Colony Collapse Disorder (CCD), a special case of collapse of honey bee colonies, has resulted in significant losses for beekeepers. CCD-colonies show abundance of pathogens which suggests that they have a weakened immune system. Since honey bee viruses are major players in colony collapse and given the important role of viral RNA interference (RNAi) in combating viral infections we investigated if CCD-colonies elicit an RNAi response. Deep-sequencing analysis of samples from CCD-colonies from US and Israel revealed abundant small interfering RNAs (siRNA) of 21-22 nucleotides perfectly matching the Israeli acute paralysis virus (IAPV), Kashmir virus and Deformed wing virus genomes. Israeli colonies showed high titers of IAPV and a conserved RNAi-pattern of matching the viral genome. That was also observed in sample analysis from colonies experimentally infected with IAPV. Our results suggest that CCD-colonies set out a siRNA response that is specific against predominant viruses associated with colony losses.

To evaluate symptoms, extent, and possible causes of colony decline and losses in Israel, we carried out (1) a survey of honeybee colony losses and potential causes via mail and phone; (2) systematic sampling of healthy and problematic beehives after requeening in the winter; (3) detection of Varroa and pathogens including, viruses and Nosema ceranae, by microbiological means and sensitive RT-PCR. From 58 beekeepers (46 000 colonies) interviewed, 40% complained of extensive colony loses during 2008. Examination and sampling for pests and pathogens of 113 hives in the winter of 2009 showed 35% of hives with Nosema and 21% with V. destructor. The most frequent viruses detected were Black Queen Cell Virus, Israeli Acute Paralysis Virus, and Deformed Wing Virus. A significant negative correlation was found between worker population in the hive and the presence of viral and Nosema infections. Apis mellifera / Bee viruses / Varroa / Nosema

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The determinants of Colony Collapse Disorder (CCD), a particular case of collapse of honey bee colonies, are still unresolved. Viruses including the Israeli acute paralysis virus (IAPV) were associated with CCD. We found an apiary with colonies showing typical CCD characteristics that bore high loads of IAPV, recovered some colonies from collapse and tested the hypothesis if IAPV was actively replicating in them and infectious to healthy bees. We found that IAPV was the dominant pathogen and it replicated actively in the colonies: viral titers decreased from April to September and increased from September to December. IAPV extracted from infected bees was highly infectious to healthy pupae: they showed several-fold amplification of the viral genome and synthesis of the virion protein VP3. The health of recovered colonies was seriously compromised. Interestingly, a rise of IAPV genomic copies in two colonies coincided with their subsequent collapse. Our results do not imply IAPV as the cause of CCD but indicate that once acquired and induced to replication it acts as an infectious factor that affects the health of the colonies and may determine their survival. This is the first follow up outside the US of CCD-colonies bearing IAPV under natural conditions.

The aim of this study was to explore the extent of varroa mite resistance to fluvalinate in Israel and to determine the underlying biochemical mechanism. Assays at different apiaries indicated varroa mite resistance at three of the five sites tested. Dose response assays conducted with tau-fluvalinate on mites obtained from different sites indicated uneven resistance. A monooxygenase assay revealed an increased rate (approximately 20-fold) of activity in mites that were not controlled by the pesticide, as compared to activity in mites from untreated colonies. A minor, 1.5-2.5 fold, increase of esterase activity was also noted in the resistant mites. This first demonstration of a fluvalinate-resistance mechanism in varroa mites points to the need for more vigorous resistance management practices to control the pest.