An archaeal CBASS system eliminates viruses without killing the host cells

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Detalles Bibliográficos
Publicado en:bioRxiv (Feb 13, 2025)
Autor principal: Choudhary, Deepak Kumar
Otros Autores: Singla, Himani, Vassover, Dana, Golan, Noam, Reshef, Leah, Hadar Shukrun, Gophna, Uri
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Cold Spring Harbor Laboratory Press
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Acceso en línea:Citation/Abstract
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022 |a 2692-8205 
024 7 |a 10.1101/2024.09.12.612678  |2 doi 
035 |a 3166351656 
045 0 |b d20250213 
100 1 |a Choudhary, Deepak Kumar 
245 1 |a An archaeal CBASS system eliminates viruses without killing the host cells 
260 |b Cold Spring Harbor Laboratory Press  |c Feb 13, 2025 
513 |a Working Paper 
520 3 |a Many cyclic-oligonucleotide-based antiphage signalling systems (CBASS) defend against viral infections using a TIR-SAVED domain protein that depletes cellular NAD+ levels, eventually leading to cell dormancy or death. This abortive infection strategy is beneficial in stopping fast lytic infections, as cells die before spreading the virus to neighboring cells. However, many archaea are infected by chronic "temperate" viruses that coexist with their hosts for extended periods. In such situations, abortive infection could be detrimental, as the cost of immunity may outweigh that of infection. In this study, we examine an archaeal Type II-C CBASS system from Haloferax strain Atlit 48N that was heterologously expressed in the model organism Haloferax volcanii DS2. We demonstrate that this system protects against a chronically infecting virus, HFPV-1, and enables clearing of the virus after several passages without killing the host. Moreover, cells that have cleared the virus become substantially more resistant to future HFPV-1 infections, without acquiring CRISPR spacers from that virus. Cell death during viral infection only occurs after extensive incubation with HFPV-1. These findings suggest that CBASS could be beneficial even for archaea exposed to chronic infecting viruses, potentially explaining why such systems are relatively common in archaea.Competing Interest StatementThe authors have declared no competing interest.Footnotes* Author contribution section added, this is now required by most journals. 
653 |a Infections 
653 |a Chronic infection 
653 |a Cell death 
653 |a Viruses 
653 |a Oligonucleotides 
653 |a Dormancy 
653 |a Viral infections 
653 |a CRISPR 
700 1 |a Singla, Himani 
700 1 |a Vassover, Dana 
700 1 |a Golan, Noam 
700 1 |a Reshef, Leah 
700 1 |a Hadar Shukrun 
700 1 |a Gophna, Uri 
773 0 |t bioRxiv  |g (Feb 13, 2025) 
786 0 |d ProQuest  |t Biological Science Database 
856 4 1 |3 Citation/Abstract  |u https://www.proquest.com/docview/3166351656/abstract/embedded/75I98GEZK8WCJMPQ?source=fedsrch 
856 4 0 |3 Full text outside of ProQuest  |u https://www.biorxiv.org/content/10.1101/2024.09.12.612678v2