating prospects for research on parasitic manipulation by suggesting for the first time that behaviour manipulation could be symbiont-mediated.

Parasitoids modulate host development for the survival of their offspring, but the mechanisms underlying this phenomenon remain largely unknown. Here, we found that the endoparasitoid Cotesia vestalis disrupted the larval-larval ecdysis in its host Plutella xylostella by the 20-hydroxyecdysone (20E) synthesis pathway. After parasitization by C. vestalis , the 20E peak of host larvae disappeared before the onset of ecdysis and the expression of ecdysone synthesis genes was significantly downregulated. We further found that a Cotesia vestalis bracovirus (CvBV) gene CvBV_28 − 5 was transiently high-level expressed prior to the host’s 20E peak, enabling the precise suppression of this critical developmental signal. Consistently, the knockdown of CvBV_28 − 5 affected the expression of 20E response transcription factors in the cuticle and several ecdysis-related genes. Furthermore, we found that CvBV_28 − 5 bound directly to the Raf, a MAP3K member of the MAPK pathwaythat functions as a critical regulator of ecdysone synthesis genes in hosts. Collectively, our results provide the first evidence that parasitoids modulate host ecdysis by affecting MAPK-20E signaling during a defined developmental window and provide novel insights into the mechanism of parasitoid regulation of host development.

Aedes aegypti mosquitoes are a major vector of arboviruses that oviposit in both artificial containers (i.e., buckets, tires, cans) and natural containers (i.e., coconut husks, tree holes). These diverse container types will seed the larvae microbiome with differing bacterial communities. While the larval microbiome has been shown to alter adult susceptibility to arboviruses including dengue (DENV) and Zika virus (ZIKV), it is not known if exposure to different bacterial communities found between container types impacts adult Ae. aegypti interactions with arboviruses. To address this, rainwater was collected from an artificial container (plastic buckets) and a natural container (coconut husks) from three different collection sites and the microbiomes were preserved. Larval exposure to plastic bucket-derived microbiomes resulted in adults with increased susceptibility to ZIKV compared to larval exposure to coconut husk-derived microbiomes from all three collection sites, indicating that the container type, independent of collection environment, drives variation in adult susceptibility to ZIKV. 16S amplicon sequencing of larvae exposed to the preserved microbiomes revealed that bacterial community structure differed between plastic bucket and coconut husk derived communities at each collection site, but a conserved plastic- or coconut-derived bacterial community across collection sites was not identified. However, water from coconut husks had significantly more total bacterial abundance than water from plastic buckets. Normalization of bacterial loads between container types resulted in similar ZIKV infection rates. Together, these data suggest that larval exposure to specific container type-associated microbiomes alters adult susceptibility to ZIKV, largely driven by differences in total bacterial density between container types. Results from this study will help understand how the urbanization-driven expansion of Ae. aegypti into new/different oviposition sites might affect arbovirus susceptibility.

Symbiotic relationships may provide organisms with key innovations that aid in the establishment of new niches. For example, during oviposition, some species of parasitoid wasps, whose larvae develop inside the bodies of other insects, inject polydnaviruses into their hosts. These symbiotic viruses disrupt host immune responses, allowing the parasitoid’s progeny to survive. Here we show that symbiotic polydnaviruses also have a downside to the parasitoid’s progeny by initiating a multitrophic chain of interactions that reveals the parasitoid larvae to their enemies. These enemies are hyperparasitoids that use the parasitoid progeny as host for their own offspring. We found that the virus and venom injected by the parasitoid during oviposition, but not the parasitoid progeny itself, affected hyperparasitoid attraction toward plant volatiles induced by feeding of parasitized caterpillars. We identified activity of virus-related genes in the caterpillar salivary gland. Moreover, the virus affected the activity of elicitors of salivary origin that induce plant responses to caterpillar feeding. The changes in caterpillar saliva were critical in inducing plant volatiles that are used by hyperparasitoids to locate parasitized caterpillars. Our results show that symbiotic organismsmay be key drivers of multitrophic ecological interactions. We anticipate that this phenomenon is widespread in nature, because of the abundance of symbiotic microorganisms across trophic levels in ecological communities. Their role should be more prominently integrated in community ecology to understand organization of natural and managed ecosystems, as well as adaptations of individual organisms that are part of these communities.

The effect of temperature on insect biology is well understood under constant temperature conditions, but less so under more natural, fluctuating conditions. A fluctuating temperature profile around a mean of 26°C can alter Aedes aegypti vector competence for dengue viruses as well as numerous life-history traits, however, the effect of fluctuations on mosquitoes at critical thermal limits is unknown. We investigated the effects of large and small daily temperature fluctuations at low (16°C) and high (35-37°C) mean temperatures, after we identified these temperatures as being thresholds for immature development and/or adult reproduction under constant temperature conditions. We found that temperature effects on larval development time, larval survival and adult reproduction depend on the combination of mean temperature and magnitude of fluctuations. Importantly, observed degree-day estimates for mosquito development under fluctuating temperature profiles depart significantly (around 10-20%) from that predicted by constant temperatures of the same mean. At low mean temperatures, fluctuations reduce the thermal energy required to reach pupation relative to constant temperature, whereas at high mean temperatures additional thermal energy is required to complete development. A stage-structured model based on these empirical data predicts that fluctuations can significantly affect the intrinsic growth rate of mosquito populations. Our results indicate that by using constant temperatures, one could under- or over-estimate values for numerous life-history traits compared to more natural field conditions dependent upon the mean temperature. This complexity may in turn reduce the accuracy of population dynamics modeling and downstream applications for mosquito surveillance and disease prevention.