Spring Harbor Laboratory Press, Cold Spring Harbor,

NY; 1

Spring Harbor Laboratory Press, Cold Spring Harbor,

NY; 1982. 27. Jiang SC, Kellogg CA, Paul JH: Characterization of marine temperate phage-host systems isolated from Mamala Bay, Oahu, Hawaii. Appl Environ Microbiol 1998, 64:535–542.PubMed 28. Verma V, Harjai K, Chhibber S: Characterization of a T7-like lytic bacteriophage of Klebsiella pneumoniae B5055: a potential therapeutic agent. Curr Microbiol 2009, 59:274–281.PubMedCrossRef 29. Capra ML, Quiberoni A, Reinheimer JA: Thermal and chemical resistance of Lactobacillus casei and Lactobacillus paracasei bacteriophages. Lett selleck compound Appl Microbiol 2004, 38:499–504.PubMedCrossRef 30. Whiteford N, Skelly T, Curtis C, Ritchie ME, Lohr A, Zaranek AW, Abnizova I, Brown C: Swift: primary data analysis for the Illumina Solexa sequencing platform. Bioinformatics 2009, 25:2194–2199.PubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions JJ conceived of the study and designed all the experiments and drafted the manuscript; ZJL, SWW, and DHH performed all phage-related experiments; SMW, YYM, and JW analyzed the clinical bacteria strains; FL and XDC participated in the TEM investigation; YHL, GXL, and check details XTW analyzed the phage genome. GQZ and ZQW participated in the design of the study and coordination

and helped to draft the manuscript. All authors read and approved the final manuscript.”
“Background Human immunodeficiency virus (HIV) infection leads to a progressive loss of CD4+ T cell numbers and function, impairing immune responses and rendering the host susceptible to secondary opportunistic infections

[1–3]. Opportunistic infections (OI) of the oral mucosa are presented in up to 80% of HIV-infected patients [4], often causing debilitating lesions that contribute to deterioration in nutritional health. While, several studies have examined the effects of HIV infection on oral mucosal immunity in patients with OI [5, 6], questions regarding the role of epithelial pathogenesis remain to be answered. Although the underlying mechanisms remain unknown, the oral epithelium appears to be Sulfite dehydrogenase more permeable and perturbed during HIV infection [7]. Studies in the simian immunodeficiency virus (SIV) non-human primate model may provide some mechanistic clues. Similar to the intestinal mucosa [8, 9], SIV infection leads to a rapid down regulation of genes that mediate oral epithelial regeneration [10]. In addition to increasing barrier permeability, impairment of epithelial regenerative capacity is likely to enhance susceptibility to OI by disrupting homeostatic interactions with the overlying RG7420 cost protective microbiota (microbiome). The human oral microbiome is a complex polymicrobial community in delicate balance.

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