A queen bee larvae disease caused by the black queen cell virus (bqcv) is mostly infected with Western bees, and weak groups are susceptible to infestation. Studies have proven that healthy bee colonies have the potential to hide viruses. For example, in 2004, researchers found 4 viruses on a worker bee body, and 93% of queen bees were detected to have 2 to 5 potential infections.
More than 20 bee viruses have been reportedly completely isolated and identified so far, but the connection between them and the death of bees is not yet fully understood. Whether valosporosis and sporangiasis are associated with viral infections and whether it is an additional factor contributing to the death of bees. Black Wangtai virus (bqcv) is one of three bee viruses closely associated with bee spore disease, which has been linked to spore disease causing bee death.
Black Wangtai virus is a single-stranded positive-chain rna virus belonging to the genus Cripivirrus, dicistroviridae. Pre-pupae in queen and worker bees are isolated for the first time and found in the cells of dead pupae. Each of these dead pupae contains at least 1012 isohadic virions with a diameter of 30 nm. As can be seen from the name of the virus, the royal bee platform walls and pupae have turned black. The bqcv virion contains a positive single-stranded RNA genome and 4 capsid proteins with protein molecular weights of 34, 32, 29 and 6kda. BQCV isolated in South Africa by Leat et al. has 8550 nucleotide genomes, excluding poly(a) tails.
BQCV is a widely transmitted disease found in Europe, North America, South Africa, and Australia. In the United States, it is a common bee virus disease; in Australia, it also causes the death of queen bee larvae. In 2005, a survey in the United States showed that 86% of 29 queen bees were positive for bqcv. In 2004, France completed a census of six bee viruses, including bqcv. In summer, adult bees have a 58% chance of contracting bqcv, while pupae have a very small chance of infection, with only 2% being positive for the virus. Adult bees from 24 bee farms were positive for the virus throughout the year, suggesting chronic BQCV infection in these colonies. Siede and Buchler report that the larvae of both worker and male bees are infected with BQCV, although not often observed. The first observation of male wasps was the disease at two apiaries in hesse, Germany, where male bee larvae were found to be bqcv and severe, with some of the larvae already dead.
In the early stages of bqcv infection, pupae are pale yellow with a tough cystic outer skin similar to bee cystic larval disease. The onset of the virus is during the capped nesting phase of the royal bee pupae, and the onset is concentrated in the early spring and summer. The larvae infected with bqcv quickly turn black after death, and finally, the walls of the royal chamber also change from dark brown to black. In the Yuwang group, because the number of Wangtai is large and concentrated, the incidence is higher.
Unlike cystic larval disease viruses, bqcv does not proliferate when ingested by worker bee larvae. The virus proliferates rapidly when it is injected into pupae; the virus does not proliferate when injected into adult bees. In 1995, the Scott-Dupree and McCarthy study confirmed that the presence of microsporidium microsporidium co-infection in host bees increased the proliferation of bqcv virus. Microsporidium infects the midgut epithelium of bees, enhancing the sensitivity of bqcv infection to the digestive tract, which is the main route of transmission of the virus.
However, the virus appears to be a complex of microsporidium pathogenicity, and the observed viral changes in spore disease illustrate this phenomenon. For example, in Toledo, Spain, there was a colony of 80 colonies of bees infected with bqcv, resulting in a large number of adult bees dying. Death symptoms resemble sporangiasis infections, including diarrhea, bloating, midgut edema (abnormal accumulation of aqueous fluid), and an enlarged rectum filled with a transparent liquid substance.
Bailey et al. report that under laboratory conditions, oral infection of bqcv by adult bees relies entirely on the presence of microsporidium. The close association between bqcv and microsporidium is highly susceptible to infection in bee colonies, reflecting the consistency of their proliferation and transmission processes. Bees infected with both bqcv and microsporidiosis will live longer than those infected with microsporidium only. Therefore, mixed infection of microsporidium and bqcv is more harmful than infection of microsporidium alone.
Strict control of the infestation of bee colonies by bee sporangia is the main control measure for this disease. The researchers examined 10 queen bees and found that bqcv was found in both the queen's excreta and intestines, bqcv in 2/3 of the queen's ovaries, and bqcv was absent in the queen's hemolymphatic and fertilized sacs. Microsporidium and bqcv spread and proliferate somewhat similarly. Testing of queen bee feces proves that there is a route of transmission of the virus transmitted by food (feeding) in the colony. The number of viruses is much higher in the intestine than in the ovaries, and the intestines are the main sites of viral replication.
Bee viruses can be detected at all stages of bee development, such as eggs, larvae, pupae, and adult bees. Thus, it can be assumed that the queen bee is infected by the virus, and the virus is transmitted vertically from the queen to the egg. Relevant studies have confirmed that the queen bee can indeed be infected by viruses, and even multiple viruses can be detected at the same time on a single queen bee. Of the 3 to 5 different viral infections, including bqcv, 100% of eggs can be detected with virus, 27% of larvae can detect virus, and adults can detect 3%. The queen bee is positive for only two viruses, bqcv and residual wing virus, with bqcv infection rates of 100% eggs, 22% larvae, and 5% adults. In order to further prove the vertical transmission of the virus, the researchers tested the virus of the surface-disinfected eggs and the queen bee's ovaries, and the virus was detected in the surface-disinfected eggs, which is another strong evidence of the spread of the virus through the ovaries.
Although valet mites are vectors of virus transmission and have an effect on potential viral infections in bees, bqcv does not occur with valerian mites. Tentcheva tested samples of tile mites from 36 French apiaries and showed that there was an 86% chance of no black king virus disease occurring, which meant that bqcv would not be transmitted through tile mites.
The infection process that activates latent viruses in bees is not well understood. Anderson and GIBBS injected table salt water into healthy Australian bee colonies, and BQCV infection was not apparent. The activated virus proliferates to a measurable limit, and the pupa incubates at 35 °C for 3 days. This indicates that when bqcv antiserum is injected, activated bqcv replication is inhibited. In addition, activated bqcv was more infectious during the pupal stage, while replication of Kashmir virus and bee cystic larval virus was suppressed. More in-depth research is needed to demonstrate what determines the outbreak of Black Throne virus disease.
For example, when bqcv occurs during the brooding of a queen, the virus spreads rapidly, preventing the growing queen from laying eggs. It is difficult to identify the status of the virus, and given the close link between the virus and spore disease, strict control of the infestation of bee colonies by bee sporangia is the main control measure to control this disease.
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