A new archaeal virus that suppresses the transcription of host immunity genes
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Abstract
In some extreme environments, archaeal cells have been shown to have chronic viral infections, and such infections are well-tolerated by the hosts and may potentially protect against more lethal infections by lytic viruses. We have discovered that a natural Haloferax strain (48N), which is closely related to the model organism Haloferax volcanii, is chronically-infected by a lemon-shaped virus, which we could purify from the medium. The chronic infection by this virus, which we named LSV-48N, is never cleared, despite the multiple defense systems of the host that include CRISPR-Cas, and two CBASS systems. Curing 48N of its virus by genetic engineering, led to radical changes in the gene expression profile of 48N and a dramatic improvement in its growth rate. Remarkably, the cured 48N is the fastest-growing haloarchaeon reported to date, with a generation time of approximately 1 hour at 45°C compared to the typical 2.5 hours of H. volcanii or its infected isogen, and faster than any known haloarchaeon. The virus subverts host defenses by reducing their transcription and interfering with the CRISPR spacer acquisition machinery. Our results suggest that the slow growth of many halophilic archaea could be due to the effects of proviruses within their genomes that consume resources and alter the gene expression of their hosts.
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However, a comparison of the expression levels of defense genes in 48N and cured-48N showed that these defense systems, and additional ones, such as Hachiman, were strongly downregulated in the infected strain
This is a really cool finding! We saw something conceptually similar when studying the transcriptional regulation of CRISPR-Cas systems in Pseudomonas aeruginosa. We found that numerous Pseudomonas phages had their own copies of a bacterial gene that was involved in CRISPR-Cas transcriptional repression, and these phage transcription factors were capable of down regulating expression of the CRISPR-Cas system in Pseudomonas. (see https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7190418/)
I'm wondering if you see any cases where these viruses encode host-like proteins? Perhaps that represents a similar case where the virus has stolen …
However, a comparison of the expression levels of defense genes in 48N and cured-48N showed that these defense systems, and additional ones, such as Hachiman, were strongly downregulated in the infected strain
This is a really cool finding! We saw something conceptually similar when studying the transcriptional regulation of CRISPR-Cas systems in Pseudomonas aeruginosa. We found that numerous Pseudomonas phages had their own copies of a bacterial gene that was involved in CRISPR-Cas transcriptional repression, and these phage transcription factors were capable of down regulating expression of the CRISPR-Cas system in Pseudomonas. (see https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7190418/)
I'm wondering if you see any cases where these viruses encode host-like proteins? Perhaps that represents a similar case where the virus has stolen defense system regulators and is using them to control host gene expression.
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despite the lack of sequence similarity of any of the ORFs encoded by the provirus to any known capsid protein.
Have you considered using structural homology searches to ID the capsid protein? In this paper (https://www.nature.com/articles/s41396-023-01474-1) they were able to use that approach assign function to archaea virus genes of unknown function, and successfully ID'ed a capsid gene.
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