Latent infection of an active giant endogenous virus in a unicellular green alga
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Abstract
Latency is a common strategy in a wide range of viral lineages, but its prevalence in giant viruses remains unknown. Here we describe the activity and viral production from a 617 kbp integrated giant viral element in the model green alga Chlamydomonas reinhardtii . We resolve the integrated viral region using long-read sequencing and show that viral particles are produced and released in otherwise healthy cultures. A diverse array of viral-encoded selfish genetic elements are expressed during GEVE reactivation and produce proteins that are packaged in virions. In addition, we show that field isolates of Chlamydomonas sp. harbor latent giant viruses related to the C. reinhardtii GEVE that exhibit similar infection dynamics, demonstrating that giant virus latency is prevalent in natural host communities. Our work reports the largest temperate virus documented to date and the first active GEVE identified in a unicellular eukaryote, substantially expanding the known limits of viral latency.
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Abstract
Really exciting work! Congrats to the authors.
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These monocultures all have continued to grow well in the laboratory and have not undergone any crashes, similar to CC-2937, demonstrating that the virus is not lethal.
If you are trying to assess viral virulence or cytoxicity of reactivation, I dont think this is the best measure. Unless all the latent infections are simultaneously reactivating and lysing the cells, it would be difficult to see the impact on cell viability.
If you want to see if the GEVEs are directly lytic, you could try infecting naive strains that do not have the GEVE and measuring OD. If it crashes and there is a viral bloom, probably about to directly lyse cells through lytic replication. If that doesn't happen, it is harder to interpret bc it might be just very slow-growing lysing and also forming some latent infections. Alternatively it might be 100% latent …
These monocultures all have continued to grow well in the laboratory and have not undergone any crashes, similar to CC-2937, demonstrating that the virus is not lethal.
If you are trying to assess viral virulence or cytoxicity of reactivation, I dont think this is the best measure. Unless all the latent infections are simultaneously reactivating and lysing the cells, it would be difficult to see the impact on cell viability.
If you want to see if the GEVEs are directly lytic, you could try infecting naive strains that do not have the GEVE and measuring OD. If it crashes and there is a viral bloom, probably about to directly lyse cells through lytic replication. If that doesn't happen, it is harder to interpret bc it might be just very slow-growing lysing and also forming some latent infections. Alternatively it might be 100% latent --> and replicating and spreading only through sporadic reactivation.
If you want to see if induction is lethal, you could try triggering synchronized induction by treating with a DNA damage agent (there might be something better to trigger induction for these viruses, that's just what I would do if they were phages)
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Our proteomic analysis detected group B and C Fanzors in the virions, as well as the Gag protein from the LTR retrotransposon (Fig. 4). To our knowledge, this is the first example of the packaging of proteins from mobile elements into viral capsids, and it suggests that the effectors are active immediately upon cellular entry during viral infection. Work in bacteriophages has shown that HEGs can mediate inter-viral competition during co-infection [35,36], suggesting that Fanzors and other selfish genetic elements encoded in GEVEs may also play a similar role
This is an interesting but somewhat surprising result. Given that these parasites are associated with diverse MGEs, I'm surprised that they've evolved to be recognized and packaged by one specific MGE. Are you sure that these are truly packaged?
When I have done mass spec on …
Our proteomic analysis detected group B and C Fanzors in the virions, as well as the Gag protein from the LTR retrotransposon (Fig. 4). To our knowledge, this is the first example of the packaging of proteins from mobile elements into viral capsids, and it suggests that the effectors are active immediately upon cellular entry during viral infection. Work in bacteriophages has shown that HEGs can mediate inter-viral competition during co-infection [35,36], suggesting that Fanzors and other selfish genetic elements encoded in GEVEs may also play a similar role
This is an interesting but somewhat surprising result. Given that these parasites are associated with diverse MGEs, I'm surprised that they've evolved to be recognized and packaged by one specific MGE. Are you sure that these are truly packaged?
When I have done mass spec on phages, I have seen that proteins that are really highly expressed during infection but that are not packaged can be carried over into the phage particle prep, even if you are purifying and concentrating particles via CsCl gradients. If your mass spec is sensitive enough, you will pick them up. I have used buffer exchange to differentiate between true packaged proteins and carryover proteins - carryovers get diluted out with buffer exchanges, whereas true packaged proteins do not. We did that in this paper here (https://www.cell.com/cell/fulltext/S0092-8674(19)30846-3) when we were trying to figure out if phage anti-CRISPR proteins got packaged or not.
It might be worth trying some buffer exchange experiments to convince yourself either way of this interesting result!
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