Slow Paralysis Virus Research Articles

Detection of Lotmaria passim, Crithidia mellificae and Replicative Forms of Deformed Wing Virus and Kashmir Bee Virus in the Small Hive Beetle (Aethina tumida).

Knowledge regarding the honey bee pathogens borne by invasive bee pests remains scarce. This investigation aimed to assess the presence in Aethina tumida (small hive beetle, SHB) adults of honey bee pathogens belonging to the following groups: (i) bacteria (Paenibacillus larvae and Melissococcus plutonius), (ii) trypanosomatids (Lotmaria passim and Crithidia mellificae), and (iii) viruses (black queen cell virus, Kashmir bee virus, deformed wing virus, slow paralysis virus, sacbrood virus, Israeli acute paralysis virus, acute bee paralysis virus, chronic bee paralysis virus). Specimens were collected from free-flying colonies in Gainesville (Florida, USA) in summer 2017. The results of the molecular analysis show the presence of L. passim, C. mellificae, and replicative forms of deformed wing virus (DWV) and Kashmir bee virus (KBV). Replicative forms of KBV have not previously been reported. These results support the hypothesis of pathogen spillover between managed honey bees and the SHB, and these dynamics require further investigation.

Detection of replicative Kashmir Bee Virus and Black Queen Cell Virus in Asian hornet Vespa velutina (Lepelieter 1836) in Italy

Information concerning the pathogenic role of honey bee viruses in invasive species are still scarce. The aim of this investigation was to assess the presence of several honey bee viruses, such as Black Queen Cell Virus (BQCV), Kashmir Bee Virus (KBV), Slow Paralysis Virus (SPV), Sac Brood Virus (SBV), Israeli Acute Paralysis Virus (IAPV), Acute Bee Paralysis Virus (ABPV), Chronic Bee Paralysis Virus (CBPV), in Vespa velutina specimens collected in Italy during 2017. Results of this investigation indicate that among pathogens, replicative form of KBV and BQCV were detected, assessing the spillover effect of both these viruses from managed honey bees to hornets.

Detection of honey bee ( Apis mellifera) viruses with an oligonucleotide microarray

In recent years, declines in honey bee ( Apis mellifera L.) colonies have been observed to varying degrees worldwide with the worst losses in the USA being termed Colony Collapse Disorder (CCD). Pathogen load and the prevalence of honey bee viruses have been implicated in these losses and many diseased hives have multiple viruses present. We have designed and tested an oligonucleotide microarray which enables the simultaneous detection of nine honey bee viruses: Acute bee paralysis virus, Black queen cell virus, Chronic bee paralysis virus, Deformed wing virus, Kashmir bee virus, Sacbrood virus, Israel acute paralysis virus, Varroa destructor virus 1 and Slow paralysis virus. The microarray can be used to robustly diagnose nine viruses in one test.

Transmission of deformed wing virus and slow paralysis virus to adult bees (Apis mellifera L.) by Varroa destructor

SummaryTo investigate the role of the parasitic mite Varroa destructorin the transmission of slow paralysis virus (SPV) and deformed wing virus (DWV) and to gain some insight into host-parasite-pathogen interactions, virus transmission experiments were carried out with adult honey bees in two periods of the year (early July and late September) using either five or ten mites exposed to bee pupae injected with either DWV or SPV for two different time periods of virus acquisition (five or ten days). No significant differences were observed between the proportions of bees becoming infected after mites were exposed to injected pupae for five or ten days regardless the type of virus (DWV or SPV). There was a significant difference in the proportion of bees subsequently infected in relation to the time of year at which the experiments were undertaken. For both DWV and SPV, a greater proportion of adult bees became infected by the mites during September trials than during July trials. Significantly more adult bees were infected with DWV in comparison with SPV. The results strongly support the suggestion that transmission of DWV and SPV occurs during the feeding activities of mites.

The prevalence of viruses of honey bees in Britain

SUMMARYAdult individuals of honey bee colonies in Britain are commonly infected with several small RNA viruses. Black queen cell virus and bee virus Y are the commonest and occur most frequently about June, together with Nosema apis with which both viruses are intimately but independently associated. Bee virus X is less common than bee virus Y and showed no pronounced seasonal fluctuations in local surveys, but was detected mostly in winter and early spring. Sacbrood virus occurred in adults of most local colonies in summer, chronic paralysis virus and cloudy wing particle occurred commonly but without seasonal variations and acute paralysis occurred commonly throughout the active season of bees but does not multiply sufficiently to cause overt disease. Slow paralysis virus was rare.

Viruses Attacking the Honey Bee

Publisher Summary Honey bee viruses possess small unenclosed particles containing ribonucleic acid (RNA). Each known type of virus native to bees may represent a group of related but distinguishable strains that differ in certain ways, including their virulence for any one strain of bee. Different virus strains may also vary in host range. Two of the diseases of bees caused by viruses have been recognized since the beginning of the century. One of them is sacbrood of the larval bee that is caused by a “filterable virus” and was one of the first virus diseases to be identified in insects. The second disease, paralysis of the adult bee, is caused by a filterable virus, but the agents causing these diseases were identified until much later. This chapter describes the methods of identification, properties, virus multiplication, and spread of infection of several honey bee virus. These viruses include sacbrood virus, chronic bee-paralysis virus, acute bee-paralysis virus, Arkansas bee virus, bee virus X, slow-paralysis virus, and Nodamura virus. Several other possible bee viruses such as particles associated with “Shiny-Black” disease and a possible satellite virus are also described in the chapter. The mechanisms that prevent the viruses from multiplying and attacking may differ in the host.

Three previously undescribed viruses from the honey bee.

SUMMARY Arkansas bee virus, bee virus X and slow paralysis virus, isolated from adult honey bees, have isometric particles, contain RNA and are serologically unrelated to each other or to the other known bee viruses. Arkansas bee virus particles are 30 nm in diam. sediment at 128S, have a buoyant density in CsCl of 1.37 g/ml and kill bees injected with them in about 3 weeks. Bee virus X particles are 35 nm in diam., sediment at 187S, have a buoyant density of 1.36 g/ml, multiply when fed to young bees kept at 30 °C but not at 35 °C nor when injected, and have not by themselves been associated with symptoms or mortality, although they killed bees when injected in combination with sacbrood virus. Slow paralysis virus particles are 30 nm in diam., sediment at about 176S, have a buoyant density of 1.35 g/ml and kill bees injected with them in about 12 days.

On the structure of the virus causing sacbrood of the honey bee

Honey bee viruses possess small unenclosed particles containing ribonucleic acid (RNA). Each known type of virus native to bees may represent a group of related but distinguishable strains that differ in certain ways, including their virulence for any one strain of bee. Different virus strains may also vary in host range. Two of the diseases of bees caused by viruses have been recognized since the beginning of the century. One of them is sacbrood of the larval bee that is caused by a “filterable virus” and was one of the first virus diseases to be identified in insects. The second disease, paralysis of the adult bee, is caused by a filterable virus, but the agents causing these diseases were identified until much later. This chapter describes the methods of identification, properties, virus multiplication, and spread of infection of several honey bee virus. These viruses include sacbrood virus, chronic bee-paralysis virus, acute bee-paralysis virus, Arkansas bee virus, bee virus X, slow-paralysis virus, and Nodamura virus. Several other possible bee viruses such as particles associated with “Shiny-Black” disease and a possible satellite virus are also described in the chapter. The mechanisms that prevent the viruses from multiplying and attacking may differ in the host.