Common Honey Bee Viruses

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Viruses could attack at different developing stages and castes of the honey bees, including eggs, larvae, pupae, adult worker bees, adult drones, and queen of the colonies. Although bee viruses usually persist as inapparent infections and cause no overt signs of disease, they can dramatically affect honey bee health and shorten the lives of infected bees under certain conditions (Ball and Allen, 1988; Martin, 2001). Of 18 viruses identified to attack honey bees, six viruses, namely, Deformed wing virus (DWV), Black queen cell virus (BQCV), Sacbrood virus (SBV), Kashmir bee virus (KBV), Acute bee paralysis virus (ABPV), and Chronic bee paralysis virus (CBPV) are the most common infections and have been objects of active research currently.

A. Deformed wing virus

DWV was first isolated from diseased adult bees in Japan (Bailey and Ball, 1991). The occurrence and distribution of DWV has since been worldwide. Except for Oceania, the infection of DWV so far has been reported in Europe, North America, South America, Africa, Asia, and the Middle East (Allen and Ball, 1996; Antunez et al, 2006; Ellis and Munn, 2005). The infection of DWV has also been identified in A. cerana in China (Bailey and Ball, 1991).

DWV is one of a few bee viruses that cause well-defined disease symptoms in infected bees. Typical disease symptoms of DWV infection include shrunken, crumpled wings, decreased body size, and discoloration in adult bees. However, the mechanism by which the DWV causes the morphological deformities of the infected hosts is unclear. Aside from the adult stage, DWV infection is also detected in other stages of bee development, including egg, larvae, and pupae. When pupae at the normally multiplies slowly and rarely kills the pupae, instead mostly causing deformity and early death in newly emerged adult bees. Adult honey bees infected with DWV usually appear normal but are believed to have a reduction in life span (Bailey and Ball, 1991; Ball and Bailey, 1997; Kovac and Crailsheim, 1988).

DWV appears to be the most prevalent infection in A. mellifera in recent years. Our 5-year field survey carried out in Beltsville, MD showed that DWV infection occurred in 100% of the apiaries investigated (Y. P. C., unpublished observation). Similar results were reported previously by Tentcheva et al. (2004b) who observed that DWV was detected in over 97% of French apiaries when the adult bee population was examined. A study on the prevalence and distribution pattern of viruses in Austria demonstrated that DWV was present in 91% of tested bee samples (Berenyi et al., 2006). Although high prevalence of DWV is not geographically related, some seasonal variation in virus incidence was observed and the frequency of DWV infection in both adult bees and pupae increased considerably from summer to autumn during the year (Tentcheva et al., 2004a,b). The striking high incidence of DWV infection in honey bees obtained from these studies indicate that DWV is prevalent over a wide range of geographic locations and is likely to become an important cause of mortality in honey bee colonies whenever a viral disease outbreak occurs, and warrants further investigation in the epidemiology and pathogenesis of this pathogen.

Bee colonies infected with DWV are often found to be associated with the infestation of a parasitic mite, Varroa destructor (Anderson and Trueman, 2000). Both laboratory and field studies showed that the varroa mite is an effective vector of the DWV (Ball and Allen, 1988; Bowen-Walker et al., 1999; Martin et al., 1998; Nordstrom, 2003; Nordstrom et al., 1999; Shen et al., 2005b). Varroa mites acquire the virus from infected bees and transmit it to uninfected bees, which either develop morphological deformities or die after the mites feed on them for a period of time. Studies of virus status in varroa mites showed that DWV was present in 100% of varroa mites collected from Thailand (Chantawannakul et al., 2006) and that varroa mites appeared to be DWV positive in 100% of French apiaries (Tentcheva et al., 2004b). Evaluation of DWV infection in individual bees showed that DWV was detected in 69% of bees collected from mite-infested colonies in Poland (Topolska et al., 1995), and in over 90% of bees from mite-infested colonies in England (Ball, 2001). The high frequency of DWV in mites and mite-infested bee colonies suggests that the significant increase in prevalence of DWV infection in recent years is likely associated with the worldwide infestation of varroa mites in honey bees. It also suggests that the varroa mite may play a major role in colony collapse due to the outbreak of viral disease.

B. Sacbrood virus

SBV is the most widely distributed of all honey bee viruses. Since its first identification in the United States in 1913 (White, 1913), infection of SBV has been found on every continent where A. mellifera honey bees are present (Allen and Ball, 1996; Bradbear, 1988; Ellis and Munn, 2005).

SBV attacks both brood and adult stages of bees, but larvae about 2-day old are most susceptible to SBV infections (Ball and Bailey, 1997). SBV affects adult bees without causing obvious signs of disease, but the infected adult bees may have a decreased life span (Bailey, 1969; Bailey and Fernando, 1972). The initial spread of SBV within a colony occurs when nurse bees become infected while removing larvae killed by SBV. Virus particles accumulate in the hypopharyngeal glands of the nurse bees and infected nurse bees can then spread the virus throughout the colony by feeding larvae with their glandular secretion and exchanging food with other adult bees including foraging bees. Infected foraging bees spread the virus by passing it from their glandular secretions to the pollen loads as they collect pollen. Young larvae become infected with the virus by ingesting virus-contaminated food. The SBV starts to replicate in the larva, and the infected larva turns pale yellow after the brood cell is capped. As the disease progresses, the skin of the larva becomes leathery and the larva fails to pupate because it cannot digest the old cuticle. A large amount of fluid containing millions of SBV particles accumulates between the body of a diseased larva and its saclike skin. Affected larvae appear to be a water-filled sac when removed from the cell. Sacbrood derives its name from the saclike appearance of the diseased larvae.

Infection of SBV can be readily diagnosed in the field because of the characteristic symptoms produced in diseased brood. Typically, when bee colonies are heavily infected with SBV, there are a number of partially uncapped or completely uncapped brood cells scattered among capped brood that can be found on the brood frame. Dead larva becomes a dark, brittle scale can be easily removed from the brood cell, a characteristic that differs from a bacterium-caused brood disease, American foulbrood.

Prevalence of SBV in honey bees has been found to be prominently seasonal. Frequencies of SBV infection in spring and summer were significantly higher than in autumn (Anderson and Gibbs, 1988; Bailey et al., 1981; Tentcheva et al., 2004b). The incidence of SBV has been believed to be positively correlated with the number of susceptible brood and young workers in the colonies. During the seasons of spring and summer, the rich sources of pollen and nectar stimulate brood rearing and a great number of new workers hatch from the brood cells, providing opportunities for SBV to attack bees and multiply in the colonies. The seasonal variation in SBV indirectly reflects variable susceptibility of different bee developmental stages to the virus infection.

SBV infection has been associated with varroa mite infestation. SBV was detected in large amount of adult bees from varroa mite-infested colonies (AntUnez et al., 2006; Ball, 1989; Berenyi et al., 2006). Detection of SBV in varroa mites (Chantawannakul et al., 2006; Shen et al., 2005a; Tentcheva et al., 2004b) indicates that varroa mites have the potential to transmit the virus in the bee colonies, although varroa mite as a vector in transmitting SBV has not yet been experimentally demonstrated.

A new strain of SBV has been identified in the eastern honey bee, A. cerana, from Thailand in 1982. Infection of Thai SBV (TSBV) was also detected in India. TSBV is serologically related to SBV but not physiochemically identical to SBV (Bailey, 1982b).

C. Black queen cell virus

BQCV was first isolated from dead queen larvae and prepupae sealed in their cells that had turned dark brown to black along with the walls of the cell (Bailey and Woods, 1977), hence the designation of the name. The infection of BQCV in bees has been reported in North America, Central America, Europe, Oceania, Asia, Africa, and the Middle East (Allen and Ball, 1996; Ellis and Munn, 2005).

BQCV mainly affects developing queen larvae and pupae in the capped-cell stage. High incidences of the virus infection are observed in queen-rearing colonies in spring and early summer (Laidlaw, 1979). Diseased larvae have a pale yellow appearance and a tough saclike skin, a disease symptom also seen in SBV-infected larvae. BQCV readily multiplies in the pupal stage of the honey bees. Infected pupae turn dark and die rapidly. The wall of the queen cell eventually becomes dark colored, a characteristic symptom of BQCV infection. Worker bees can also be infected by BQCV but normally do not exhibit outward disease symptoms. BQCV does not multiply in bees when the virus particles are ingested.

Our 5-year field survey in Beltsville, MD showed that BQCV was the second most common infection of honey bees in the field after DWV (Y. P. C., unpublished observation). In 1993, Anderson (1993) reported that BQCV was the most common cause of queen larvae mortality in Australia. A study conducted by Tentcheva et al. (2004b) indicated that BQCV infection was more prevalent in adult bees than in pupae and that the incidence of BQCV was higher in spring and summer than in autumn. This result was consistent with a previous finding by Laidlaw (1979) that BQCV was more prevalent in spring and summer during the year.

In the field, BQCV disease outbreak has been linked with infection of a protozoan, Nosema apis. When the incidence of N. apis infection was high during the spring and summer, the infection of BQCV was more prevalent in honey bees (Bailey, 1981). It has been observed that BQCV multiplied rapidly in adult bees infected with N. apis (Bailey, 1982a).

BQCV is believed to be transmitted to queen brood via glandular secretion of nurse bees during the feeding (Bailey, 1982a). N. apis infects midgut tissues of the adult bees, increasing the susceptibility of the alimentary tract to infection by BQCV. Bailey et al. (1981) reported that honey bees infected with BQCV were found to be infected with N. apis simultaneously from all parts of England and Wales during 1979. Field survey of Austrian apiaries showed that N. apis was found to be present in 78% of BQCV-positive bee samples and that 75% of N. apis-infected colonies were also infected with BQCV (Berenyi et al., 2006). Similar results were also obtained from a survey carried out in France (Tentcheva et al., 2004b). Although positive association between the BQCV and N. apis infections has been documented in the field observations, definite experimental evidence for deciphering the mechanism of N. apis in activation and transmission of BQCV infection remains to be determined.

Varroa mites are thought to sometimes act as a vector for BQCV (Bailey, 1976). Detection of BQCV in varroa mites collected from a Thai honey bee apiary supports this assumption (Chantawannakul et al., 2006). However, an investigation conducted by Tentcheva et al. (2004b) yielded a different result; BQCV was never detected in any of the varroa mites they examined. Further studies to confirm the role of varroa mites as a vector in BQCV transmission will be necessary.

D. Kashmir bee virus

The origin of KBV in the bee species is obscure. KBV was first isolated from adult western honey bees, A. mellifera, that were experimentally inoculated with an extract prepared from the diseased Asian honey bee (A. cerana) in Kashmir, northwestern region of India, hence the name (Bailey and Woods, 1977). Subsequently, KBV has been detected in A. mellifera collected from Australia (Bailey et al., 1979). The detection of KBV in the natural population of A. mellifera in Australia was unexpected because A. cerana, which is assumed to be the original host of KBV, does not exist there. Later, strains of KBV have been found in A. mellifera from Canada and New Zealand (Allen and Ball, 1995; Anderson, 1985), Fiji (Anderson, 1990), Spain (Allen and Ball, 1995), and the United States (Bruce et al., 1995; Hung et al., 1995). The unexpected emergence of KBV in the countries such as Australia and New Zealand might be due to the importation of bees from North American or other countries where KBV is endemic. So far, infection of KBV in A. mellifera has also been documented in several countries in Europe and Oceania (Allen and Ball, 1996; Ellis and Munn, 2005; Siede et al., 2005).

KBV attacks all stages of the bee life cycle (Hornitzky, 1981,1982) and commonly persists within brood and adult bees as an inapparent infection (Anderson and Gibbs, 1988; Dall, 1985). The disease and mortality caused by KBV infection occurs in different developing stages of bees without clearly defined disease symptoms. Among all of the viruses infecting honey bees, KBV is considered to be the most virulent under laboratory conditions. It multiplies quickly once a few viral particles are introduced into the bee hemolymph and can cause bee mortality within 3 days. However, KBV does not cause infection when adult bees are fed with food mixed with KBV particles. The virus probably invades the bees through the cuticle by direct contact between live bees (Bailey et al., 1979).

KBV is genetically, serologically, and pathologically closely related to another bee virus ABPV. Infection of KBV in honey bees resembles infection caused by ABPV in several ways. For example, both viruses usually persist as inapparent infections in bees and replicate readily only when injected into the hemolymph of adult bees (Anderson, 1991). Immunodiffusion tests showed that strains of KBV from Canada and Spain were even more serologically closely related to ABPV than were other KBV strains (Allen and Ball, 1995). Molecular analysis revealed KBV and ABPV share about 70% sequence homology over the entire genome, although there are significant differences in several critical areas of the genomes between the two viruses (De Miranda et al., 2004). Phylogenetic analyses suggest that KBV and ABPV are distinct viruses and can be inferred to be different species, even though there is no clear geographic and ecological separation between the two viruses (De Miranda et al., 2004; Evans, 2001).

Incidence of KBV infection in honey bees is less prevalent, as compared with other highly prevalent bee viruses such as DWV, BQCV, and SBV. Field survey of honey bee viruses on a large geographic scale of France showed that KBV was found in 17% of the apiaries for adult population, and 5% of the apiaries for pupae versus 97% and 94% of the apiaries with DWV infection for adult and pupae, and 86% and 80% of apiaries with SBV infection for adult and pupae, 86% and 23% with SBV infection for adult and pupae, respectively (Tentcheva et al., 2004b). Although KBV has been considered to be more widespread in the United States than in Europe (Allen and Ball, 1996), field survey from 2002 to 2006 in Maryland indicated that the incidence of KBV infection varied significantly from year to year with more than 50% of apiaries with KBV infection in 2002 and about 10-20% of the apiaries with KBV infection for the rest of the years (Y. P. C., unpublished observation).

Although KBV usually persists as an inapparent infection in honey bees, infection of KBV can be activated to a lethal level in the presence of varroa mites (Bailey et al., 1979). A high mite-infestation level could result in high virulence in the bee colonies (Hung et al., 1996b). It has been experimentally proven that varroa mites were effective vectors of KBV. They transmitted KBV in the same way as they transmitted DWV in bee colonies (Chen et al., 2004b). Varroa mites acquired KBV from virus-infected bees and transferred the virus to virus-negative hosts during feeding. Varroa mites also acquired virus from KBV-positive mites by cohabiting in the same cell with virus-positive mites via a bee host intermediary. A subsequent study conducted by Shen et al. (2005b) further supports the role of varroa mites as a vector in transmitting KBV in bees.

E. Acute bee paralysis virus

ABPV was first discovered during laboratory infectivity tests with CBPV (Bailey et al., 1963). When bees were experimentally inoculated with purified CBPV particles, the bees remained flightless and trembling for about 5-7 days before they died. In contrast, when healthy bees were injected with extract prepared from a group of apparently healthy bees and incubated for 5-6 days, most of the bees became flightless and died quickly. Virus particles were isolated from the extracts of those apparently healthy bees that caused bee acute paralysis, hence the designation of the name to distinguish it from CBPV (Bailey et al., 1963). Since its first identification, the presence of ABPV in honeybees of A. mellifera has been reported in North America, Central and South America, Europe, Oceania, Asia, Africa, and the Middle East (Allen and Ball, 1996; Ellis and Munn, 2005).

ABPV can be detected in both brood and adult stages of bee development. In the field, ABPV commonly occurred in apparently healthy adult bees, particularly during the summer, and infection of ABPV was rarely noticed to be associated with disease or mortality of bees (Bailey, 1965b; Bailey et al., 1981). Spread of ABPV in the colonies is probably via salivary gland secretion of infected adult bees when glandular secretions are fed to young larvae or mixed in the pollen. Infected larvae either die before they are sealed in brood cell if large amounts of virus particles were ingested, or survive to emerge as inapparently infected adult bees (Bailey and Ball, 1991).

ABPV is considered to be the second most-prevalent virus in Austria (Berenyi et al., 2006), though it has been a sporadic infection in the United States only for the last 5 years based on our survey results (unpublished observation). ABPV has been identified as a major cause for the decline and collapse of bee colonies that were also infested with varroa mites in Europe and the United States (Antunez et al., 2006; Bakonyi et al., 2002; Ball, 1989; Ball and Allen, 1988; Berenyi et al., 2006; Faucon et al, 1992; Hung et al., 1996c; Kulincevic et al., 1990). The laboratory experiments by Ball (1989) demonstrated that varroa mites can act as a virus vector and transmit ABPV from severely infected bees to healthy adult bees and brood via feeding activities. Detection of ABPV in varroa mites further supports the possible role of varroa mites in the virus transmission (Allen et al., 1986; Bakonyi et al., 2002; Chantawannakul et al., 2006; Tentcheva et al., 2004b). In addition to acting as a vector of the virus, the varroa mite is also believed to serve as an activator of ABPV in infected bees.

Detection of large amounts of the virus in diseased or dead bees from colonies heavily infested with varroa mites suggests that infestation of varroa mites may stimulate the virus to replicate to the amounts sufficient to cause bee disease and mortality (Ball and Allen, 1988; Faucon et al., 1992; Hung et al., 1996c; Kulincevic et al., 1990). While varroa mites might activate ABPV replication, replication of the virus in bees can be also induced by some other factors. Previous studies showed that ABPV was present in bees from apiaries where no APBV-positive varroa mites were detected (Tentcheva et al., 2004b) and that replication of ABPV can be activated to detectable concentrations by injection of potassium phosphate buffer (Hung et al., 1996c), suggesting that the varroa mite is not the sole factor contributing to the disease outbreaks of ABPV infection.

F. Chronic bee paralysis virus

CBPV was identified as a cause of adult bee paralysis by Bailey et al. (1963) after long suspicion that the tracheal mite, Acarapis woodi, was the culprit of the paralysis. Later, CBPV was extracted from naturally paralyzed bees as one of the first viruses isolated from honey bees (Bailey et al., 1968). CBPV has since been detected in adult bees of A. mellifera from every continent except South America (Allen and Ball, 1996; Ellis and Munn, 2005).

CBPV mainly attacks adult bees and causes two forms of "paralysis" symptoms in bees (Bailey, 1975). The most common one is characterized by an abnormal trembling of the body and wings, crawling on the ground due to the flight inability, bloated abdomens, and dislocated wings. The other form is identified by the presence of hairless, shiny, and black-appearing bees that are attacked and rejected from returning to the colonies at the entrance of the hives by guard bees. Both forms of symptoms can be seen in bees from the same colony. The variation in the disease symptoms may reflect differences among individual bees in inherited susceptibility to the multiplication of the virus (Kulincevic and Rothenbuhler, 1975; Rinderer et al, 1975).

While CBPV causes the same symptoms of trembling and the inability to fly in infected bees that ABPV does, the two viruses are different in several ways: CBPV is the less virulent of the two viruses, as CBPV takes several days to kill the diseased bees while ABPV takes only 1 day; the shapes of the two viruses are different—CBPV particles are asymmetric and ABPV particles are isometric; there are many more virus particles of CBPV than of ABPV in naturally paralyzed bees (Bailey, 1965a).

Laboratory tests were carried out to investigate the infectivity of CBPV by injecting purified virus particles into the hemolymph of bees, spraying virus preparation on the surfaces of bees, or mixing virus particles with colony food (Bailey and Ball, 1991; Bailey et al., 1983). The results showed that CBPV was readily transmitted to bees by topical application of virus particles after hairs on the surface of the body were denuded. The results also showed that CBPV is not readily replicated to the level sufficient to cause disease when the virus was introduced in bees via food. Accordingly, CBPV naturally spread best among bees when the colonies were the most crowded. The close contact of overcrowded bees breaks hairs from the cuticle, allowing CBPV to spread from diseased bees to healthy bees via their exposed epidermal cytoplasm. It is likely that any factors that result in decreased foraging activities and crowded conditions in the bee colonies may lead to disease outbreaks of CBPV.

It has been reported that CBPV is very widespread in Britain and infects most bees and causes mortality in bee colonies (Bailey et al., 1981). The incidence of CBPV in Britain declined from 8% in 1947 to less than 2% by 1963 based on the samples submitted by beekeepers. The decrease in CBPV incidence coincided with the decline in the total number of bee colonies during that period of time (Bailey et al., 1983). In Austria, CBPV was found to be present in different geographic regions and infection of CBPV was detected in 10% of bee colonies suffering from various diseases (Berenyi et al., 2006). A field survey in France showed that CBPV was the least prevalent of all examined viruses and that infection of CBPV was detected only in adult bees with the maximum frequency of 4% in the colonies. Infection of CBPV also did not appear to follow any seasonal pattern (Tentcheva et al., 2004b). In the United States, incidence of CBPV has been very sporadic for the last 5 years and less than 1% of bees were identified with CBPV infection in the colonies. Field survey in France and Thailand showed that all examined varroa mites were negative for CBPV. This result suggests that the varroa mite is unlikely a vector of CBPV.

CBPV is often associated with the ''satellite'' virus, chronic paralysis virus associate (CPVA). CPVA is a single-stranded, isometric RNA satellite virus that is of unknown significance. It is serologically unrelated to CBPV but cannot multiply in the absence of CBPV (Ball et al, 1985).

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