Bacteriophage Gene Products That Cause Human Disease

Bishai, William R.; Murphy, John R.

doi:10.1007/978-1-4684-5490-1_12

Cited by 48 publications

(38 citation statements)

References 172 publications

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“…The interest in prophages of corynebacteria stems from early work demonstrating that the diphtheria toxin is encoded by corynephage beta, morphologically a siphovirus with a 35-kb genome containing cohesive ends (17). Physical maps of the phage genome demonstrated that the toxin is encoded near the attachment site of the phage.…”

Section: Corynebacteriummentioning

confidence: 99%

Prophage Genomics

Canchaya

Proux

Fournous

et al. 2003

Microbiol Mol Biol Rev

637

621

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The majority of the bacterial genome sequences deposited in the National Center for Biotechnology Information database contain prophage sequences. Analysis of the prophages suggested that after being integrated into bacterial genomes, they undergo a complex decay process consisting of inactivating point mutations, genome rearrangements, modular exchanges, invasion by further mobile DNA elements, and massive DNA deletion. We review the technical difficulties in defining such altered prophage sequences in bacterial genomes and discuss theoretical frameworks for the phage-bacterium interaction at the genomic level. The published genome sequences from three groups of eubacteria (low- and high-G+C gram-positive bacteria and γ-proteobacteria) were screened for prophage sequences. The prophages from Streptococcus pyogenes served as test case for theoretical predictions of the role of prophages in the evolution of pathogenic bacteria. The genomes from further human, animal, and plant pathogens, as well as commensal and free-living bacteria, were included in the analysis to see whether the same principles of prophage genomics apply for bacteria living in different ecological niches and coming from distinct phylogenetical affinities. The effect of selection pressure on the host bacterium is apparently an important force shaping the prophage genomes in low-G+C gram-positive bacteria and γ-proteobacteria

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Section: Corynebacteriummentioning

confidence: 99%

Prophage Genomics

Canchaya

Proux

Fournous

et al. 2003

Microbiol Mol Biol Rev

637

621

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“…The scheme represents a modified version inspired by a comprehensive diphtheria review (Murphy, 1996) Diphtheria pathogenesis is largely determined by the capacity of virulent C. diphtheriae biotypes (see below) to produce the deadly DT and to colonize and multiply in skin lesions or nasopharyngeal cavities. Since both determinants are encoded by the bacterium carrying a lysogenic beta prophage (Freeman, 1951;Bishai & Murphy, 1988), virulence results from the combined effects of the bacterial and phage genomes (Fig. 3).…”

Section: Manifestations Pathogenesis and Epidemiology Of Diphtheriamentioning

confidence: 99%

“…Intriguingly, DT is specified for by tox, a gene carried on one of a family of related corynebacteriophages integrated into the host chromosome of C. diphtheriae (Fig. 4) (for review, see Bishai & Murphy 1988). That DT is encoded by the prophage gene was demonstrated when non-pathogenic strains of C. diphtheriae became lysogenically converted upon infection with a bacterial virus known as 340 beta phage (Freeman, 1957;Holmes & Barksdale, 1969).…”

Section: Diphtheriae and Diphtheria Toxin (Dt) Productionmentioning

confidence: 99%

“…The latter scenario is predominantly found in bacterial species and accounts for lysogenic conversions, phenomena in which phenotypes of the microbial host including pathogenicity, growth performance and production of virulence factors and toxins can be significantly affected by expression of prophage encoded genes. Prominent examples for phage-dependent toxin expression and disease formation include exotoxin-associated scarlet fever by Streptocoocus pyogenes (Johnson et al, 1986;Broudy et al, 2001), dysentery causing Shiga toxins Stx1 and Stx2 from Shigella dysenteriae (Newland et al, 1985;Willshaw et al, 1985;Huang, et al, 1986), phage CTXφ encoded cholera toxin from Vibrio cholera (Waldor & Mekalanos, 1996;Faruque & Nair, 2002) and diphtheria toxin encoded on a beta prophage from lysogens of Corynebacterium diphtheriae (Holmes & Barksdale, 1969;Bishai & Murphy 1988). Together 334 with tRNase ribotoxins and anticodon nucleases from prokaryal and eukaryal microbes that have been shown to be encoded by transposable elements as well as circular and nonconventional linear DNA plasmids (Tokunaga et al, 1990;Kaufmann, 2000;Schaffrath & Meinhardt, 2005;Schaffrath et al, 1999), all of these genetic constellations implicate scenarios in which killer phenotypes have been evolved and spread by way of viral DNA transduction pathways or other forms of horizontal gene transfer.…”

Section: Introductionmentioning

confidence: 99%

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Diphtheria Disease and Genes Involved in Formation of Diphthamide, Key Effector of the Diphtheria Toxin

Uthman¹,

Liu²,

Giorgini³

et al. 2012

Insight and Control of Infectious Disease in Global Scenario

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“…This led to the discovery of H. somnus DNA similar to bacteriophage DNA. The existence of phage-encoded virulence factors in several bacterial species has been described (6). Phage conversion can occur due to the acquisition of a phage-encoded toxin or altered expression of bacterial toxins due to the lysogenic state (5,31,43,45,68).…”

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confidence: 99%

Cloning and characterization of bacteriophage-like DNA from Haemophilus somnus homologous to phages P2 and HP1

1997

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In an attempt to identify and characterize components of a heme uptake system of Haemophilus somnus, an Escherichia coli cosmid library of H. somnus genomic DNA was screened for the ability to bind hemin (Hmb ؉ ). The Hmb ؉ phenotype was associated with a 7,814-bp HindIII fragment of H. somnus DNA that was subcloned and sequenced. Thirteen open reading frames (orfs) were identified, all transcribed in one direction, and transposon mutagenesis identified orf7 as the gene associated with the Hmb ؉ phenotype. Orf7 (178 amino acids) has extensive homology with the lysozymes of bacteriophages P-A2, P21, P22, PZA, -29, -vML3, T4, or HP1. The orf7 gene complemented the lytic function of the K gene of phage P2 and the R gene of phage . A lysozyme assay using supernatants from whole-cell lysates of E. coli cultures harboring plasmid pRAP501 or pGCH2 (both of which express the orf7 gene product) exhibited significant levels of lysozyme activity. The orf6 gene upstream of orf7 has the dual start motif common to the holins encoded by lambdoid S genes, and the orf6 gene product has significant homology to the holins of phages HP1 and P21. When expressed from a tac promoter, the orf6 gene product caused immediate cell death without lysis, while cultures expressing the orf7 gene product grew at normal rates but lysed immediately after the addition of chloroform. Based on this data, we concluded that the Hmb ؉ phenotype was an artifact resulting from the expression of cloned lysis genes which were detrimental to the E. coli host. The DNA flanking the cloned lysis genes contains orfs that are similar to structural and DNA packaging genes of phage P2. Polyclonal antiserum against Orf2, which is homologous to the major capsid precursor protein (gpN) of phage P2, detected a 40,000-M r protein expressed from pRAP401 but did not detect Orf2 in H. somnus lysates. The phage-like DNA was detected in the serum-susceptible preputial strains HS-124P and HS-127P but was absent from the serum-resistant preputial strains HS-20P and HS-22P. Elucidation of a potential role for this cryptic prophage in the H. somnus life cycle requires more study.

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Bacteriophage Gene Products That Cause Human Disease

Cited by 48 publications

References 172 publications

Prophage Genomics

Prophage Genomics

Diphtheria Disease and Genes Involved in Formation of Diphthamide, Key Effector of the Diphtheria Toxin

Cloning and characterization of bacteriophage-like DNA from Haemophilus somnus homologous to phages P2 and HP1

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