Acute bee paralysis

The viruses of the acute bee paralysis complex are among the deadliest agents for the honey bee. In a colony with few mites, they usually circulate quietly, without visible symptoms. But when varroa injects them directly into pupae, a handful of particles is enough to kill: a colony can then collapse within weeks, in late summer or autumn¹.

The complex brings together three very closely related viruses: acute bee paralysis virus (ABPV), Kashmir bee virus (KBV) and Israeli acute paralysis virus (IAPV), which was linked in 2007 to colony collapse disorder (CCD) in the United States. This page explains how to recognise them, how to tell them apart from other causes of mortality, and how to prevent them by controlling varroa.

The agents: three viruses from one family

Dicistroviridae

ABPV, KBV and IAPV are small, non-enveloped, single-stranded RNA viruses of the family Dicistroviridae. Their genome carries two successive open reading frames, hence the family name: one encodes the replication proteins, the other the capsid proteins^{2, 8}. They are classified in the genus Aparavirus. They are so close that recombination between strains has been described^{1, 5}.

Despite a similar name and similar symptoms, they are unrelated to the chronic bee paralysis virus (CBPV), which belongs to an entirely different group.

Three discoveries, three stories

• ABPV. It was described in England in 1963 by Bailey and colleagues at Rothamsted, during experiments on chronic paralysis. Injected into healthy bees, it killed them much faster than the chronic virus, hence its name^{4, 1}.
• KBV. It was identified in the mid-1970s from material from the Asian hive bee Apis cerana, originating in Kashmir and India¹.
• IAPV. It was purified in 2002 from dead bees in Israel, then characterised and published in 2007^{1, 5}.

Worldwide, but unevenly distributed

All three viruses are present on most continents, although data remain patchy for parts of Africa, Central Asia and South America. According to the reference review, ABPV is the most common in Europe, KBV is mostly reported from North America and New Zealand, and IAPV was first associated with the Middle East and Australia¹. In France, a national study carried out in the early 2000s detected ABPV in many apiaries, with a clear increase as the season progressed¹¹.

IAPV and colony collapse disorder

In 2007, a US team used metagenomics to survey the microorganisms in colonies affected by CCD, in which hives lose their adult bees without visible corpses. Of all the agents detected, IAPV was the one most strongly correlated with affected colonies⁶. The authors presented it as a marker of CCD, not as its proven cause.

Later work qualified this result:

• IAPV was already present in the United States before CCD appeared, and it has become permanently established in bee populations⁸.
• The descriptive study of CCD published in 2009 did not find a single pathogen explaining the syndrome. Above all, it showed that bees from collapsed colonies carried more pathogens at once, and in larger quantities, pointing to an interaction between diseases and other stress factors⁷.
• A 2014 review concludes that IAPV is not consistently associated with CCD, but that its ability to increase bee mortality is firmly established⁸.

CCD is now generally considered multifactorial; IAPV may play an aggravating role without explaining the whole phenomenon.

How these viruses spread

Varroa, the main amplifier

Varroa is an efficient vector of all three viruses. Transmission studies show that it passes ABPV from bee to bee very efficiently, without the virus apparently replicating in the mite itself¹. For IAPV, experiments have shown that bees exposed to virus-carrying mites become infected, and that the viral load then increases in the bee⁹.

The route of infection changes everything. Orally, massive doses of virus are needed to kill a bee. By injection into the haemolymph, which is what varroa does when feeding, fewer than a hundred particles are enough to cause death within a few days¹. Varroa thus turns a silent infection into a lethal one.

Other routes

• Food and contact. The viruses are found in faeces, royal jelly, honey, pollen and the hypopharyngeal glands of nurse bees. They therefore circulate through food sharing, larval feeding and cannibalism of brood^{1, 8}.
• Vertical transmission. IAPV has been detected in eggs, larvae and queen ovaries, and ABPV in drone semen: the queen can pass the virus on to her offspring^{1, 8}.
• Between colonies. Robbing, drifting and exchanging frames move both viruses and mites.

Why it matters

Without varroa, these viruses persist at low levels. With it, everything changes. The mite population peaks in late summer, just as the colony is raising its winter bees. Viral loads also rise over the season: ABPV tends to peak in late summer, KBV rather in autumn^{1, 11}.

Infected pupae die in their cells or emerge doomed. The colony loses young bees faster than it replaces them, attracts robbers and dies out before winter, or goes into winter too weak to survive.

ABPV was heavily implicated in varroa-related colony losses in Europe in the 1980s and 1990s¹. More recently, the large German bee monitoring project showed that ABPV infection detected in autumn was significantly associated with colony death the following winter, usually together with heavy varroa infestation¹⁰.

Recognising the disease

Symptoms

The signs are not specific and often go unnoticed.

• Bees that tremble, cannot fly and crawl in front of the hive, then die within a few days.
• In affected bees, gradual loss of hair from the thorax and abdomen, which take on a dark, shiny appearance (described for ABPV and IAPV)¹.
• Patchy brood, pupae dead in their cells, sometimes without characteristic lesions.
• Rapid population decline in late summer or autumn, often with stores still present.
• Usually, accompanying signs of varroosis: deformed wings, spotty brood.

Unlike chronic paralysis, heaps of paralysed bees in front of the hive are rarely seen. The disease moves so fast from paralysis to death that sick bees do not have time to accumulate¹.

Do not confuse with

Starvation or nosema can also produce crawling bees. Only the laboratory can decide.

Diagnosis

What you can do in the apiary

1. Measure varroa infestation by alcohol wash or sugar roll. High infestation in late summer makes a viral cause very likely.
2. Examine the brood: dead pupae, perforated cappings, deformed wings in young bees.
3. Compare colonies in the apiary: collapse limited to the most infested colonies points to viruses; simultaneous mortality across the whole apiary points to poisoning.

Laboratory testing

Diagnosis relies on RT-PCR, usually real-time (RT-qPCR), which detects and quantifies viral RNA in a sample of bees¹.

Two points of caution when interpreting results:

• Because these viruses are widespread, a positive result does not prove on its own that they caused the deaths. What matters is a high viral load in sick bees.
• Because the three viruses are so similar, specific primers are needed: some early KBV primers also detected the other viruses of the complex¹.

Live, symptomatic bees are the preferred sample, stored according to the laboratory’s instructions; old corpses are poorly suited to analysis.

Regulations

In France, the acute paralysis viruses are not regulated diseases: detecting them triggers no official animal health measures. However, any sudden mass mortality of bees should be reported to the state veterinary services (DDPP or DDETSPP), in particular to rule out poisoning.

In several regions, the French Honey Bee Mortality and Weakening Observatory (OMAA) offers a single reporting desk: the beekeeper calls a regional number and the report is directed to the appropriate scheme, whether it concerns a regulated disease, acute mass mortality or colony weakening¹². The status of these viruses and reporting procedures vary between countries.

Prevention and management

No treatment

There is no authorised medicine against these viruses. RNA interference approaches have given experimental results against IAPV⁸, but they are not a treatment available to beekeepers.

Control varroa

This is the decisive measure. Preventing acute paralysis is all about keeping varroa from reaching high levels when winter bees are being raised^{1, 10}: count before and after the summer treatment, treat early after the last harvest with an authorised medicine according to the label, treat the whole apiary at the same time, then carry out a broodless winter treatment. Details are on the Varroa page.

Limit spread

General good beekeeping practices complement varroa control³:

• Reduce entrances at the end of the season and avoid anything that triggers robbing.
• Close up dead or dying colonies quickly, as they are sources of viruses and mites.
• Do not move frames from a sick colony to a healthy one.
• Requeen chronically weak colonies and favour hygienic lines.
• Ensure good nutrition for winter bees.

For general hygiene rules, see Apiary biosecurity and Disinfecting equipment.

Most common mistakes

• Looking for an antiviral treatment instead of counting and treating mites.
• Treating too late, in September or October, when winter bees are already infected.
• Concluding it is poisoning without counting mites, or the reverse.
• Uniting a sick colony with a healthy one.
• Leaving dead hives open to robbing.
• Reading a positive PCR as proof of the cause of death, without considering viral load and context.

Frequently asked questions

My bees are trembling in front of the hive: is it acute or chronic paralysis? You cannot tell by eye. Heaps of black, trembling bees in spring or summer suggest chronic paralysis; a heavily infested colony emptying out in late summer suggests acute paralysis. Only PCR can confirm.

Is the Israeli virus the cause of CCD? Not on its own. It was strongly associated with affected colonies in 2007, but later studies did not confirm a consistent link. CCD is now considered multifactorial.

Can an affected colony be saved? Rarely, if the collapse is advanced. Efforts are mainly directed at neighbouring colonies that are still healthy.

Should the equipment of a colony that died of acute paralysis be destroyed? No. Clean the equipment and check that no other disease, especially foulbrood, is involved before reusing the frames.

Is honey from an affected colony safe to eat? These insect viruses pose no risk to humans. However, do not feed these stores to other colonies.

References

1. de Miranda J.R., Cordoni G., Budge G. (2010). The Acute bee paralysis virus-Kashmir bee virus-Israeli acute paralysis virus complex. Journal of Invertebrate Pathology 103: S30-S47. doi.org
2. Chen Y.P., Siede R. (2007). Honey bee viruses. Advances in Virus Research 70: 33-80. doi.org
3. FAO, IZSLT, Apimondia, CAAS (2021). Good beekeeping practices for sustainable apiculture. FAO Animal Production and Health Guidelines No. 25.
4. Bailey L., Gibbs A.J., Woods R.D. (1963). Two viruses from adult honey bees (Apis mellifera Linnaeus). Virology 21(3): 390-395. doi.org
5. Maori E., Lavi S., Mozes-Koch R., Gantman Y., Peretz Y., Edelbaum O., Tanne E., Sela I. (2007). Isolation and characterization of Israeli acute paralysis virus, a dicistrovirus affecting honeybees in Israel: evidence for diversity due to intra- and inter-species recombination. Journal of General Virology 88(12): 3428-3438.
6. Cox-Foster D.L., Conlan S., Holmes E.C., Palacios G., Evans J.D., Moran N.A. et al. (2007). A metagenomic survey of microbes in honey bee colony collapse disorder. Science 318(5848): 283-287. doi.org
7. vanEngelsdorp D., Evans J.D., Saegerman C., Mullin C., Haubruge E., Nguyen B.K. et al. (2009). Colony collapse disorder: a descriptive study. PLoS ONE 4(8): e6481. doi.org
8. Chen Y.P., Pettis J.S., Corona M., Chen W.P., Li C.J., Spivak M. et al. (2014). Israeli acute paralysis virus: epidemiology, pathogenesis and implications for honey bee health. PLoS Pathogens 10(7): e1004261. doi.org
9. Di Prisco G., Pennacchio F., Caprio E., Boncristiani H.F. Jr., Evans J.D., Chen Y. (2011). Varroa destructor is an effective vector of Israeli acute paralysis virus in the honeybee, Apis mellifera. Journal of General Virology 92(1): 151-155.
10. Genersch E., von der Ohe W., Kaatz H., Schroeder A., Otten C., Büchler R. et al. (2010). The German bee monitoring project: a long term study to understand periodically high winter losses of honey bee colonies. Apidologie 41(3): 332-352. doi.org
11. Tentcheva D., Gauthier L., Zappulla N., Dainat B., Cousserans F., Colin M.E., Bergoin M. (2004). Prevalence and seasonal variations of six bee viruses in Apis mellifera L. and Varroa destructor mite populations in France. Applied and Environmental Microbiology 70(12): 7185-7191. doi.org
12. Plateforme ESA, OMAA monitoring group (2022). L'Observatoire des mortalités et des affaiblissements de l'abeille mellifère (OMAA) : un système de surveillance innovant (in French). plateforme-esa.fr

Updated : October 8, 2026
Written by : Apisanitas editorial team
Reviewed by : Review in progress