Inter‐viral conflicts that exploit host CRISPR immune systems of S ulfolobus

Summary Infection of S ulfolobus islandicus   REY 15 A with mixtures of different S ulfolobus viruses, including STSV 2, did not induce spacer acquisition by the host CRISPR immune system. However, coinfection with the tailed fusiform viruses SMV 1 and STSV 2 generated hyperactive spacer acquisition in both CRISPR loci, exclusively from STSV 2, with the resultant loss of STSV 2 but not SMV 1. SMV 1 was shown to activate adaptation while itself being resistant to CRISPR ‐mediated adaptation and DNA interference. Exceptionally, a single clone S ‐1 isolated from an SMV 1 +  STSV 2‐infected culture, that carried STSV 2‐specific spacers and had lost STSV 2 but not SMV 1, acquired spacers from SMV 1. This effect was also reproducible on reinfecting wild‐type host cells with a variant SMV 1 isolated from the S ‐1 culture. The SMV 1 variant lacked a virion protein ORF114 that was shown to bind DNA . This study also provided evidence for: (i) limits on the maximum sizes of CRISPR loci; (ii) spacer uptake strongly retarding growth of infected cultures; (iii) protospacer selection being essentially random and non‐directional, and (iv) the reversible uptake of spacers from STSV 2 and SMV 1. A hypothesis is presented to explain the interactive conflicts between SMV 1 and the host CRISPR immune system.