Latency of Insect Viruses

Podgwaite, J. D.; Mazzone, H.M.

doi:10.1016/s0065-3527(08)60266-3

Cited by 36 publications

(32 citation statements)

References 87 publications

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“…It is possible that the open wounds allowed DWV entry into the bee host from the cell environment (Kanbar and Engels, 2003) or that DWV replication was increased by the wounding trauma itself (Boncristiani et al, 2013). This suggests the intriguing possibility that honey bee viruses may be activated by several different stressors (Podgwaite and Mazzone, 1986), including mite feeding. The bacterial cofactor effect reported earlier (Yang and Cox-Foster, 2005) may represent another general stressor or be due to the injection trauma itself.…”

Section: Discussionmentioning

confidence: 99%

Immunogene and viral transcript dynamics during parasitic Varroa destructor mite infection of developing honey bee (Apis mellifera) pupae

Kuster

Boncristiani

Rueppell

2014

Journal of Experimental Biology

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The ectoparasitic Varroa destructor mite is a major contributor to the ongoing honey bee health crisis. Varroa interacts with honey bee viruses, exacerbating their pathogenicity. In addition to vectoring viruses, immunosuppression of the developing honey bee hosts by Varroa has been proposed to explain the synergy between viruses and mites. However, the evidence for honey bee immune suppression by V. destructor is contentious. We systematically studied the quantitative effects of experimentally introduced V. destructor mites on immune gene expression at five specific time points during the development of the honey bee hosts. Mites reproduced normally and were associated with increased titers of deformed wing virus in the developing bees. Our data on different immune genes show little evidence for immunosuppression of honey bees by V. destructor. Experimental wounding of developing bees increases relative immune gene expression and deformed wing virus titers. Combined, these results suggest that mite feeding activity itself and not immunosuppression may contribute to the synergy between viruses and mites. However, our results also suggest that increased expression of honey bee immune genes decreases mite reproductive success, which may be explored to enhance mite control strategies. Finally, our expression data for multiple immune genes across developmental time and different experimental treatments indicates co-regulation of several of these genes and thus improves our understanding of the understudied honey bee immune system.

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Section: Discussionmentioning

confidence: 99%

Immunogene and viral transcript dynamics during parasitic Varroa destructor mite infection of developing honey bee (Apis mellifera) pupae

Kuster

Boncristiani

Rueppell

2014

Journal of Experimental Biology

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“…Many insect species have been found to be inapparently infected with viruses (Bailey & Gibbs, 1964;Brun & Plus, 1980;Evans & Harrap, 1982;Podgwaite & Mazzone, 1986;Scotti et al, 1981). These infections differ from acute infections in that they may persist in their hosts for many generations causing little or no harm or recognizable symptoms, yet in certain circumstances they may be stimulated or activated to yield greater numbers of particles and initiate acute infections.…”

Section: Introductionmentioning

confidence: 99%

“…These infections differ from acute infections in that they may persist in their hosts for many generations causing little or no harm or recognizable symptoms, yet in certain circumstances they may be stimulated or activated to yield greater numbers of particles and initiate acute infections. Little is known of how the viruses become activated, of the state and site of inapparent infections, of interactions between viruses in the inapparent state, or of how viruses establish inapparent infections in their hosts (Podgwaite & Mazzone, 1986).…”

Section: Introductionmentioning

confidence: 99%

Inapparent Virus Infections and their Interactions in Pupae of the Honey Bee (Apis mellifera Linnaeus) in Australia

Anderson

Gibbs

1988

Journal of General Virology

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SUMMARYWhen honey bee pupae from seemingly healthy Australian colonies were injected with various salt solutions, inapparent infections of black queen-cell virus (BQCV), Kashmir bee virus (KBV), sacbrood virus (SBV) and, occasionally, cricket paralysis virus were activated. The activated viruses replicated to detectable concentrations after pupae were incubated at 35 °C for 3 days. Inapparent infections of SBV, but not the other viruses, were also activated merely by incubating pupae at 35 °C. The replication of activated BQCV, KBV or SBV was specifically suppressed by injecting pupae with rabbit antisera against the particles of each virus. However, a greater proportion of activated SBV infections occurred in groups of pupae in which the replication of activated KBV was suppressed than in groups of pupae in which KBV was not suppressed. In addition, a greater proportion of activated BQCV infections occurred in pupae in which the replication of both KBV and SBV was suppressed than in groups of pupae that were not injected with KBV and SBV antisera. Results from one group of pupae treated in this way indicated that about 40~ were infected with KBV, about 43~ with SBV and about 15~ with BQCV. There was no evidence of interference between the viruses in the establishment of inapparent infections of pupae, but clear evidence of interference during or after activation. These results have implications for the use of pupae for virus propagation.

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“…Persistent virus infection in insects is an obscure phenomenon which is difficult to study and is thus a poorly understood field (Podgwaite & Mazzone, 1986). When cells persistently infected with Hz-1 virus are challenged with the same virus, homologous virus interference occurs ).…”

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confidence: 99%

Apoptosis resulting from superinfection of Heliothis zea virus 1 is inhibited by p35 and is not required for virus interference.

Lee

Chao

1998

Journal of General Virology

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Superinfection of Spodoptera frugiperda insect cells that are persistently infected with Heliothis zea 1 (Hz-1) virus induces general cellular apoptosis and subsequently results in homologous virus interference. Since apoptosis correlates closely with both a significant decrease in yield of virus progeny and expansion of virus infection among cells, further experiments were designed to verify the direct association of apoptosis with homologous interference. It was found that superinfection-induced apoptosis can be efficiently blocked by the stable transfection of p35 into cells before or after the

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Latency of Insect Viruses

Cited by 36 publications

References 87 publications

Immunogene and viral transcript dynamics during parasitic Varroa destructor mite infection of developing honey bee (Apis mellifera) pupae

Immunogene and viral transcript dynamics during parasitic Varroa destructor mite infection of developing honey bee (Apis mellifera) pupae

Inapparent Virus Infections and their Interactions in Pupae of the Honey Bee (Apis mellifera Linnaeus) in Australia

Apoptosis resulting from superinfection of Heliothis zea virus 1 is inhibited by p35 and is not required for virus interference.

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