The FISH image - FISH stands for a visualisation method called fluorescence in situ hybridisation - shows amoebae infected simultaneously with the Viennavirus (for the first time isolated in this study and therefore named by the research team) and the bacterial symbiont. In the image, the amoebae are shown in magenta, their symbionts in cyan and DNA in yellow. The larger yellow structures are the virus factories, which are still in the initial phase here and cannot produce infectious viruses.
Credit: Patrick Arthofer
Here we have a very nice example of the reality of biology that devotees of the childish intelligent [sic] design notion, must either ignore or explain away as an unexplained mystery if they are to retain their childish superstition.
Similar example abound in nature, when one looks beneath the superficial of course, as I showed in my popular book, The Unintelligent Designer: Refuting The Intelligent Design Hoax, but this is an especially nice one.
It involved an amoeba, a bacterium - chlamydia - 'designed' to infect the amoeba, and a giant virus, also designed to infect the amoeba. The problem is, when the amoeba is infected with chlamydia, it gains protection against the giant virus. This was discovered by scientists from the University of Vienna, Austria, and the Université de Poitiers in France, led by microbiologist Matthias Horn from the Centre for Microbiology and Environmental Systems Science at the University of Vienna.
Giant viruses are unique in that they are several times larger than normal viruses and contain genes normally only found in cellular organisms such as bacteria, animals, plants and fungi. Fortunately, they are harmless to all but Protista such as amoebae which they infect then takeover to turn them into virus factories. Their only purpose seems to be to kill amoebae and produce more giant viruses. Biologists believe the reason for such a large, relatively complex virus is due to an evolutionary arms race between the virus and chlamydia, each vying for control of the host amoeba. The exact evolutionary pathway remains to be worked out, but it looks like another example of horizontal gene transfer.
Chlamydia are infectious bacteria which infect many species, including humans where they are a serious, sexually transmitted pathogen. The species that infects amoebae is closely related to the human pathogen and normally takes up residence in the amoeba where is slows down growth. In that respect it behaves like a parasite, but it also behaves like a symbiont when it protects the amoeba against infection by the giant virus.
So, let's just summarise what intelligent [sic] design advocates have to believe. This is based on the assumption that a designer such as the one believed in by Creationists, i.e. an omniscience, omnipotent creator god, would have known exactly what its creations would do, so designed them for that very purpose and no other:
- The amoeba was intelligently [sic] designed to live in a wide range of environment where it is an important lower tier in the food chain and is basic to recycling environmental nutrients bound up in the bacteria they eat, which would have consumed the dead plant and animal matter from higher up the food chain. Apart from that it just produces more amoebae to replace those eaten by the species higher up the food chain.
- The chlamydia in question were intelligently [sic] designed to live inside the amoebae to slow down their growth and so prevent them doing what they were intelligently [sic] designed to do. Apart from that, they just produce more chlamydia.
- Giant viruses were intelligently [sic] designed to infect amoebae and destroy them to prevent them doing what they were intelligently [sic] designed to do. Apart from that, they produce more giant viruses.
- The genetic complexity of these giant viruses is almost certainly because the intelligent [sic] designer has had to continually redesign them to overcome the problem it intelligently [sic] created by intelligently [sic] designing chlamydia to defend the amoebae, to enable the virus to kill the amoebae and prevent them doing what they were intelligently [sic] designed to do.
Little wonder then that Creationists do everything they can to avoid learning about these things, in case they have to cope with the resulting cognitive dissonance because understanding these things might cause them to have some doubts about their superstition, and that might make their imaginary putative intelligent [sic] designer very angry indeed.
Here is how the news release from Vienna University explains it all, obviously in scientific terms which make a lot more sense than the childish Creationist explanation:
Chlamydia protect protozoa from deadly viral infections
Amoebae receive surprising support in defense against viruses: The bacteria they are infected with prevent them from being destroyed by giant viruses. A research team led by microbiologist Matthias Horn from the Centre for Microbiology and Environmental Systems Science at the University of Vienna have investigated how a virus infection proceeds when the amoebae are simultaneously infected with chlamydia. The research team shows for the first time that intracellular bacteria known as symbionts protect their host against viruses. Amoebae are protists, i.e. single-celled microorganisms with a cell nucleus. Protists play a key role in food webs and ecosystem processes. Consequently, the results of the study suggest that the interaction between symbionts and viruses influence the flow of nutrients in ecosystems. The study is now published in the journal PNAS.
Intracellular bacteria: Friend not foe?
Under natural conditions, protists including the studied amoebae are often infected by bacterial symbionts, which include chlamydiae. Chlamydiae are primarily known as human pathogens. However, close relatives of these pathogenic chlamydiae have been discovered in a variety of animals and protists.Since, according to current knowledge, chlamydial infection leads to a slower growth rate of the infected host, chlamydiae are commonly considered to be parasitic.
Our study shows that chlamydiae are actually mutualists rather than parasites here, since they protect the protists against lethal infections by giant viruses. After all, slower growth is better than dying.
If chlamydiae protect the protists from being destroyed by viruses, they are not merely ensuring that their hosts remain a source of food for small animals. Beyond that, the bacterial symbionts could influence the entire nutrient cycle in ecosystems.
Patrick Arthofer, first author
PhD student
Centre for Microbiology and Environmental Systems Science (CMESS)
University of Vienna, Vienna, Austria.
Giant viruses and their unicellular hosts
Infections with bacteria, but also those with viruses, shape how populations of protists develop. The researchers from the University of Vienna and the Université de Poitiers in France wanted to know how a viral infection proceeds when protists are simultaneously infected with bacteria. In order to study a situation that might also occur in natural environments, the scientistsfirst isolated amoebae, bacteria, and a giant virus from the same environmental sample. Giant viruses have only been known for about 20 years. Their discovery challenges many previously held assumptions about viruses, for they are not only multiple times larger than all previously known viruses, but also possess genes that were previously thought to be characteristic of cellular organisms such as bacteria, animals, plants and fungi. According to current knowledge, they are completely harmless to animals and humans. Their natural hosts are single-celled organisms with a cell nucleus, the protists. When giant viruses infect a host cell, they remodel the entire host cell and set up a so-called "virus factory". This viral factory produces hundreds of new virus particles until the host cell bursts and releases the new viruses. The study of virus-symbiont interactions could therefore provide answers to the question of how giant viruses evolved.If the protist is infected with bacterial symbionts, this very process is blocked. Our study shows that the presence of the chlamydia does not prevent the virus from being taken up. However, the viruses subsequently cannot form a functional virus factory. A common hypothesis is that these intracellular interactions between giant viruses and bacterial symbionts have played a role in giant viruses becoming so complex
In general, a closer look at virus-symbiont interactions tells us something about ecosystem dynamics.
Matthias Horn, senior author Centre for Microbiology and Environmental Systems Science
University of Vienna, Vienna, Austria
Bacteria that protect against viruses influence food webs
Protists are widespread - living in waters, seawater and seabeds, among other places. They feed on bacteria, thus absorbing the nutrients bound in the bacteria and, when being eaten themselves, pass them on to animals such as small crustaceans. By this means only, the animals have access to the nutrients provided by bacteria. If the protists are killed by viruses, the nutrients released can only be metabolised once again by bacteria. Future research will show to what extent this process affects the functioning of ecosystems. In a next step, the scientists therefore want to investigate the exact mechanism behind the bacteria-mediated protection of protists from giant viruses. Additionally, Anouk Willemsen, co-author of the paper and virologist at CMESS, is focusing specifically on giant viruses: In a research project recently approved by the European Research Council (ERC), she is investigating how giant viruses have acquired their complexity.
The team give more technical details in the abstract to their open access paper published in PNAS:
AbstractOf course, anyone with a basic understanding of logic and biology could explain why the Creationist explanation for these sorts of systems is childish and trivially refutable as the work of a single intelligence because any designer of such a system could not conceivably be described as intelligent without a substantial redefinition of the word 'intelligent' so that it becomes indistinguishable from 'utterly stupid', unless this putative designer has a right hand which doesn't know what it's left hand is doing, and who forgets whet it designed yesterday and why it designed it. They could also explain how evolution alone is sufficient to explain it all perfectly well without the need to include magic and magic designers, stupid or otherwise, in the explanation.
Protists are important regulators of microbial communities and key components in food webs with impact on nutrient cycling and ecosystem functioning. In turn, their activity is shaped by diverse intracellular parasites, including bacterial symbionts and viruses. Yet, bacteria–virus interactions within protists are poorly understood. Here, we studied the role of bacterial symbionts of free-living amoebae in the establishment of infections withnucleocytoplasmic large DNA viruses (Nucleocytoviricota). To investigate these interactions in a system that would also be relevant in nature, we first isolated and characterized a giant virus (Viennavirus, family Marseilleviridae) and a sympatric potential Acanthamoeba host infected with bacterial symbionts. Subsequently, coinfection experiments were carried out, using the fresh environmental isolates as well as additional amoeba laboratory strains. Employing fluorescence in situ hybridization and qPCR, we show that the bacterial symbiont, identified as Parachlamydia acanthamoebae, represses the replication of the sympatric Viennavirus in both recent environmental isolates as well as Acanthamoeba laboratory strains. In the presence of the symbiont, virions are still taken up, but viral factory maturation is inhibited, leading to survival of the amoeba host. The symbiont also suppressed the replication of the more complex Acanthamoeba polyphaga mimivirus and Tupanvirus deep ocean (Mimiviridae). Our work provides an example of an intracellular bacterial symbiont protecting a protist host against virus infections. The impact of virus–symbiont interactions on microbial population dynamics and eventually ecosystem processes requires further attention.Graphical abstract of the study: It shows how a giant virus infection (orange hexagon) causes the amoeba to produce virus particles until the host cell bursts and thus dies. If the amoeba is infected with a bacterial symbiont (turquoise circles), the virus can enter the amoeba, but the symbiont blocks it and the amoeba survives.
Credit: Patrick Arthofer
Arthofer, Patrick; Delafont, Vincent; Willemsen, Anouk; Panhölzl, Florian; Horn, Matthias
Defensive symbiosis against giant viruses in amoebae
Proceedings of the National Academy of Sciences (PNAS) (2022) 119(36);e2205856119. DOI:10.1073/pnas.2205856119
Copyright: © 2022 The authors.
Published by PNAS. Open access
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)
The amoebae gain from playing host to chlamydia, at the relatively small cost of a reduced growth rate; chlamydia gain by have a host to live inside and both gain from the protection against the virus; the virus also gains in the long-term by evolving ways to overcome the protection provided by chlamydia, although that was probably important at some point in the past, it seems to be at something of an impasse at the moment.
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