Beeologics - Dedicated to Restoring Bee Health

Among honey bee pathogens, viruses are one of the most major threats to the health and well-being of honey bees and cause serious concern for researchers and beekeepers.

Viruses were first identified as a new class of pathogens infecting honey bees when at the beginning of the 20th century, a US scientist discovered that a filterable agent from diseased bee larvae could cause sacbrood disease in the honey bee. Since then, at least 18 viruses have been reported to infect honey bees worldwide. Understanding of these virus infections has grown considerably over the last three decades. Symptoms of disease, such as paralysis, have been used as diagnostic markers for different viruses. However, it has been established that different strains of the same virus and environmental factors can contribute to make this form of diagnosis unreliable at best. In addition, the fact that many apiaries have multiple viruses makes this form of differentiation between viruses obsolete. Thus, developing simple, alternative diagnostic methods has become has become a top priority.

Viruses are obligate intracellular parasites that can only multiply inside living host cells utilizing the host cell's metabolic machinery. Honey bee viruses usually enter the host through the alimentary tract during feeding or trauma on the body surface, though they can also directly enter the blood circulation via bites by varroa mites or other insects. In order to survive, viruses must have ways to invade hosts and be transmitted from one host to another. Although bee viruses multiply abundantly and fatally when injected into bee hemolymph, the initial infection site of most honey bee viruses usually occurs through the cuticle by direct contact between healthy and infected bees or in the alimentary tract when bees ingest virus-contaminated food. Viruses can attack at different development stages and castes of the honey bees, including eggs, larvae, pupae, adult worker bees, adult drones, and queen of the colonies. The densely crowded populations and high contact rate between colony members provide an ideal environment for transmission of pathogens. They are transferred both horizontally (between bees, through infested food/ feces or vectored by hive pests, predominantly varroa mites), or vertically (transferred from queen to offspring).

Although bee viruses usually persist as unapparent 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. Since both horizontal and vertical transmission pathways have been demonstrated, they represent important survival strategies for viruses. Indeed, viruses choose the appropriate transmission pathway based on the developmental, physiological, ecological, and epidemiological conditions that abound. When colonies are under noncompetitive and healthy conditions, viruses may remain in bee colonies via vertical transmission and exist in a persistent or latent state. However, under stressful conditions, such as infestation of varroa mites, coinfection of other pathogens such as N. apis, or decline in food supply, viruses switch to horizontal transmission and start to replicate. Other environmental factors, such as cold temperature and unfavorable flying conditions for long periods of time that keep all the bees in their hives may create similar circumstances. For example, this may lead to in-hive fecal deposition from the bee gastrointestinal tract, a major source of replicating viruses in the bee, which can be a major cause of rapid spread of disease within the community. High numbers of produced virions then become much more infectious, leading to the death of hosts and possible collapse of the whole bee colony.

Some of the more common viruses that infect honey bee colonies include:

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A. Deformed Wing Virus (DWV)
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. Adult honey bees infected with DWV usually appear normal but are believed to have a reduced life span. In addition, it has been shown that DWV infected bees have impaired learning capabilities. DWV has been shown to be one of the most prevalent infections in honey bees in recent years, and is known to be transferred by the varroa mites. Studies of DWV status in varroa showed that it was present in up to 100% of mites surveyed.

B. Sacbrood Virus (SBV)
SBV attacks both brood and adult stages of bees, but larvae about two days old are most susceptible to SBV infections. SBV affects adult bees without causing obvious signs of disease, but as in other viral infections, the infected adult bees may have a decreased life span. 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. 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 water-filled sacs when removed from the cell.

Prevalence of SBV in honey bees has been found to be prominently seasonal. During the 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. Just as in DWV, SBV is found in and vectored by varroa mites.

C. Black Queen Cell Virus (BQCV)
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, hence the designation of the name. BQCV mainly affects developing queen larvae and pupae in the capped-cell stage. It too is extremely common, second only to DWV. BQCV disease outbreak has been linked with infection of a protozoan, Nosema apis. Although this positive association between the BQCV and N. apis infections has been documented in the field observations, definite experimental evidence for deciphering cause and effect have yet to be determined.

D. Kashmir Bee Virus (KBV)
KBV was detected in honey bees collected from Australia in 1979. It attacks all stages of the bee life cycle and commonly persists within brood and adult bees as an unapparent infection. 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, like its almost indistinguishable relative Israeli Acute Paralysis Virus, 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 three days. KBV is also genetically, serologically, and pathologically closely related to another bee virus Acute Bee Paralysis Virus. Infection of KBV in honey bees resembles the infection caused by ABPV in several ways. KBV usually persists as an unapparent infection in honey bees. This virus is also efficiently vectored by varroa mites, but the mites may also activate latent infection to a lethal level.

E. Acute Bee Paralysis Virus (ABPV)
Since its first identification, the presence of ABPV in honey bees of A. mellifera has been reported in North America, Central and South America, Europe, Oceania, Asia, Africa, and the Middle East. 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 cells if large amounts of virus particles were ingested, or survive to emerge as unapparently infected adult bees.

Viruses Summary
Phylogenetic analysis shows that KBV, APBV, and IAPV are very closely related, as are DWV and SBV. This probably points to common and recent ancestry. For example, KBV and IAPV are >95% identical, except for a relatively small region of the genome that seems to have been recently incorporated into IAPV (or alternatively discarded from KBV).

A virus causes infection by invading host cells, multiplying new virions, and exiting the host cell to attack others. As part of their survival strategies, hosts have evolved effective mechanisms to defend against viral invaders by employing multifaceted immune responses. Virulence and pathogenesis are the consequences of the complex interactions between the infecting virus and host immunity. While the humoral and cellular immune responses to bacterial and fungal infections have been characterized and documented in honey bees, relatively little is known concerning how honey bees recognize and fight viral infections. The commonly observed phenomenon that viruses persist in apparently healthy colonies as latent infections is a good indication that honey bees have the innate ability to resist the multiplication of virus infections.

Recent work has indicated that RNA interference (RNAi) is a natural, conserved mechanism of antiviral immunity in plants, vertebrates, and insects. RNAi is an RNA-dependent gene silencing process triggered by a long double-stranded RNA (dsRNA). When dsRNA is introduced into a cell, a specific RNaseIII endonuclease, Dicer, binds and cleaves dsRNA to produce double-stranded fragments of 20-25 base pairs with 2-nt 3? overhangs, called small interfering RNAs (siRNAs). The siRNAs are integrated into the RNA-induced silencing complex (RISC) to activate the RISC. Activated RISC bind to homologous mRNA and cause sequence-specific degradation of the target mRNA. Positive-stranded RNA viruses are vulnerable to RNAi because the viruses replicate their genomes through complementary strands resulting in dsRNA replication intermediates. Since the genomes of most honey bee viruses are positive-stranded RNA molecules, RNAi is an important defense mechanism against viruses in honey bees.

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Bee Viruses