bioRxiv Science⌕ Search

Biology subjects

McKee, R. C.

Publications and source records attributed to McKee, R. C..

2 recordsLinked to original sources

Primary and secondary antiviral RNAi responses throughout Varroa destructor life stages reveal the vertical transmission of viruses

One of the most devastating threats to global honey bee health is the ectoparasitic mite and viral vector Varroa destructor, yet the transmission dynamics of viruses carried by mites are poorly understood. RNA interference (RNAi) is a major antiviral defence mechanism in invertebrates including Varroa, where actively replicating viruses are degraded into virus-derived small interfering RNAs (vsiRNAs). Insects typically produce 20-22 nt vsiRNAs with sense and antisense polarity, however established viral infections in V. destructor lead to the production of 24-nt antisense vsiRNA fragments, which could indicate the presence of secondary siRNA synthesis. To better understand viral infection and transmission dynamics in V. destructor, we conducted small RNA sequencing of male and female mites throughout development, from egg to reproductive stages. Viral community structure was largely driven by developmental stage, with younger and older life stages clustering separately. We identified five viruses that are consistently degraded into antisense 24-nt vsiRNA across all developmental stages, suggesting that these viruses are transmitted vertically and form part of Varroas core virome. This includes the highly diverse Varroa destructor virus 2 (VDV-2), for which we observe eight distinct VDV-2 strains that simultaneously co-infect individual mites throughout development. In contrast, sense and antisense 23-nt vsiRNA fragments are generated in response to the honey bee pathogen, Iflavirus aladeformis (deformed wing virus A, DWV-A) in eggs, but the vsiRNA size profile transitions to 24-nt antisense fragments at later life stages. Our results suggest that once a virus is first acquired by Varroa, a primary 23-nt sense and antisense antiviral response precedes the production of secondary 24-nt antisense vsiRNAs as the infection progresses. We confirm this observation using synthetic dsRNA, which show both primary and secondary siRNA processing, revealing how exogenous dsRNA processing occurs in Varroa. These results show distinct primary and secondary antiviral RNAi responses across V. destructor life stages and demonstrate how vsiRNA profiles can be used to infer virus transmission routes and long-term persistence within vector populations.

genetics↗

Virus replication in the honey bee parasite, Varroa destructor

Arthropod vectors such as mites and ticks introduce an alternative viral transmission route between their hosts. The ectoparasitic mite Varroa destructor is the leading threat to the health of Western honey bees (Apis mellifera) primarily through its action as a vector of viruses. However, it is unclear whether viruses transmitted by V. destructor actively infect and replicate in mites, which could facilitate increased transmission and select for more virulent strains. To better understand the role of V. destructor as a vector, we took advantage of differences between bee and mite antiviral RNA interference pathways to identify the host specificity of replicating viruses. We used small RNA sequencing of individual V. destructor mites to examine viral small interfering RNA (vsiRNA) profiles of Deformed wing virus genotypes (DWV-A and DWV-B), associated with colony declines, as well as nine other viruses present in our samples. We found active replication of six V. destructor-associated viruses, including a novel virus, Varroa destructor virus 9 (VDV-9), and replication of two honey bee associated viruses, including both DWV-A and -B genotypes, suggesting that mites are biological vectors for important bee pathogens. We show that the antiviral RNAi response can be used define the host range of viruses in host-parasite interactions, such as honey bees and their parasites, enabling a better understanding of the role of a vector in the evolution and spread of honey bee pathogens.

genetics↗