The ectoparasitic mite, Varroa destructor , is unarguably the leading cause of honeybee ( Apis mellifera ) mortality worldwide through its role as a vector for lethal viruses, in particular, strains of the Deformed wing virus (DWV) and Acute bee paralysis virus (ABPV) complexes. This multi-level system of host-parasite-pathogen interactions makes it difficult to investigate effects of either the mite or the virus on natural host survival. The aim of this study was to remove confounding effects of varroa to examine the role of virus susceptibility in the enhanced survival of a naturally adapted Swedish mite-resistant (MR) honeybee population, relative to mite-susceptible (MS) honeybees. Caged adult bees and laboratory reared larvae, from varroa-free colonies, were inoculated with DWV and ABPV in a series of feeding infection experiments, while control groups received virus-free food. Virus infections were monitored using RT-qPCR assays in individuals sampled over a time course. In both adults and larvae the DWV and ABPV infection dynamics were nearly identical between MR and MS groups, but MS adults suffered significantly higher mortality than MR adults. Results suggest virus tolerance, rather than reduced susceptibility or virus resistance, is an important component of the natural survival of this honeybee population.

Plant viruses cause a variety of diseases in susceptible hosts. The disease symptoms often include leaf malformations and other developmental abnormalities, suggesting that viruses can affect plant development. However, little is known about the mechanisms underlying virus interference with plant morphogenesis. Here, we show that a C-4 type zinc-finger (ZF) protein, p12, encoded by a carlavirus (chrysanthemum virus B) can induce cell proliferation, which results in hyperplasia and severe leaf malformation. We demonstrate that the p12 protein activates expression of a regulator of cell size and proliferation, designated upp-L (upregulated by p12), which encodes a transcription factor of the basic/helix-loop-helix family sufficient to cause hyperplasia. The induction of upp-L requires translocation of the p12 protein into the nucleus and ZF-dependent specific interaction with the conserved regulatory region in the upp-L promoter. Our results establish the role of the p12 protein in modulation of host cell morphogenesis. It is likely that other members of the conserved C-4 type ZF family of viral proteins instigate reprogramming of plant development by mimicking eukaryotic transcriptional activators.

Adenovirus encodes for the pVII protein, which interacts and modulates virus DNA structure in the infected cells. The pVII protein is synthesized as the precursor protein and undergoes proteolytic processing by viral proteinase Avp, leading to release of a propeptide sequence and accumulation of the mature VII protein. Here we elucidate the molecular functions of the propeptide sequence present in the precursor pVII protein. The results show that the propeptide is the destabilizing element targeting the precursor pVII protein for proteasomal degradation. Our data further indicate that the propeptide sequence and the lysine residues K26 and K27 regulate the precursor pVII protein stability in a co-dependent manner. We also provide evidence that the Cullin-3 E3 ubiquitin ligase complex alters the precursor pVII protein stability by association with the propeptide sequence. In addition, we show that inactivation of the Cullin-3 protein activity reduces adenovirus E1A gene expression during early phase of virus infection. Collectively, our results indicate a novel function of the adenovirus propeptide sequence and involvement of Cullin-3 in adenovirus gene expression.

The parasitic mite, Varroa destructor, in combination with the viruses it vectors, is the main cause for global colony losses of the European honeybee, Apis mellifera. However, an isolated honeybee population established in 1999 on the Island of Gotland, Sweden has naturally acquired resistance to the mite, and has survived without mite control treatment for more than 18 years. A recent study has shown that this mite resistant (MR) population also appears to be resistant to Black queen cell virus (BQCV) and Sacbrood virus (SBV) and tolerant to Deformed wing virus (DWV), relative to nearby mite susceptible (MS) honeybee populations. In this study, RNA sequencing was employed to corroborate these previous findings and identify other viral factors that may play a role in the enhanced survival of this mite resistant honeybee population. Two additional honeybee-infecting viruses, Apis rhabdovirus-1 (ARV-1) and Lake Sinai virus (LSV), were identified and near-complete genomes of these two viruses were obtained. Phylogenetic analyses of the assembled virus sequences revealed consistent separation between the MR and MS honeybee populations, although it is unclear whether this is due to pre-existing differences between the viruses in the two populations when they were established, and isolated, or due to virus genetic adaptation towards reduced virulence in the MR population, to promote colony survival. Reverse transcription quantitative polymerase chain reaction(RT-qPCR) analyses show higher ARV and LSV titres in MS colonies compared to MR colonies, gradually increasing from summer to autumn 2009, and reaching maximum titres in the following spring 2010. While the DWV and BQCV titres in MR colonies increased between autumn 2009 and spring 2010, the SBV practically disappeared entirely by spring 2010. Possible explanations for the apparent virus tolerance or resistance in the Gotland mite-resistant honeybee population are discussed.

Virus accumulation was reduced when the 8K ORF was disrupted but D RNA was produced. Conversely, the virus accumulated at higher titers when the 8K ORF was intact and D RNA production was blocked. These data demonstrate that the D RNA interferes with virus infection and therefore should be referred to as a defective interfering RNA (DI RNA). The 8K protein was shown to be a weak silencing suppressor. This study provides an example of the interplay between a pathogen and its molecular parasite where virus accumulation was differentially regulated by the 8K protein and DI RNA, indicating that they play antagonistic roles and suggesting a mechanism by which the virus can attenuate replication, decreasing viral load and thereby enhancing its efficiency as a parasite.T he small genome size of RNA viruses means that most viral proteins are multifunctional and that viruses adopt several different strategies for gene expression including overlapping open reading frames (ORFs). In the course of infection many RNA viruses produce defective RNAs (D RNAs), which are deleted versions of the viral genome (see references 1 and 2 for a review). Because they lack essential genetic information, in plants D RNAs are totally dependent on the infectious helper virus for replication, encapsidation, and cell-to-cell and long-distance movement. Interference occurs when D RNA reduces symptom production by the parent virus or/and reduces multiplication of the helper virus; hence, the term defective interfering RNA (DI RNA) is used.Production of D RNA molecules during replication cycles seems to be a common occurrence in many viruses. D and DI RNAs of plant viruses, including DNA and negative-and positivestranded RNA viruses, have been described and characterized previously (1, 2). In some instances, for example, the criniviruses, DI RNAs consist of a mosaic of the multipartite parental viral genome (3). Multiple-deletion DI RNAs are typical for several members of genus Tombusvirus, and these DI RNAs have been extensively studied (4, 5). On the other hand, single-deletion D and DI RNAs have been reported in Potexvirus and Tobravirus genera as well as in several soilborne viruses of the genera Furo-, and Benyvirus (1).Although the DI RNA could represent up to 60% of virusspecific RNA in the infected plants, as in case of tombusviruses, the percentage of encapsidated DI RNAs could be as low as 3 to 4%, and most DI RNAs are not transmitted by vectors (1, 2, 6). Moreover, while most DI RNAs can efficiently accumulate in inoculated tissue, they do not always move systemically, as exemplified by cucumber mosaic virus (CMV) D RNA, which moves long distances in tobacco species but not in tomato, zucchini squash, or muskmelon (1,7,8).Three major mechanisms of interference by DI RNAs have been recognized (reviewed in references 2 and 5). These mechanisms are the following: (i) competition for viral and host resources, which impairs virus replication and attenuates the symptoms; (ii) DI RNA-triggered gene-silencing response; (iii) modulation of the...