Black queen cell virus

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Black queen cell virus
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Diagram of a picorna-like virus protein
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(unranked): Virus
Realm: Riboviria
Kingdom: Orthornavirae
Phylum: Pisuviricota
Class: Pisoniviricetes
Order: Picornavirales
Family: Dicistroviridae
Genus: Triatovirus
Species:
Black queen cell virus

The black queen cell virus (BQCV) is a virus that infects honey bees, specifically Apis mellifera , Apis florea , and Apis dorsata . [1] Infection of the latter two species is more recent and can be attributed to genetic similarity and geographical closeness. [1]

Contents

Description

Black queen cell virus was originally described in 1977, but its genome was not sequenced until 2000. [2] BQCV can currently be found most commonly in Australia [3] and parts of South Africa. [4] BQCV visibly affects the pupae of queen bees, causing them first to turn yellow and then black, and eventually die. [5] These pupae come from queen bees that seem healthy and show no symptoms of being infected with this virus, as it only manifests itself with visible symptoms in the larvae. [4] Although only the larvae are visibly affected by this disease, adults can also be infected, but asymptomatically. [6] Transmission occurs by a parasite called Nosema apis, which lives in the intestines of honey bees. [4] BQCV can also be transmitted from nurse bees to larvae when they feed, and from hive to hive when the bees travel between them and when infected queen bees are distributed to other hives, [5] There are no vaccines or treatment forms available to treat bees infected with this virus, [7] therefore sanitation is the best way to prevent the spread. Sanitation practices include replacing the comb of the hive and requeening. [7] Requeening simply means that the queen of the hive is replaced with a new, and in the case of infected hives, healthy queen. [8]

Viral classification

Black queen cell virus comes from the order Picornavirales , which are also known as picorna-like viruses. [9] Families within the Picornavirales order include Picornaviridae , Comoviridae , Dicistroviridae , Marnaviridae , and Sequiviridae . [10] Of these, BQCV belongs to the Dicistroviridae family, which means that it is a virus that infects arthropods. [10] This family contains twelve viruses within the genus Cripavirus , [2] and others in the genera Aparavirus and Triatovirus .

Virus structure

The black queen cell virus contains 60 copies of the capsid proteins VP1, VP2, and VP3. [6] The capsid is the shell of the virus that holds the virus's genetic material. VP4 proteins, which are sometimes also found in the capsid, do not affect the virus's infectivity, [6] or ability to be transmitted. The surface of the virion has large protrusions, which are formed by the VP1 and VP3 proteins and are located between the 5- and 3-fold axes of the icosahedral capsid. [6] An icosahedral capsid is formed from 20 triangular faces, put together in such a way that it resembles a sphere. [11] The axes are found where the faces come together.

Due to these protrusions, BQCV is larger than most other picornaviruses. [6] The capsid is also characterized by plateaus (around the 3-fold axes) and depressions (around the 2-fold axes). [6]

Viral genome

Black queen cell virus is a nonenveloped RNA virus. [6] It has a linear, single-stranded, positive sense RNA genome encased in an icosahedral capsid (described above). [6] Viruses with icosahedral symmetry have triangulation numbers, which describe the faces in terms of the number of facets (smaller triangles inside the faces) each contains. [11] BQCV is a pseudo-T=3 capsid, meaning that it is mathematically a T=1 capsid, but the way the capsid is structured makes it look like T=3. [6] The genome of this virus contains 8550 nucleotides and it is polyadenylated. [4] Nucleotides "are organic molecules that serve as the monomer units for forming the nucleic acid polymers deoxyribonucleic acid (DNA) and ribonucleic acid (RNA)". There are four different nucleotides that can make up a genome. In BQCV, 29.2% of its genome is made up of A nucleotides, 30.6% is U nucleotides, 18.5% is C nucleotides, and 21.6% is G nucleotides. [4] A genome is polyadenylated when it has a poly(A) tail at the end, or a string of only adenine (A) bases. The black queen cell virus contains two open reading frames (ORFs), which is a "continuous stretch of codons that contain a start codon (usually AUG) and a stop codon (usually UAA, UAG or UGA)". ORF1 and ORF2 "encode polyproteins containing non-structural and structural (capsid-forming) subunits, respectively". [6]

Replication cycle

The family Dicistroviridae, as a whole, will be used as the model to explain replication of black queen cell virus.

Entry into cell

The virus enters the host cell by clathrin-mediated endocytosis. [2] Clathrin-mediated endocytosis "is a process by which cells absorb metabolites, hormones, other proteins – and in some cases viruses – by the inward budding of plasma membrane vesicles". This absorption begins after the virus binds to a receptor on the cell membrane. Once the virus is inside the cell, the virus is uncoated and the genome (RNA) is released into the cytoplasm. [2]

Replication

After the virus has entered the host cell, it must replicate its genome. In dicistroviruses, the 5’ VPg protein primes synthesis of RNA and inhibits translation of cellular mRNA, which improves translation of viral mRNA. [2] The ORF1 (discussed earlier) codes for the replication enzymes, specifically RNA-dependent RNA polymerase, [2] which helps with RNA replication. The genome of the virus has a positive strand of RNA, which is used as a template to synthesize the negative strand RNA. This negative strand is then used as a template to synthesize more genomic RNA. [2]

Viral interaction with host

The main host of black queen cell virus is the honey bee genus Apis. [6] There are also several bumblebee species that are now hosts for this virus. [6] One major impact that this virus has on its host is its ability to produce offspring. [2] The offspring are still produced by infected individuals, but they do not survive. Another way that this virus interacts with its host is by interfering with cellular mRNA production, in favor of its own mRNA production. [2]

Another important interaction that BQCV has with its host is its resistance to host cell mechanisms. [3] This resistance is accomplished by a cap structure that black queen cell virus has on the 5’ end of its genome. A cap structure has many functions. It protects the mRNA from being degraded, it ensures efficient translation, and it helps the mRNA travel from the cytoplasm to the nucleus, which is the site of replication. [12] It is possible to study these viral interactions with host cells because of the ability that scientists have to produce mutations in the viral genome and analyze the effect that it has on the host cell. [3]

Associated diseases

There are many diseases or viruses that can be associated with black queen cell virus. One such disease is Nosema disease. If a honey bee is infected with Nosema apis, there is a much higher chance that that same bee will contract BQCV. [4] Nosema disease can be treated in infected honey bees with Flumidil-B. [7] Another virus that can be associated with BQCV is Sacbrood virus. This virus manifests itself with similar symptoms to those of BQCV but it affects the worker bees of the hive, instead of the queen bee. [5]

Black queen cell virus is also similar to a few other viruses within the family Dicistroviridae. Kashmir bee virus (KBV), Israeli acute paralysis virus (IAPV), and acute bee paralysis virus (ABPV) all are related to BQCV very closely, but all have much less easily defined symptoms. [9] Structurally, BQCV is the most similar to TrV and to iflaviruses. [6] Iflaviruses also infect insects, just like black queen cell virus. [6]

The human viruses that are closest to BQCV include hepatitis A and human parechovirus. These are both from the family Picornaviridae and they may “form evolutionary intermediates between human and insect viruses”. [6]

Interactions

BQCV interacts with parasites to make the virus more prone to causing mortality. [3] Parasites, particularly Varroa destructor , are commonly found in bee colonies that are also infected with viruses. The parasites can activate the virus if it is latent and can also act as a vector to transmit the virus to other uninfected bees. [3] The results of both of these functions of the parasite in these colonies is the increase of the infectivity and the mortality rate related to the virus.

Some members of the family Dicistroviridae are being used as pest control. [2] Some examples include the control of the olive fruit fly with CrPV and the control of Helicoverpa armigera with Helicoverpa armigera stunt virus. [2] However, black queen cell virus is not used in this way because bee colonies are important to agriculture and to economics.

Related Research Articles

<span class="mw-page-title-main">Capsid</span> Protein shell of a virus

A capsid is the protein shell of a virus, enclosing its genetic material. It consists of several oligomeric (repeating) structural subunits made of protein called protomers. The observable 3-dimensional morphological subunits, which may or may not correspond to individual proteins, are called capsomeres. The proteins making up the capsid are called capsid proteins or viral coat proteins (VCP). The capsid and inner genome is called the nucleocapsid.

<span class="mw-page-title-main">Poliovirus</span> Enterovirus

Poliovirus, the causative agent of polio, is a serotype of the species Enterovirus C, in the family of Picornaviridae. There are three poliovirus serotypes: types 1, 2, and 3.

<i>Hepadnaviridae</i> Family of viruses

Hepadnaviridae is a family of viruses. Humans, apes, and birds serve as natural hosts. There are currently 18 species in this family, divided among 5 genera. Its best-known member is hepatitis B virus. Diseases associated with this family include: liver infections, such as hepatitis, hepatocellular carcinomas, and cirrhosis. It is the sole accepted family in the order Blubervirales.

<span class="mw-page-title-main">Rubella virus</span> Species of virus

Rubella virus (RuV) is the pathogenic agent of the disease rubella, transmitted only between humans via the respiratory route, and is the main cause of congenital rubella syndrome when infection occurs during the first weeks of pregnancy.

Pseudoviridae is a family of viruses, which includes three genera.

<i>Dicistroviridae</i> Family of viruses

Dicistroviridae is a family of viruses in the order Picornavirales. Invertebrates, including aphids, leafhoppers, flies, bees, ants, and silkworms, serve as natural hosts. There are 15 species in this family, assigned to three genera. Diseases associated with this family include: DCV: increased reproductive potential. extremely pathogenic when injected with high associated mortality. CrPV: paralysis and death.

<i>Cowpea chlorotic mottle virus</i> Species of virus

Cowpea chlorotic mottle virus, known by the abbreviation CCMV, is a virus that specifically infects the cowpea plant, or black-eyed pea. The leaves of infected plants develop yellow spots, hence the name "chlorotic". Similar to its "brother" virus, Cowpea mosaic virus (CPMV), CCMV is produced in high yield in plants. In the natural host, viral particles can be produced at 1–2 mg per gram of infected leaf tissue. Belonging to the bromovirus genus, cowpea chlorotic mottle virus (CCMV) is a small spherical plant virus. Other members of this genus include the brome mosaic virus (BMV) and the broad bean mottle virus (BBMV).

<i>Deformed wing virus</i> Species of virus

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.

<i>Marnaviridae</i> Family of viruses

Marnaviridae is a family of positive-stranded RNA viruses in the order Picornavirales that infect various photosynthetic marine protists. Members of the family have non-enveloped, icosahedral capsids. Replication occurs in the cytoplasm and causes lysis of the host cell. The first species of this family that was isolated is Heterosigma akashiwo RNA virus (HaRNAV) in the genus Marnavirus, which infects the toxic bloom-forming Raphidophyte alga, Heterosigma akashiwo. As of 2021, there are twenty species across seven genera in this family, as well as many other related virus sequences discovered through metagenomic sequencing that are currently unclassified.

<span class="mw-page-title-main">Bacteriophage Qbeta</span> Species of virus

Bacteriophage Qbeta, commonly referred to as Qbeta or Qβ, is a species consisting of several strains of positive-strand RNA virus which infects bacteria that have F-pili, most commonly Escherichia coli. Its linear genome is packaged into an icosahedral capsid with a diameter of 28 nm. Bacteriophage Qβ enters its host cell after binding to the side of the F-pilus.

<i>Picornavirales</i> Order of viruses

Picornavirales is an order of viruses with vertebrate, invertebrate, protist and plant hosts. The name has a dual etymology. First, picorna- is an acronym for poliovirus, insensitivity to ether, coxsackievirus, orphan virus, rhinovirus, and ribonucleic acid. Secondly, pico-, meaning extremely small, combines with RNA to describe these very small RNA viruses. The order comprises viruses that historically are referred to as picorna-like viruses.

Vesivirus is a genus of viruses, in the family Caliciviridae. Swine, sea mammals, and felines serve as natural hosts. There are two species in this genus. Diseases associated with this genus include: respiratory disease, Feline calicivirus (FCV); conjunctivitis, and respiratory disease.

<i>Cafeteria roenbergensis virus</i> Species of virus

Cafeteria roenbergensis virus (CroV) is a giant virus that infects the marine bicosoecid flagellate Cafeteria roenbergensis, a member of the microzooplankton community.

<span class="mw-page-title-main">Chronic bee paralysis virus</span> Virus which infects bees

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. Chronic bee paralysis virus infection is a factor that can contribute to or cause the sudden collapse of honeybee colonies. Since honeybees serve a vital role in ecological resilience, it is important to understand factors and diseases that threaten them.

<i>Slow bee paralysis virus</i> Species of virus

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.

Triatoma virus (TrV) is a virus belonging to the insect virus family Dicistroviridae. Within this family, there are currently 3 genera and 15 species of virus. Triatoma virus belongs to the genus Cripavirus. It is non-enveloped and its genetic material is positive-sense, single-stranded RNA. The natural hosts of triatoma virus are invertebrates. TrV is a known pathogen to Triatoma infestans, the major vector of Chagas disease in Argentina which makes triatoma virus a major candidate for biological vector control as opposed to chemical insecticides. Triatoma virus was first discovered in 1984 when a survey of pathogens of triatomes was conducted in the hopes of finding potential biological control methods for T. infestans.

Black beetle virus (BBV) is a virus that was initially discovered in the North Island of New Zealand in Helensville in dead New Zealand black beetles in 1975.

<i>Tupanvirus</i> Proposed genus of viruses

Tupanvirus is a genus of viruses first described in 2018. The genus is composed of two species of virus that are in the giant virus group. Researchers discovered the first isolate in 2012 from deep water sediment samples taken at 3000m depth off the coast of Brazil. The second isolate was collected from a soda lake in Southern Nhecolândia, Brazil in 2014. They are named after Tupã (Tupan), a Guaraní thunder god, and the places they were found. These are the first viruses reported to possess genes for amino-acyl tRNA synthetases for all 20 standard amino acids.

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.

References

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