Beekeeping/Kashmir Bee Virus

Kashmir bee virus
This virus is widely diffused in Australia and in the United States, where it is endemic, it has been reported in Europe only rarely (Tentcheva et al., 2004; Berènyi et al., 2006). Like most dicistroviruses (Christian and Scotti, 1998; Valles et al., 2007; de Miranda et al., 2010), KBV persists at low titres in apparently healthy colonies until several stress factors activate the viral multiplication causing the death of the colony. The KBV overt infection occurs in different developing stages of bees without clearly defined disease symptoms. In last decade, this potentially lethal virus is becoming more important as one of several viruses closely associated with colony collapse in apiaries infested by V. destructor (Hung et al., 1995, 1996c; Ball and Bailey, 1997; de Miranda et al., 2004; Todd et al., 2007; Ribière et al., 2008; Pettis et al., 2008; de Miranda et al., 2010a, 2010b).

KBV is genetically and serologically closely related to ABPV (Allen and Ball, 1996; de Miranda et al., 2004); both these viruses were discovered as a contaminant during transmission studies of CBPV (Bailey et al., 1963; de Miranda et al., 2004). Probably these two viruses originate from a common ancestor and evolved independently in secluded geographic regions (Berènyi et al., 2006). Both viruses are able to co-infect the same colony (Hung et al., 1996; de Miranda et al., 2004) and even within the same bee (Evans, 2001; de Miranda et al., 2004). Although these two viruses are closely related they are readily distinguished by RT-PCR (Stoltz et al., 1995; Evans, 2001; de Miranda et al., 2004), moreover the VP4 proteins of ABPV and KBV particles are serologically distinct (Stoltz et al., 1995; de Miranda et al., 2004). Indeed, between these two viruses there are significant differences concerning critical areas of the genome such as the 5’ NTR (de Miranda et al., 2004). This region contains primary and secondary RNA structures that are fundamental for the binding of the viral RNA polymerase for genome replication (Gromeier et al., 1999).

In experimental infections KBV is resulted extremely lethal to adults and larvae, (Bailey et al., 1963; Dall, 1985; Bailey and Ball, 1991; Ribière et al., 2008; de Miranda et al., 2010a, 2010b), with less than 100 particles required to cause death within a few days, and the same effect can also be achieved by feeding around 1011 virus particles per bee (Bailey et al., 1963; Bailey and Woods, 1974; Bailey and Ball, 1991; Nordström, 2000; Maori et al., 2007a; Ribière et al., 2008; de Miranda et al., 2010a, 2010b). In natural infections KBV affects all stages of the bee life cycle and commonly persists within brood and adults apparently healthy (Anderson and Gibbs, 1988; Dall, 1985; de Miranda et al., 2004, 2010a, 2010b). The transmission of KBV in natural infected colonies may be occurred through multiple routes (Shen et al., 2005). The detection of KBV in brood food, honey, pollen royal jelly and faeces confirm the oral transmission of infection via contaminated food resources in the colony (Shen et al., 2005; Chen et al., 2006a; Chen and Siede, 2007a, 2007b; de Miranda et al., 2010a, 2010b). The detection of viral genome in Varroa mites and their salivary secretions (Shen et al., 2005; Hung and Shimanuki, 1999; Hung, 2000) suggests that the parasite may act as vector of KBV even if further studies will be needed to clarify the effective role of Varroa as biological or physical vector.

In recent years the virus has proved to be a most important marker of Colony Collapse Disorder (CCD) (Pettis, 2008; de Miranda et al., 2010a, 2010b). CCD is characterized by rapid loss of the colony’s adult bee population. At the final stages of collapse, the queen is attended by only a few newly emerged adult bees (Pettis et al., 2007; Maori et al., 2009). CCD poses a serious threat to apiculture and agriculture worldwide and CCD-related losses (direct and indirect) have been estimated at $75 billion (Swinton et al., 2007; Maori et al., 2009). Further work is, therefore, required to elucidate the precise role of KBV plays in this syndrome and the possible existence of other environmental and biological factors that could be able to play an important role in the spread of CCD.