Intestinal bacteria have been implicated in the initiation and amplification of inflammatory bowel disease (IBD). The dysbiosis theory, reviewed by Tamboli et al (Gut 2004; 53: 1), is that an imbalance between putative ‘‘harmful’’versus ‘‘protective’’bacterial species may promote chronic intestinal inflammation. Although several studies published so far support this hypothesis, the most vexing question posed by Tamboli et al remains ‘‘what is the origin of dysbiosis?’’. Bacteriophages outnumber bacteria by a factor of 10 in many natural ecosystems, exert a strong influence on bacterial diversity and population structure, and are probably involved in dysbiosis by destabilising bacterial communities. 1 They could be involved indirectly through gene transfer and genome reorganisation within the bacterial population or directly as immunomodulating agents2 or by steric competition for microbe-associated molecular patterns on bacterial surfaces. However, bacteriophages are a neglected component of the gut microbiota. The first viral metagenomic study demonstrated a wide diversity (1200 genotypes) of uncultured bacteriophage species. 3 The present study aimed at measuring the total viral community associated with the gut mucosa and comparing viral abundance between healthy individuals and patients with Crohn’s disease (CD), and also between the ulcerated and non-ulcerated mucosa of these patients.