Evolution of the Sacbrood Virus

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 RNA virus. Most of the structural genes are located at the 5' end of the genome and the non-structural genes at the 3' end. The virus contains a region that encodes a 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. Overall, the structure of this virus is similar to others in the Picornavirales order, but it has evolved a unique feature. The difference in SBV comes from the functional protein responsible for the viral genome delivery in host cells. In most Picornavirales, the capsid contains the functional protein VP4 for this. SBV, instead of having VP4, has a small protein attached to the surface of the capsid, called MiCP. 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. These pores will form on the capsid when exposed to and acidic pH, which would happen upon entry to any host cells. == Evolutionary lineages ==

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. AC genotype will infect A. cerana and AM genotype will infect A. mellifera. 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. There are numerous strains in this lineage, most coming from China. Throughout the evolution of the AC lineage, there have been some major colony devastations due to SBV. Most notably, there was a 100% wipeout of A. cerana in Thailand in 1976. Some of these detrimental effects include increased accumulation of ecdysial fluid, cuticle coloration, and possibly death. As for studies on the different subgroups in the AC genotype, they have revealed that the sequence changes between those do not cause significant changes in SBV's pathogenicity. 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. == New advances ==

Pathogenicity Studies on the evolution of SBV have ramped up recently due to increased death in honeybees seen almost globally. 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. 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. 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. == References ==