Prophages belonging to Sa3int and Sa2int group were the most prevalent. of the bacterial genome. Phage integrase genes were found in 55/58 (~95?%) strains and 97/211 (~46?%) prophages. Prophages belonging to Sa3int integrase group (phiNM3, JS01, phiN315) (39/97, 40%) and Sa2int (phi2958PVL) (14/97, 14%) were the most prevalent prophages and harboured multiple virulence genes such as isolated from CRS patients and their possible role in disease development. These findings provide a platform for future investigations into potential tripartite associations between bacteria-prophage-human immune system, evolution and CRS disease pathophysiology. including but not limited to toxin secretion, biofilm formation, niche adaptation. As chronic rhinosinusitis (CRS) is usually often associated with persistence of clinical isolates carrying Sa3int group prophages encoding human immune evasion factors like were predominantly found in CRS patients with nasal polyps. These findings provide a platform for investigation into the contribution of those factors in the pathophysiology of CRS and their potential use as diagnostic, prognostic and therapeutic targets. Our findings will not only be of interest to clinicians but also will equally be BI6727 (Volasertib) important in disease epidemiology particularly inflammatory diseases, including but not limited to CRS as prophage associated toxins have been known to cause deadly outbreaks in the past. Highlights In total, 211 prophage regions were identified in 58?genomes isolated from chronic rhinosinusitis (CRS) patients suggesting widespread distribution of prophage elements in clinical strains colonizing nasal niche. Sa2int and Sa3int group prophages belonging to family and genus were most frequently found in from CRS patients. isolated from CRS patients with nasal polyps predominantly harboured intact Sa3int group prophages encoding human immune evasion cluster (IEC) genes. Prophages in did not encode any antibiotic resistant genes (ARGs). Summary Prophages of modulate bacterial fitness on multiple levels like infectivity, toxicity, virulence regulation, immune evasion and microbiome competition as they arm bacteria with accessory genes. These properties allow to persist in a nasal niche, possibly contributing to the severity and phenotype of infections like chronic rhinosinusitis (CRS). Here, we report that isolated from CRS patients carried at least one prophage and contributed up to 7.7?% of the total bacterial Tmem27 genome. Intact prophages were more frequently identified in CRS patients with nasal polyp (CRSwNP) compared to patients without nasal polyp (CRSsNP). Prophages belonging to Sa3int and Sa2int group were the most prevalent. Further, isolates from CRSwNP patients often harboured Sa3int prophages encoding human immune evasion cluster genes. In summary, prophage encoded accessory genes may play a significant role in the pathogenicity of and impact CRS disease phenotype as well as severity. Data Summary Genomes of previously sequenced (is considered a commensal capable of colonizing diverse ecological niches within human and animals and is BI6727 (Volasertib) carried by ~30?% of the human population asymptomatically [7, 8], it is also one of the most invasive, highly pathoadaptive, opportunistic pathogens and etiological agent of diverse human and animal maladies including CRS. An increased colonization of was exhibited in patients with CRSwNP (64%) but not in patients with CRSsNP (33%) versus control (20%) patients suggesting contribution of in CRS [9, 10]. Of further concern BI6727 (Volasertib) is the emergence and spread of methicillin resistant (MRSA) and vancomycin resistant (VRSA). The successful pathoadaptive evolution of virulent is largely due to acquisition of large mobile genetic elements (MGEs) carrying virulence, toxin and resistance genes [11]. Such MGEs include plasmids, transposons (Tn), insertion sequences (Is usually), pathogenicity islands (SaPIs), staphylococcal cassette chromosomes (SCCs) and (pro)phages. They can be exchanged between strains by horizontal gene transfer (HGT) and/or transferred to progeny through vertical gene transfer (VGT) [12C14]. Among multiple MGEs contributing to virulence and pathogenicity of increased biofilm formation, enhanced -hemolysin activity and reduced vancomycin sensitivity. There is growing evidence that accessory genes carried by prophages of significantly modulate bacterial fitness as they carry multiple VFs. These VFs include human immune evasion cluster (IEC) comprising the genes and which encodes staphylokinase, chemotaxis inhibitory protein of (CHIPS), staphylococcal complement inhibitor (SCIN) and enterotoxin A/P (SEA or SEP) respectively in different combinations [28]..