Picornalike Viruses of Hymenopterans Wasps and Bees

With its wide host range it is not surprising that CrPV has been isolated from the hymenopterans, the European honeybee, Apis mellifera, the common wasp, Vespa vulgaris, and the German wasp, V. germanica. However, there have been a number of other picorna-like viruses isolated from the honeybee. A 'filterable virus', identified years later as sacbrood virus (SBV), was isolated in 1913 from A. mellifera and later from the Asiatic hive bee A. cerana. Despite their economic importance as pollinators, which far outweighs their value as honey producers, only a few laboratories worldwide have studied the bee viruses. Most of the isolations and characterization studies were carried out at the Rothamsted Experimental Station in England by Leslie 'Bill' Bailey in a 20-year period beginning in the mid-1960s. Table 2 lists the eight viruses from a total of 15 different viruses, that have properties that merit them being designated picorna-like (see also Table 1).

The causative agent of sacbrood was first described in 1913 but it was not until 1964 that it was found to have picorna-like virus properties (SBV). Prior to this, in 1963, acute bee paralysis virus (ABPV) had been described as having picorna-like properties. Although capable of causing paralysis when injected into adult honeybees, ABPV was not initially reported to be associated with any naturally occurring disease symptoms in the UK. However, it has since been found to kill larvae, pupae and adult bees in colonies in other parts of the world when found in association with the parasitic mite Varroa jacobsoni. In the UK ABPV is most frequently detected during the late summer months when colony numbers are at their greatest but drops quickly to a low level over the autumn and winter months. ABPV particles are icosahedral, composed of four capsid proteins and contain single-stranded RNA.

Kashmir bee virus (KBV) was initially isolated from A. cerana in Kashmir and India. Several strains of KBV were subsequently isolated from the European honeybee in Australia and New Zealand as well as from the wasp V. germanica and has since been shown to be pandemic in A. mellifera populations. Initially it was thought to cause extensive mortality in hives. Later studies showed that KBV normally exists in a latent state but that infections with other bee pathogens such as the microsporidian Nosema apis and the foul brood bacterium Melisococcus pluton can trigger virus replication leading to death. Some data suggest that KBV has a serological relationship to ABPV. However, this may be a nonspecific reaction similar to the serological crossreactivity detected between CrPV and the mammalian picornavirus EMCV or an example of convergent evolution since they can both be transmitted through the salivary glands. Molecular studies on the genome of KBV and ABPV will likely resolve these alternatives.

Other picorna-like viruses have been reported for the European honeybee: Berkeley bee paralysis virus (BBPV), black queen cell virus (BQCV), Egypt bee virus (EBV), and slow paralysis virus (SPV). A 30 nm virus, called deformed wing virus, was isolated from A. mellifera in Japan but no detailed characterization has been done so this isolate is not included in Table 1.

Slow paralysis virus was isolated from A. mellifera bees in Britain during field surveys for bee virus X in the early 1970s. It has been found occasionally in honeybees in the UK and causes paralysis of adult A. mellifera bees approximately 12 days after injection. As the name implies this aspect of its pathology distinguishes it from the faster-acting acute and chronic paralysis viruses. BQCV is commonly found in association with N. apis. As the name implies it was first isolated from dead pupae found in queen cells that exhibited a dark brown to black discoloration. The virus is not particularly infectious when fed to larvae or adult bees or injected into the latter. Nevertheless it is a common infection in beehives in the UK, particularly during the early summer months. Apart from the original isolation and description, little is known of either BBPV or EBV.

Experimental manipulations such as the injection of buffer solutions or sera into pupae, or raising the incubation temperature, can induce replication of inapparent viral infections. Conversely, injections of antisera specific to a particular virus into pupae can neutralize or suppress the induction of that virus if it is present. Some experiments using such techniques have suggested a replicative hierarchy among some honeybee viruses. For instance in one series of experiments carried out in Australia, in the absence of suppression, injection with buffer induced primarily KBV. If KBV was neutralized then SBV and BQCV were induced with SBV out-replicating BQCV. If both KBV and SBV were suppressed then BQCV replicated to high levels.

Except for the CrPVBEE isolate, none of the bee viruses have been found to replicate in any insect cell line and no bee cell line exists. This means that detailed studies on the replication of this important class of viruses is lacking although there are substantial data on their biology and pathology.

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