For most of us viruses are confusing. Many people are unable to distinguish between viruses and bacteria and expect them to be much the same kind of thing, which they are not. Viruses don’t fit easily in to the various categories of living things we are used to dealing with, and actually whether they even are living organisms is arguable, and how they came to be still more controversial. Which is why there is never a clear answer about how we might kill a harmful virus.
Viruses are not cells and can’t reproduce on their own, and some see them merely as parcels of genetic material (most often RNA) that have just gone rogue, a molecular accident. To coin a phrase ‘bad news in a protein coat’, although, not all viruses are harmful. For others they are an extreme simplification evolved from ancient living cells. At the moment, the former guess seems the more likely.
Part of the reason for that is a growing understanding about how cells communicate. While we have known for a long time the cells can secrete chemicals, it’s only in the last ten years or so that scientists have realised that they do much more. Cells produce small ‘packages’ of molecules, including the RNA that can be translated into proteins or which affect gene expression, in great quantities all the time, and in every body fluid they have tested. These packages are produced as ‘bud’s from the cell wall, or from within the cell contents and released through the cell wall, and many of them are uncannily like viruses in size and structure. Not un-naturally this has led to speculation that maybe extra-cellular vesicles and viruses were two extremes on the same continuum.
The evidence that ‘messenger’ fragments of RNA in extra-cellular vesicles are a form of communication is substantial, and we are beginning to realise how widespread this is, finding it throughout animal and plant kingdoms. What is also becoming clear that part of this communication is involved in the on-going ‘war’ between infectious viral agents and their hosts, facilitating or defending against invasion. Viral RNA communicated to another organism in an extra-cellular vesicle can pre-emptively prepare a response, a non-infectious vesicle-virus ‘inoculating’ a host against the infectious ‘real thing’. Scientists have also found instances where host genetic material and viral genetic material have become intertwined over millennia, not just as junk or contamination, but conferring new functions on the host. Viruses seem to provide a ‘library’ of genetic material, freely used by all other organisms.
Instances of RNA ‘interference’ (iRNA) in honey bee biology have popped up in recent years. It has been suggested that iRNA (or gene ‘silencing’) has a role in determining honey bee castes (worker vs queen) and other epigenetic effects, and that a honey bee virus (IAPV, once talked about as a candidate for causing CCD) can be treated with iRNA from the right dsRNA fed in syrup. An iRNA treatment for varroa mites is the subject of a US patent*. iRNA is now known to be an important response to control viral infections in many insects, not just bees. What the latest paper from Maori et al (who hold the RNA/varroa patent) suggests is that social honey bees have the ability to pass an acquired immune response to each other and to larvae while food sharing, providing long-term, intergenerational, colony level protection circumventing a non-existent hereditary mechanism and boosting a naturally depauperate immune response.
“It is generally agreed that RNAi evolved as a defense mechanism against selfish nucleic acids and further diversified to regulate endogenous gene expression. The presence of differential naturally occurring RNA among worker and royal jellies points towards a potential effect of transmissible RNA on genome function in recipient bees. Indeed, supplementing jelly with endogenous or exogenous miRNAs that are naturally enriched in worker jelly affected gene expression as well as developmental and morphological characters of newly emerged workers and queens. We speculate that bee to-larva RNA transfer could also play a role in epigenetic dynamics among honey bees…”
Esther Nolte-‘t Hoen, Tom Cremer, Robert C. Gallo, and Leonid B. Margolis (2016). Extracellular vesicles and viruses: Are they close relatives? PNAS August 16, 2016 vol. 113 no. 33 9155–9161. www.pnas.org/cgi/doi/10.1073/pnas.1605146113
Knip M, Constantin ME, Thordal-Christensen H (2014). Trans-kingdom Cross-Talk: Small RNAs on the Move. PLoS Genet 10(9): e1004602. doi:10.1371/journal.pgen.1004602
Zhu, K., Liu, M., Fu, Z., Zhou, Z., Kong, Y., Liang, H., Lin, Z., Luo, J., Zheng, H., Wan, P., et al. (2017). Plant microRNAs in larval food regulate honeybee caste development. PLoS Genet. 13, e1006946.
Garbian, Y., Maori, E., Kalev, H., Shafir, S., and Sela, I. (2012). Bidirectional transfer of RNAi between honey bee and Varroa destructor: Varroa gene silencing reduces Varroa population. PLoS Pathog. 8, e1003035.
Eyal Maori, Yael Garbian, Vered Kunik, Rita Mozes-Koch, Osnat Malka, Haim Kalev, Niv Sabath, Ilan Sela and Sharoni Shafir, A transmissible RNA pathway in honey bees (2018). bioRxiv preprint, doi:http://dx.doi.org/10.1101/299800.