Chronic bee paralysis virus (CBPV) commonly affects adult Apis mellifera honey bees and causes a chronic paralysis that can easily spread to other members of a colony. Bees infected with CBPV begin to show symptoms after 5 days and die a few days after. [1] Chronic bee paralysis virus infection is a factor that can contribute to or cause the sudden collapse of honeybee colonies. [2] Since honeybees serve a vital role in ecological resilience, it is important to understand factors and diseases that threaten them.
Although CBPV infects mainly adult bees, the virus can also infect bees in earlier developmental stages, though developing bees typically have significantly lower viral loads compared to their adult counterparts. Death as a result of CBPV infection in developing bees or brood losses due to viral infection are low or nonexistent. [3]
Bees that have been infected with CBPV may harbor millions of viral particles, with half of them concentrated in the head region of the infected honey bee. As a result, the virus has neurotropic activity, allowing the virus to cause nervous system damage in infected honey bees. Specifically, research has identified that viral particles concentrate primarily in two centers of the brain to replicate after infecting the host. The first replication center is the mushroom bodies, which play a role in sensory processing, memory, learning, and motor control, and the second replication center the central body, the center of the insect brain that primarily control locomotion, behavior, bodily orientation, and arousal. [3] [4]
Chronic bee paralysis virus shares similarities to the virus families Nodaviridae and Tombusviridae , but CBPV is distinct enough from the two existing families and consequently is considered a new family of viruses. As a result, CBPV has yet to be fully classified. [5] [6] Chronic bee paralysis virus is a single-stranded positive-RNA virus with five fragments, two large fragments and three small fragments. [6] The first large fragment is suspected to encode an RNA-dependent RNA polymerase, as it possesses 8 conserved domains of an RNA-dependent RNA polymerase. [3] The second large fragment is thought to encode for the virus capsid protein, which is reported to be a capsid protein of 23.5 kDa and four polypeptides of 75, 50, 30 and 20 kDa. [7] [6] [8] The virus capsid is hypothesized to have icosahedral symmetry. [3]
Chronic bee paralysis virus is also found to facilitate the growth and reproduction of a satellite virus, called Chronic bee paralysis associate satellite virus (CBVA), which has three small (+) single-stranded RNA fragments. The three small (+) single-stranded RNA fragments appear inconsistently in the Chronic bee paralysis virus, which lends to the idea that the three RNAs are not components of CBPV but of a satellite virus that relies on CBPV activity in order to proliferate. [2] Additionally, the three small RNA fragments each have molecular weights of 0.35 x 106 (1100 nucleotides), which exactly matches the molecular weights of the three (+) ssRNA fragments of CBVA. [9]
Chronic bee paralysis virus is transmitted through two main mechanisms. The first mechanism is viral transmission through bee feces, which remains on the hive floor and can be picked up on the furry legs of other bees and ingested orally. [10] The second mechanism is through close contact between bees in the hive. Worker bees are the most susceptible to infection, since they travel the hive most frequently. The infection may spread between hives as a result of indirect contact or direct contact between honey bees. [11] Research shows that mainly adult honey bees can be infected with chronic bee paralysis virus by a topical contact with infected feces or by ingestion of virion-containing substances. [3]
Chronic bee paralysis virus is transmitted to honey bees through a ubiquitous parasite common to honey bee hives, Varroa mites ( Varroa destructor ). Varroa mites are known to harbor many viruses for which honey bees are susceptible and permissive. [12] The parasitic mites attach themselves to honey bees externally and feed off of the hemolymph of their hosts. [12] This exchange of fluids between the parasitic mites and the hosts allows for CBPV particles to enter fluid transfer systems in the honey bee body. The mechanisms by which chronic bee paralysis virus gains entry into honey bee cells is currently unknown.
Like other positive sense single-stranded RNA viruses, Chronic bee paralysis virus replicates in the cytoplasm of honeybee cells. The first large (+) RNA fragment in the CBPV genome likely encodes for an RNA-dependent RNA polymerase, which makes many copies of viral RNA. After many copies of the genome have been produced, the honey bee host's cellular processes will translate the viral RNA into functional proteins which can cause propagation of the virus inside the host. The virus replicates at the highest levels in the head of the honeybee, reaching an average of 107 copies of the virus in an infected worker bee head and as many as 1011 copies of the virus in an infected queen bee head. Chronic bee paralysis virus particles have been found to concentrate in two centers; in mushroom bodies which play a role in sensory processing, memory, and learning as well as in the central body, which plays a vital role in coordinating movement. Loss of flying ability in honey bees as a result of CBPV infection can be attributed to neuron destruction in the central body. Erratic behavior in infected bees may be a result of mushroom body neuron destruction.
Infected honeybees will begin to show symptoms of the illness within five days of infection, and the infection presents in two distinct ways, with Type I infection being the more common of the two infection types.
A Type I infected bee presents with a bloated abdomen due to a fluid-filled honey sac and weak or trembling wings. Type I infected honey bees tend to crawl on the ground or cluster near the entrance of the hive, as their weakened wings lead to an inability to fly.
A Type II infected honey bee presents with complete abdominal hair loss, causing it to appear black and greasy. These bees are still able to fly 2–3 days after symptoms begin to appear, but they lose their ability to fly shortly before succumbing to the disease.
A third type of infection that is a major contributor to the spread of the virus is an infection of CBPV in which the infected bee exhibits no symptoms of the illness. The infected bee does not present with any of the classic symptoms of the disease before death, and, as a result, is able to transmit the virus beyond its own hive.
There is no known treatment for the disease currently.
Chronic bee paralysis virus is classified as an inapparent infection because there are few tell-tale symptoms that appear before the infection has progressed to a fatal degree. As many honey bees can become infected and either show symptoms days after the initial point of infection or fail to show any symptoms throughout the entire course of the illness, CBPV can infect entire hives before the virus is detected. Despite the use of infectivity and serological tests, these testing methods are often inaccurate and difficult to reproduce with consistent results. [3]
Although Chronic bee paralysis virus mainly infects honey bees, the virus has also been found to replicate in two species of carnivorous ant, Camponotus vagus and Formica rufa . These carnivorous ants become infected with CBPV through two mechanisms: eating decomposing bees who harbor the virus or by independently collecting infected honeydew. [13] While the virus does not cause any symptoms in the carnivorous ants, the commensal relationship between the virus and the ants allows the ants to serve as a reservoir for viral replication to occur. [13]
Chronic bee paralysis virus is also similar to slow bee paralysis virus and acute bee paralysis virus. Though CBPV does not fall into the same family as the other two viruses, it bears similarities to the other viruses because it causes paralysis as the fatal symptom of the infection. Slow bee paralysis, in contrast to Chronic bee paralysis virus, causes paralysis of the front two pairs of legs on honey bees (Apis mellifera), silkworms ( Bombyx mori ), and bumble bees (Bombis spp.). This paralysis eventually causes death in the infected insects. Slow bee paralysis virus is transmitted to hives through Varroa destructor mite infestations. Because of the similarities between the two viruses, Chronic bee paralysis virus is suspected to have the same mode of transmission.
Chronic bee paralysis virus is also seen to interact with satellite viruses. The three short RNA segments of the viral genome are thought to be a satellite virus. [2] Only in the presence of CBPV can the associated satellite virus proliferate.
The Apis mellifera mellifera is a subspecies of the western honey bee, evolving in central Asia, with a proposed origin of the Tien Shan Mountains and later migrating into eastern and then northern Europe after the last ice age from 9,000BC onwards. Its original range included the southern Urals in Russia and stretched through northern Europe and down to the Pyrenees. They are one of the two members of the 'M' lineage of Apis mellifera, the other being in western China. Traditionally they were called the Black German Bee, although they are now considered endangered in Germany. However today they are more likely to be called after the geographic / political region in which they live such as the British Black Bee, the Native Irish Honey Bee, the Cornish Black Bee and the Nordic Brown Bee, even though they are all the same subspecies, with the word "native" often inserted by local beekeepers, even in places where the bee is an introduced foreign species. It was domesticated in Europe and hives were brought to North America in the colonial era in 1622 where they were referred to as the English Fly by the Native Americans.
Formica rufa, also known as the red wood ant, southern wood ant, or horse ant, is a boreal member of the Formica rufa group of ants, and is the type species for that group, being described already by Linnaeus. It is native to Eurasia, with a recorded distribution stretching from the middle of Scandinavia to the northern Iberia and Anatolia, and from Great Britain to Lake Baikal, with unconfirmed reportings of it also to the Russian Far East. There are claims that it can be found in North America, but this is not confirmed in specialised literature, and no recent publication where North American wood ants are listed mentions it as present, while records from North America are all listed as dubious or unconfirmed in a record compilation. Workers' head and thorax are colored red and the abdomen brownish-black, usually with a dorsal dark patches on the head and promensonotum, although some individuals may be more uniform reddish and even have some red on the part of the gastern facing the body. In order to separate them from closely related species, specimens needs to be inspected under magnification, where difference in hairyness are among the telling characteristics, with Formica rufa being more hairy than per example Formica polyctena but less hairy than Formica lugubris. Workers are polymorphic, measuring 4.5–9 mm in length. They have large mandibles, and like many other ant species, they are able to spray formic acid from their abdomens as a defence. Formic acid was first extracted in 1671 by the English naturalist John Ray by distilling a large number of crushed ants of this species. Adult wood ants primarily feed on honeydew from aphids. Some groups form large networks of connected nests with multiple queen colonies, while others have single-queen colonies.
Nosema apis is a microsporidian, a small, unicellular parasite recently reclassified as a fungus that mainly affects honey bees. It causes nosemosis, also called nosema, which is the most common and widespread of adult honey bee diseases. The dormant stage of N. apis is a long-lived spore which is resistant to temperature extremes and dehydration, and cannot be killed by freezing the contaminated comb. Nosemosis is a listed disease with the Office International des Epizooties (OIE).
Varroa destructor, the Varroa mite, is an external parasitic mite that attacks and feeds on honey bees and is one of the most damaging honey bee pests in the world. A significant mite infestation leads to the death of a honey bee colony, usually in the late autumn through early spring. Without management for Varroa mite, honey bee colonies typically collapse within 2 to 3 years in temperate climates. These mites can infest Apis mellifera, the western honey bee, and Apis cerana, the Asian honey bee. Due to very similar physical characteristics, this species was thought to be the closely related Varroa jacobsoni prior to 2000, but they were found to be two separate species after DNA analysis.
Varroa is a genus of parasitic mesostigmatan mites associated with honey bees, placed in its own family, Varroidae. The genus was named for Marcus Terentius Varro, a Roman scholar and beekeeper. The condition of a honeybee colony being infested with Varroa mites is called varroosis.
Kakugo virus is a picorna-like virus most commonly found in the brains of worker bees. It is a subtype of the Deformed wing virus. The Kakugo virus, when resident in a bee's brain, can contribute to aggressive behaviors similar to those preeminent during a bee's guard phase in their life cycle. Kakugo is the first virus to have been found to cause aggressive behavior, although because the virus was only recently discovered to have such effects, research into the matter is limited.
Deformed wing virus (DWV) is an RNA virus, one of 22 known viruses affecting honey bees. While most commonly infecting the honey bee, Apis mellifera, it has also been documented in other bee species, like Bombus terrestris, thus, indicating it may have a wider host specificity than previously anticipated. The virus was first isolated from a sample of symptomatic honeybees from Japan in the early 1980s and is currently distributed worldwide. It is found also in pollen baskets and commercially reared bumblebees. Its main vector in A. mellifera is the Varroa mite. It is named after what is usually the most obvious deformity it induces in the development of a honeybee pupa, which is shrunken and deformed wings, but other developmental deformities are often present.
Nosema ceranae is a microsporidian, a small, unicellular parasite that mainly affects Apis cerana, the Asiatic honey bee. Along with Nosema apis, it causes the disease nosemosis, the most widespread of the diseases of adult honey bees. N. ceranae can remain dormant as a long-lived spore which is resistant to temperature extremes and dehydration. This fungus has been shown to act in a synergistic fashion with diverse insecticides such as fipronil or neonicotinoids, by increasing the toxicity of pesticides for bees, leading to higher bee mortality. It may thus play an indirect role in colony collapse disorder. In addition, the interaction between fipronil and N. ceranae induces changes in male physiology leading to sterility.
Animal viruses are viruses that infect animals. Viruses infect all cellular life and although viruses infect every animal, plant, fungus and protist species, each has its own specific range of viruses that often infect only that species.
Colony collapse disorder (CCD) is an abnormal phenomenon that occurs when the majority of worker bees in a honey bee colony disappear, leaving behind a queen, plenty of food, and a few nurse bees to care for the remaining immature bees. While such disappearances have occurred sporadically throughout the history of apiculture, and have been known by various names, the syndrome was renamed colony collapse disorder in early 2007 in conjunction with a drastic rise in reports of disappearances of western honey bee colonies in North America. Beekeepers in most European countries had observed a similar phenomenon since 1998, especially in Southern and Western Europe; the Northern Ireland Assembly received reports of a decline greater than 50%. The phenomenon became more global when it affected some Asian and African countries as well. From 1990 to 2021, the United Nation’s FAO calculated that the worldwide number of honeybee colonies increased 47%, reaching 102 million.
Camponotus vagus is a species of large, black, Palaearctic carpenter ant with a wide range that includes much of Europe, a large area of Asia, and part of Africa.
Iflaviridae is a family of positive sense RNA viruses insect-infecting viruses. Some of the insects commonly infected by iflaviruses include aphids, leafhoppers, flies, bees, ants, silkworms and wasps. The name "Ifla" is derived from the name "Infectious flacherie virus", a member species. There is one genus (Iflavirus) and 16 species in this family.
Varroa sensitive hygiene (VSH) is a behavioral trait of honey bees (Apis mellifera) in which bees detect and remove bee pupae that are infested by the parasitic mite Varroa destructor. V. destructor is considered to be the most dangerous pest problem for honey bees worldwide. VSH activity results in significant resistance to the mites.
Apocephalus borealis is a species of North American parasitoid phorid fly that attacks bumblebees, honey bees, and paper wasps. This parasitoid's genus Apocephalus is best known for the "decapitating flies" that attack a variety of ant species, though A. borealis attacks and alters the behavior of bees and wasps. These flies are colloquially known as zombie flies and the bees they infect are colloquially known as zombees. Association with honey bees has so far only been documented from California, South Dakota, Oregon, Washington, British Columbia, and Vermont.
Aparavirus is a genus of viruses in the order Picornavirales, in the family Dicistroviridae. Invertebrates, honeybee, and bumblebees serve as natural hosts. There are six species in this genus. Diseases associated with this genus include: ABPV: paralysis. This virus plays a role in sudden collapse of honey bee colonies infested with the parasitic mite varroa destructor.
Nodamura virus (NoV) is a member of the family Nodaviridae, which was originally isolated from mosquitoes in Japan near the village of Nodamura in 1956. Other members of Nodaviridae are flock house virus (FHV) and black beetle virus (BBV). NoV has been found to multiply in several insect and tick species; however, these infected individuals seem to be asymptomatic. Nodamura virus is the only member of the genus Alphanodavirus that can infect insects, fish, and mammals.
Slow bee paralysis virus (SBPV) is a virus discovered in England in 1974 that infects honeybees, bumblebees, and silkworms through Varroa destructor mite infestations. The virus causes paralysis in the front two pairs of legs of adult bees eventually killing its hosts. The virus is in the iflaviridae family of viruses. Infection by iflaviridae viruses is among the leading cause of death of honeybee colonies. As bees and silkworms are of great economic and biological importance, the virus is the subject of ongoing research.
The black queen cell virus (BQCV) is a virus that infects honey bees, specifically Apis mellifera, Apis florea, and Apis dorsata. Infection of the latter two species is more recent and can be attributed to genetic similarity and geographical closeness.
The evolution of the Sacbrood virus (SBV) is characterized by the genomic changes that have occurred in SBV since its initial discovery in 1913, which have enabled the virus to continuously infect a wide array of honeybee colonies. SBV is single stranded RNA virus (genus: Iflavirus) that most commonly infects honeybee larvae, and is known to wipe out entire honeybee colonies quickly. Due to SBV, there has been sharp declines in honey bee populations in Europe, as well as a 30% decline each year in U.S. colonies. Studies on the evolution of SBV have arisen in hopes to stop these colony devastations. SBV is one of the most widely studied honeybee viruses in terms of genomic analysis, leading to it having the highest number of complete genomes isolated compared to any other viruses known to honeybees. Through these genome studies, it has been found that there are two distinct lineages of SBV, each characterized by a high mutation rate, leading to multiple subtypes in both lineages. In studying how these lineages have evolved through time, new discoveries in their pathogenicity and different honeybee resistance mechanisms have been unveiled.