New insights of Sacbrood virus.

Abstract

Over the last several years, major efforts have been expended to study viral infection of honeybees mainly due to colony losses around the world (Allen M, et al., 1996). It seems that honeybees are infected with numerous viruses mounting to 18 so far. Infection may be asymptomatic but could still have adverse effects on the bee and may even cause death resulting in colony collapse. Sacbrood virus (SBV) is the most widely distributed of all honey bee viruses. Since its first identification in Apis mellifera L in the United State in 1913, infection of SBV has been found in almost all colonies throughout the world (Allen M, et al., 1996; Ellis J D, et al., 2005; Kim Cuc N T, et al., 2008; Ma M X, et al., 2010). SBV infects the brood and adults, but 2-day old larvae appear to be the most susceptible resulting in death (Ritter W, 1996). Diseased larvae do not pupate and ecdysial fl uid collects around the integument in the form of a “sac”, after which the disease has been designated. The color of infected larvae changes from pearly white to pale yellow. Following death, larvae dry out, making a dark brown gondola-shaped scale (Bailey L, 1975). SBV may infect adults without overt signs of disease (Anderson D L, et al., 1989; Bailey L, 1969). However, life span may become shorter (Bailey L, 1969; Wang D I, et al., 1970). Sacbrood occurs most frequently in the spring when the colony is in a very active growing phase (Bailey L, 1969). The SBV was firstly described infecting the eastern honeybee, A. cerana, in Guangdong China in 1972 and was designated the Chinese sacbrood virus (CSBV). It emerged once again in 2008 in Liaoning, China (Ma M X, et al., 2010) causing death to individual bees or the collapse of the whole colony in an epidemic outbreaks. Later, the SBV was identified in A. cerana in Thailand and in Korea in 1982 and 2008, and named Thi SBV (TSBV) and AcSBV-Kor, respectively. SBV is 26-30 nm in diameter, icosahedral, pseudo T=3 structure symmetry, nonenveloped, and featureless in appearance with sedimentation coefficient of 160S and a buoyant density in cesium chloride of 1.33 g, and belongs to Picornaviridae. The outer shell of the capsid is composed of 60 repeated structures, each consisting of one molecule of 3 subunits VP1, VP2, and VP3 (25, 28, and 31.5 kDa), but each consisting of a single molecule of four subunits VP1, VP2, VP3, and VP4 (30.5, 31.5, 37.8 kDa and 44.2 kDa, respectively) about CSBV. The capsid proteins play important roles in the protection and in the determination of host specificity, tissue tropism and regional variations. Based on phylogeny and sequence homology of SBV-VP1, the SBV strains were divided into two major groups, an AC genotype infecting Apis cerana and an AM genotype infecting Apis mellifera, and also that the virus has host specificity and regional variations (Ma M X, et al., 2013).