There are different ecological consequences from lytic and lysogenic strategies of viruses. Lytic cycles generally remove genetic material and energy from the food chain. Conversely, lysogenic cycles can cause transfer of genetic material between host bacteria (transduction) and may allow for increased bacterial survivorship. Therefore, it is important to understand these strategies and their impacts on marine ecosystems. But first, what do we know...
Viral reproduction has two cycles: lytic and lysogenic. In the lytic cycle, a bacteriophage injects viral DNA through the cell wall of the host. Next, biosynthesis occurs until progeny phages are matured. The progeny phages then burst out of the membrane and are released to the environment. For the lysogenic cycle, viral DNA is injected into the genome of the host and the DNA becomes part of the chromosome. As the bacterial host divides, the viral DNA becomes part of the daughter cells. The viral DNA remains dormant until a stimulus (e.g. ultraviolet light) excides the viral DNA. Next follows biosynthesis, maturation, and finally the progeny phages burst and are released.
Viruses, like many other strong competitors and predators, have an evolutionary dilemma: they must be successful, but not too successful so that they drive their hosts to extinction. It has been thought that lysogeny is a technique designed to ensure this; lysogeny allows the phage to survive, without killing the hosts when host numbers are few. Lysogeny also means that the phage is in the same place as the host when growth conditions improve. Generally, lysogeny would be more common in oligotrophic waters.
When host abundance is high, there is an increased likeliness of virus-host collisions and opportunities for lytic viruses – this would show a higher virus-to-microbe ratio. However, a study by Knowles et al. (2016) found the opposite. The study conducted meta-analysis approach including: (1) experimental manipulations (2) literature meta-analyses, (3) direct counts, and (4) a personal study of 24 coral reef viral metagenomics. Authors found that there was a decrease in virus-to-microbe abundance as microbe abundance increased. Authors explain that this was caused by increased lysogeny at higher abundances – results showed that as microbe abundance increased, genes that are associated with integration and excision of lysogenic viruses increased as well. But why?
Authors investigated alternate hypotheses and the leading explanation was the defense hypothesis: that the high abundance host communities were dominated by defensive, slow-growing strains of hosts, associated with low virus production. Therefore, viruses would mainly infect the more-competitive and faster-growing strains of hosts which had lower abundances. Despite this, metagenomic data showed that there was no correlation between viral-defense genes and microbe abundance.
The final explanation was the Piggyback-the-Winner hypothesis, rather than Kill-the-Winner models. This implies that viruses exploit their hosts for a more prolonged period, rather than killing them. Under the Piggyback-the-Winner dynamics, there is likely more virulence content in microbial communities than previously thought – Authors claim that this data suggests facilitation for microbialisation.
Overall, virus-host community structure may be less known than previously thought – the rules behind lysogeny and lytic strategies remain uncertain however, research shows complex virus-host interactions, from an evolutionary perspective. Research on this topic could have huge consequences to help understand virome interactions. So, more microbes... less viruses?
Reviewed paper:
Knowles, B., Silveira, C.B., Bailey, B.A., Barott, K., Cantu, V.A., Cobián-Güemes, A.G., Coutinho, F.H., Dinsdale, E.A., Felts, B., Furby, K.A. and George, E.E., 2016. Lytic to temperate switching of viral communities. Nature, 531(7595), p.466.
Viral reproduction has two cycles: lytic and lysogenic. In the lytic cycle, a bacteriophage injects viral DNA through the cell wall of the host. Next, biosynthesis occurs until progeny phages are matured. The progeny phages then burst out of the membrane and are released to the environment. For the lysogenic cycle, viral DNA is injected into the genome of the host and the DNA becomes part of the chromosome. As the bacterial host divides, the viral DNA becomes part of the daughter cells. The viral DNA remains dormant until a stimulus (e.g. ultraviolet light) excides the viral DNA. Next follows biosynthesis, maturation, and finally the progeny phages burst and are released.
Viruses, like many other strong competitors and predators, have an evolutionary dilemma: they must be successful, but not too successful so that they drive their hosts to extinction. It has been thought that lysogeny is a technique designed to ensure this; lysogeny allows the phage to survive, without killing the hosts when host numbers are few. Lysogeny also means that the phage is in the same place as the host when growth conditions improve. Generally, lysogeny would be more common in oligotrophic waters.
When host abundance is high, there is an increased likeliness of virus-host collisions and opportunities for lytic viruses – this would show a higher virus-to-microbe ratio. However, a study by Knowles et al. (2016) found the opposite. The study conducted meta-analysis approach including: (1) experimental manipulations (2) literature meta-analyses, (3) direct counts, and (4) a personal study of 24 coral reef viral metagenomics. Authors found that there was a decrease in virus-to-microbe abundance as microbe abundance increased. Authors explain that this was caused by increased lysogeny at higher abundances – results showed that as microbe abundance increased, genes that are associated with integration and excision of lysogenic viruses increased as well. But why?
Authors investigated alternate hypotheses and the leading explanation was the defense hypothesis: that the high abundance host communities were dominated by defensive, slow-growing strains of hosts, associated with low virus production. Therefore, viruses would mainly infect the more-competitive and faster-growing strains of hosts which had lower abundances. Despite this, metagenomic data showed that there was no correlation between viral-defense genes and microbe abundance.
The final explanation was the Piggyback-the-Winner hypothesis, rather than Kill-the-Winner models. This implies that viruses exploit their hosts for a more prolonged period, rather than killing them. Under the Piggyback-the-Winner dynamics, there is likely more virulence content in microbial communities than previously thought – Authors claim that this data suggests facilitation for microbialisation.
Overall, virus-host community structure may be less known than previously thought – the rules behind lysogeny and lytic strategies remain uncertain however, research shows complex virus-host interactions, from an evolutionary perspective. Research on this topic could have huge consequences to help understand virome interactions. So, more microbes... less viruses?
Reviewed paper:
Knowles, B., Silveira, C.B., Bailey, B.A., Barott, K., Cantu, V.A., Cobián-Güemes, A.G., Coutinho, F.H., Dinsdale, E.A., Felts, B., Furby, K.A. and George, E.E., 2016. Lytic to temperate switching of viral communities. Nature, 531(7595), p.466.
It is a fascinating subject! The "Piggybacking-the-winner" hypothesis is one mentioned in a paper I blogged about too (https://2015-mbio322.blogspot.com/2018/11/fish-guts-are-going-viral.html). Briefly, it was about the viral and bacterial gut microbiome of Tilapia, and they found that actually there was quite a high proportion of gut bacterial cells that were lysogenised. I reckon that was perhaps surprising at first; but put into the context of "Piggybacking-the-winner", I think it just shows that there's such an amazing variation of lifestyles and community structures in the microbiome, and we still know so little about it!
ReplyDeleteOh that's interesting! So this finding has been found in other research environments... I'll have a read and comment!
ReplyDeleteHi Rebecca and Caitlin! I also find the subject very engaging, as I've blogged about it myself (https://2015-mbio322.blogspot.com/2019/01/the-importance-of-being-temperate-when.html). In the paper I reviewed no significant relationship between the virus-to-bacteria ratio and lysogeny or lytic infections has been found. I'm not an expert on the subject, so naturally I felt prompted to do a bit research onto how and why the VBR is being influenced. This is when I stumbled upon the article Lysis, lysogeny and virus–microbe ratios from Weitz et al. (2017), which is written as an answer to the publication of Knowles et al. (2016) you've reviewed in this blogpost. In the article they argue whether using the Piggyback-the-Winner model as an explanation of the systematic decline in virus-to-microbe ratio is acceptable. I definitely recommend the read,as they propose some interesting approaches to the data!
ReplyDeleteHi again! After leaving my previous I felt obliged to do some more digging on the subject. Under the link (https://t.co/OKcCl4VddF) you will find the aforementioned publication challenging the paper from Knowles et al. (2016) alongside with a response to it from Knowles & Rohwer. It’s quite interesting to track their discussion, as it is not seldom that scientists disagree on a research. I believe this is a great example on how the acquired data or its analysis may not be straightforward sometimes. I also fully agree with Caitlin that the Piggyback-the-winner hypothesis is quite fascinating and I would love to see more research being published on the subject!
ReplyDelete