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home:pathogenesis:microbiota:interaction [09.09.2012] paulalberthome:pathogenesis:microbiota:interaction [10.13.2018] – [Bacteria affect human genes and gene expression] sallieq
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 ====== Effects of bacteria on their human host ====== ====== Effects of bacteria on their human host ======
  
-Manipulation of host cell fate and orchestrated choreography of inflammatory responses are recurrent themes in the strategies of microbial pathogens.((Relman D.A. and Falkow S. (2010). A molecular perspective of microbial pathogenecity. Mandell, Douglas, and Bennett's principles and practice of infectious diseases. G. L. Mandell, J. E. Bennett and R. Dolin. Philadelphia, PA, Churchill Livingstone/Elsevier. 7.)) + 
 +The genomes and the respective proteomes of microbes in the body frequently interact with those expressed by their human hosts. This is a key part of what is know as the interactome. The "massive"(({{pubmed>long:18582510}})) co-occurrence of protein-coding genes between microbes and humans speaks to the survival advantage of such homology, and the extent to which sequence overlap may play a key role in disease. Indeed, manipulation of host cell fate and orchestrated choreography of inflammatory responses are recurrent themes in the strategies of microbial pathogens.((Relman D.A. and Falkow S. (2010). A molecular perspective of microbial pathogenecity. Mandell, Douglas, and Bennett's principles and practice of infectious diseases. G. L. Mandell, J. E. Bennett and R. Dolin. Philadelphia, PA, Churchill Livingstone/Elsevier. 7.)) Bacteria affect host-cell pathways and human gene expression through a number of increasingly well-documented ways.
  
  
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 [{{ :home:pathogenesis:microbiota:interactome.082.png?400|**When interacting with the human body (and one another), bacteria are responsible for an imponderable number of interactions.**}}] [{{ :home:pathogenesis:microbiota:interactome.082.png?400|**When interacting with the human body (and one another), bacteria are responsible for an imponderable number of interactions.**}}]
  
-The genomes and the respective proteomes of microbes in the body frequently interact with those expressed by their human hosts. This is a key part of what is know as the interactome. The co-occurrence of protein-coding genes between microbes and humans speaks to the survival advantage of such homology, and the extent to which sequence overlap may play a key role in disease. +The genomes and the respective proteomes of microbes in the body frequently interact with those expressed by their human hosts. This is a key part of what is know as the interactome. The "massive"(({{pubmed>long:18582510}})) co-occurrence of protein-coding genes between microbes and humans speaks to the survival advantage of such homology, and the extent to which sequence overlap may play a key role in disease. Work to understand extent of protein-protein interactions between microbe and man is in its early stages, but there are some indications of its full extent
  
-Work to understand extent of protein-protein interactions between microbe and man is in its early stages, but there are some indications of its full extent. Several studies out of University of Saskatchewan have been particularly provocative.+==== Viruses ====
  
 +In a 2007 analysis of sequence similarity between hepatitis C virus (HCV) and humans Kusalik //et al.// found that pentamers from HCV polyprotein have a widespread and high level of similarity to a large number of human proteins (19,605 human proteins, that is 57.6% of the human proteome).(({{pubmed>long:17485143}})) Indeed, only a limited number of HCV pentameric fragments have no similarity to the human host. A 2011 study by the same author revised that figure: using once more pentapeptide matching, only 214 motifs – a short sequence pattern of nucleotides in a DNA sequence or amino acids in a protein – out of a total of 3,007 (7.11%) identified HCV as nonself compared to the //Homo sapiens// proteome.(({{pubmed>long:22299062}})) 
  
 +A 2008 study examined thirty viral proteomes were examined for amino acid sequence similarity to the human proteome (as well as a control of 30 sets of human proteins).(({{pubmed>long:18582510}})) Researchers found that all of the analyzed 30 viral proteomes including human T-lymphotropic virus 1, and Rubella virus had substantial overlap with the human proteome.
  
 +==== Bacteria ====
  
-==== Sequence homology ==== +Work on bacterial proteomes, while more recent, has also been illuminating. Trost //et al.// studied in 2010 forty bacterial proteomes for amino acid sequence similarity to the human proteome.(({{pubmed>long:21559180}})) All bacterial proteomes, were found to share hundreds of nonamer (nine subunit) sequences with the human proteome. The overlap is widespread, with one third of human proteins sharing at least one nonapeptide with one of these bacteria. On the whole, the bacteria-versus-human nonamer overlap is numerically defined by 47,610 total perfect matches disseminated through 10,701 human proteins. 
  
 +Expanding on this work, Trost //et al.// performed a pentapeptide and hexapeptide analyses of sequence similarities between bacterial and human DNA.(({{pubmed>long:21487508}})) He demonstrated that there does not exist a single human protein that does not harbor a bacterial pentapeptide or hexapeptide motif; as the team writes, "not even one." Interestingly the team found in a 2012 study that while pathogens and nonpathogens had comparable similarity to the human proteome, pathogens causing chronic infections were found to be more similar to the human proteome than those causing acute infections.(({{pubmed>long:22558081}})) Trost owed this discrepancy to the fact that chronic pathogens are better able to resist immune responses.
  
 +Surveys of protein-protein interactions have also been completed for //Salmonella//,(({{pubmed>long:22750305}})) (({{pubmed>long:22589098}})) //Clostridium difficile//, and //Mycobacterium tuberculosis//.(({{pubmed>long:22587966}}))
  
  
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 The highly variable range of human genetic mutations induced by bacteria have been identified with some success by researchers with the Human Genome Project. Rather than serving as markers of particular diseases, such mutations generally mark the presence of those pathogens capable of affecting DNA transcription and translation in the nucleus. The highly variable range of human genetic mutations induced by bacteria have been identified with some success by researchers with the Human Genome Project. Rather than serving as markers of particular diseases, such mutations generally mark the presence of those pathogens capable of affecting DNA transcription and translation in the nucleus.
  
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 +{{tag>Microbes_in_the_human_body}}
  
 ===== Notes and comments ===== ===== Notes and comments =====
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 +===== References =====
home/pathogenesis/microbiota/interaction.txt · Last modified: 09.14.2022 by 127.0.0.1
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