1,553
Views
5
CrossRef citations to date
0
Altmetric
Letters to the Editor

Hypervirulent Clostridium difficile ribotypes are CpG depleted

, , &
Pages 1422-1425 | Received 18 Jun 2018, Accepted 31 Jul 2018, Published online: 03 Sep 2018

References

  • Goorhuis A, Bakker D, Corver J, et al. Emergence of Clostridium difficile infection due to a new hypervirulent strain, polymerase chain reaction ribotype 078. Clin Infect Dis. 2008;47:1162–1170.
  • Vohra P, Poxton IR. Comparison of toxin and spore production in clinically relevant strains of Clostridium difficile. Microbiology. 2011;157:1343–1353.
  • Smits WK. Hype or hypervirulence: a reflection on problematic C. difficile strains. Virulence. 2013;4:592–596.
  • Simmonds P, Tulloch F, Evans DJ, et al. Attenuation of dengue (and other RNA viruses) with codon pair recoding can be explained by increased CpG/UpA dinucleotide frequencies. Proc Natl Acad Sci. 2015;112:E3633–E3634.
  • Wasson MK, Borkakoti J, Kumar A, et al. The CpG dinucleotide content of the HIV-1 envelope gene may predict disease progression. Sci Rep. 2017;7:8162.
  • Sankar S, Borkakoti J, Ramamurthy M, et al. Identification of tell-tale patterns in the 3ʹ non-coding region of hantaviruses that distinguish HCPS-causing hantaviruses from HFRS-causing hantaviruses. Emerg Microbes Infect. 2018;7:32.
  • Upadhyay M, Samal J, Kandpal M, et al. CpG dinucleotide frequencies reveal the role of host methylation capabilities in parvovirus evolution. J Virol. 2013;87:JVI–02515.
  • Upadhyay M, Vivekanandan P. Depletion of CpG Dinucleotides in papillomaviruses and polyomaviruses: a role for divergent evolutionary pressures. PloS One. 2015;10:e0142368.
  • Takata MA, Gonçalves-Carneiro D, Zang TM, et al. CG dinucleotide suppression enables antiviral defence targeting non-self RNA. Nature. 2017;550:124.
  • Vedantam G, Clark A, Chu M, et al. Clostridium difficile infection: toxins and non-toxin virulence factors, and their contributions to disease establishment and host response. Gut Microbes. 2012;3:121–134.
  • Marsh JW, Arora R, Schlackman JL, et al. Association of relapse of Clostridium difficile disease with BI/NAP1/027. J Clin Microbiol. 2012;50:4078–4082.
  • Quesada-Gómez C, López-Ureña D, Acuña-Amador L, et al. Emergence of an outbreak-associated Clostridium difficile variant with increased virulence. J Clin Microbiol. 2015;53:1216–1226.
  • Stabler RA, Gerding DN, Songer JG, et al. Comparative phylogenomics of Clostridium difficile reveals clade specificity and microevolution of hypervirulent strains. J Bacteriol. 2006;188:7297–7305.
  • Burge C, Campbell AM, Karlin S. Over-and under-representation of short oligonucleotides in DNA sequences. Proc Natl Acad Sci. 1992;89:1358–1362.
  • Dalpke A, Frank J, Peter M, et al. Activation of toll-like receptor 9 by DNA from different bacterial species. Infect Immun. 2006;74:940–946.
  • Yang X, Li D, Xu H, et al. P-258 YI clostridium difficile toxin A-associated DNA augments the host inflammatory response. Inflamm Bowel Dis. 2012;18:S113–S113.
  • Wojciechowski M, Czapinska H, Bochtler M. CpG underrepresentation and the bacterial CpG-specific DNA methyltransferase M. MpeI Proc Natl Acad Sci. 2013;110:105–110.
  • Sánchez-Romero MA, Cota I, Casadesús J. DNA methylation in bacteria: from the methyl group to the methylome. Curr Opin Microbiol. 2015;25:9–16.
  • Kansau I, Barketi-Klai A, Monot M, et al. Deciphering adaptation strategies of the epidemic Clostridium difficile 027 strain during infection through in vivo transcriptional analysis. PLoS One. 2016;11:e0158204.
  • Borriello SP. Pathogenesis of Clostridium difficile infection. J Antimicrob Chemother. 1998;41:13–19.