Evolution of the Sacbrood Virus

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The evolution of the

pathogenicity and different honeybee resistance mechanisms have been unveiled.[5]

General virology

SBV is one of the few viruses known to infect honeybees that researchers have been successful in sequencing the full genome for. SBV is a single stranded

polyprotein, which is the precursor for the main functional proteins that are cleaved to form the capsid. The main functional capsid proteins are termed VP1, VP2, and VP3.[6] Overall, the structure of this virus is similar to others in the Picornavirales order, but it has evolved a unique feature.[6] The difference in SBV comes from the functional protein responsible for the viral genome delivery in host cells.[2] In most Picornavirales, the capsid contains the functional protein VP4 for this.[2] SBV, instead of having VP4, has a small protein attached to the surface of the capsid, called MiCP.[2] Researchers believe it is this small protein that is responsible for forming pores on the capsid. The pores then enable the virus to inject its genome into the host cell.[2] These pores will form on the capsid when exposed to and acidic pH, which would happen upon entry to any host cells.[2]

Evolutionary lineages

A. mellifera
A. cerana

SBV has affected honeybees globally and is divided into two distinct lineages. The names of the lineages are derived from what species of honeybee they infect. The two types are termed AC genotype SBV and AM genotype SBV.[7] AC genotype will infect A. cerana and AM genotype will infect A. mellifera.[7] A. cerana is largely localized in many eastern countries, and there are different subgroups of the AC genotype depending on the region from which the virus was isolated.[8] For example, the Chinese Sacbrood virus, CSBV, is arguably one of the most studied subgroups and is a subgroup of the AC genotype.[8] The genomic sequence of the two lineages are slightly different, with the critical difference coming from genotypic changes in the region encoding the VP1 functional protein.[7] These structural differences can explain the pathogenic differences seen in the two types.[9] The differences in the subgroups of each lineage can be explained by SBV's high mutation rate.[3] The high mutation rate is due to the fact that SBV does not proofread during RNA replication, leading to multiple strains in both lineages.[3]

Apis cerana genotype

The AC genotype is more widely studied compared to the AM genotype.

pathogenicity.[10]

Apis mellifera genotype

Strains of the AM genotype have been identified and sequenced mainly in the U.S, U.K, Australia, and South Korea.[3] Compared to the AC genotype, the AM genotype is less studied and has fewer complete genome sequences available.[3] Though less studied overall, it was this genotype that led to the initial discovery of the virus.[1] It was first identified in the U.S. in 1913.[1] Compared to the high levels of infection with the AC genotype, the AM genotype is known to only infect about 15% of the species.[15] Typically, the AM genotype does not cause lethal consequences in A. mellifera, which has peaked researchers interest on this species of honeybee and why this species of honeybee seem to be more resistant.[3]

New advances

Pathogenicity

Studies on the evolution of SBV have ramped up recently due to increased death in honeybees seen almost globally.[4][3] The high mutations in SBV pose a constant threat to honeybee colonies, so understanding how the virus is evolving is a broadening topic in honeybee research. Recent studies have found that the AC genotype is capable of infecting A. mellifera, whereas it was thought previously that there was a species barrier between the two virus lineages.[9] Another recent study found evidence that the virus is more pathogenic in cold weather, which would explain why it is more prevalent in the early spring time.[3] The molecular mechanism behind this is currently unknown, but uncovering this in the future could help researchers and beekeepers with prevention protocols.[3]

Resistance mechanisms

Since A. mellifera do not typically experience the same detrimental effects from SBV as A. cerana, this has led to studies trying to uncover possible means of resistance in A. mellifera. It has been reported that honeybee colonies that have better hygiene are more resistant to SBV.[5] Since hygiene is a heritable behavioral trait in honeybees, a recent experimental evolution study selected colonies with better hygiene and examined their larvae survival rate over several generations.[5] They found that after multiple generations the resistance to SBV continues to increase, which offers a possible evolutionary path that honeybees will see in the future.[5] Honeybees with stronger immune systems that are able to resist infection from SBV will likely not only lead to positive selection in honeybees, but further drive the evolution of SBV to evade these mechanisms.[3]

References