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--- home:pathogenesis:microbiota:interaction [09.23.2012] – [Notes and comments] paulalbert
+++ home:pathogenesis:microbiota:interaction [09.14.2022] (current) – external edit 127.0.0.1
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-====== Effects of bacteria on their human host ======
+====== Effects of bacteria and viruses on their human host ======
+<relatedarticles> [[home:pathogenesis:microbiota:acute_infections|Acute infections]], [[https://mpkb.org/home/diseases/acute_respiratory|Acute respiratory infections]] </article>
-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.
+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"(({{pmid>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.**}}]
-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.
+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"(({{pmid>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.
 ==== 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.
+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).(({{pmid>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.(({{pmid>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).(({{pmid>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.
+==== Coronavirus ====
+Several teams researching coronavirus [[https://www.niaid.nih.gov/diseases-conditions/coronaviruses|What's the problem?]]
+[[https://www.nature.com/articles/d41586-020-00660-x?utm_source=Nature+Briefing&utm_campaign=9dd44b4364-briefing-dy-20200309&utm_medium=email&utm_term=0_c9dfd39373-9dd44b4364-43480017|Why does the coronavirus spread so easily between people?]]
+How does social distancing work? [[https://1v1d1e1lmiki1lgcvx32p49h8fe-wpengine.netdna-ssl.com/wp-content/uploads/2020/04/the-spinoff-toby-morris-siouxsie-wiles-design-graphics-illustration-coronavirus_dezeen_1704_col_1.gif|picture this]]
+[[https://www.youtube.com/watch?v=1vZDVbqRhyM|discussion of coronavirus and ACE inhibitors]]
+[[https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30183-5/fulltext|Clinical features of Covid-19 reported from Wuhan Feb2020]]
+[[https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(20)30132-8/fulltext|3 Antiviral and anti-inflammatory treatments compared]]
+[[https://www.koreabiomed.com/news/articleView.html?idxno=7428|Treatment guidelines for coronavirus (Korea 2020)]]
+[[https://www.koreabiomed.com/news/articleView.html?idxno=7718|Fewer new cases 20/3/2020 (Korea) ]]
+current evidence(({{pmid>long:    32096567}}))
+chloroquine (({{pmid>long:    32147496}}))
+neuroinvasive potential(({{pmid>long:    32104915}}))
+Unique epidemiological and clinical features(({{pmid>long:    32134116}}))
+Presumed Asymptomatic Carrier Transmission(({{pmid>long:    32083643}}))
+Discovering drugs(({{pmid>long:    32147628}}))
+breakthrough(({{pmid>long:    32074550}}))
+What we know so far(({{pmid>long:    32139372}}))
+It seems [[https://chemrxiv.org/articles/COVID-19_Disease_ORF8_and_Surface_Glycoprotein_Inhibit_Heme_Metabolism_by_Binding_to_Porphyrin/11938173|virus attacks the HEME of red blood cells, destroying their ability to absorb oxygen and carbon dioxide]] //so that gently applied// supplementary pure oxygen will be an important part of treatment.
+[[https://www.mediterranee-infection.com/wp-content/uploads/2020/03/Hydroxychloroquine_final_DOI_IJAA.pdf|small sample size survey shows hydroxychloroquine treatment is significantly associated with viral load reduction in COVID-19 patients, effect is reinforced by azithromycin.]]
+February 2020 The multicenter collaboration group of Department of Science and Technology of Guangdong Province and Health Commission of Guangdong Province for chloroquine in the treatment of novel coronavirus pneumonia developed this expert consensus after extensive discussion. It recommended chloroquine phosphate tablet, 500mg twice per day for 10 days for patients diagnosed as mild, moderate and severe cases of novel coronavirus pneumonia and without contraindications to chloroquine. (({{pmid>long:32075365}}))
+**May 2020** Results of extensive study of [[https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)31180-6/fulltext|hydroxychloroquine and chloroquine]] indicate harm rather than help from use of these drugs in coronavirus cases.
+ 032 patients (mean age 53·8 years, 46·3% women) with COVID-19 were hospitalised during the study period and met the inclusion criteria.
+Data from 671 hospitals in six continents  included patients hospitalised between Dec 20, 2019, and April 14, 2020, with a positive laboratory finding for SARS-CoV-2.
+Patients who received one of the treatments of interest within 48 h of diagnosis were included in one of four treatment groups (chloroquine alone, chloroquine with a macrolide, hydroxychloroquine alone, or hydroxychloroquine with a macrolide), and patients who received none of these treatments formed the control group. Patients for whom one of the treatments of interest was initiated more than 48 h after diagnosis or while they were on mechanical ventilation, as well as patients who received remdesivir, were excluded.
+After controlling for multiple confounding factors (age, sex, race or ethnicity, body-mass index, underlying cardiovascular disease and its risk factors, diabetes, underlying lung disease, smoking, immunosuppressed condition, and baseline disease severity),
+The main outcomes of interest were in-hospital mortality and the occurrence of de-novo ventricular arrhythmias (non-sustained or sustained ventricular tachycardia or ventricular fibrillation).
+Compared with the control group (0·3%), hydroxychloroquine (6·1%; 2·369, 1·935–2·900), hydroxychloroquine with a macrolide (8·1%; 5·106, 4·106–5·983), chloroquine (4·3%; 3·561, 2·760–4·596), and chloroquine with a macrolide (6·5%; 4·011, 3·344–4·812) were independently associated with an increased risk of de-novo ventricular arrhythmia during hospitalisation.
+When compared with mortality in the control group (9·3%), hydroxychloroquine (18·0%; hazard ratio 1·335, 95% CI 1·223–1·457), hydroxychloroquine with a macrolide (23·8%; 1·447, 1·368–1·531), chloroquine (16·4%; 1·365, 1·218–1·531), and chloroquine with a macrolide (22·2%; 1·368, 1·273–1·469) were each independently associated with an increased risk of in-hospital mortality.
+[[https://www.jbc.org/content/early/2020/04/13/jbc.RA120.013679.abstract|Remdesivir believed to inhibit RNA synthesis in virus and coronavirus]]
+[[https://www.mediterranee-infection.com/azithromycin-and-ciprofloxacin-have-a-chloroquine-like-effect-on-respiratory-epithelial-cells/|Azithromycin and ciprofloxacin have a chloroquine-like effect on respiratory epithelial cells]]
+Drug used for Ebola is being tested on 600 participants in a study started March 15, 2020 and expected to complete in May 2020 [[https://www.clinicaltrials.gov/ct2/show/NCT04292730|Treatment study]]
+[[https://www.monash.edu/discovery-institute/news-and-events/news/2020-articles/Lab-experiments-show-anti-parasitic-drug,-Ivermectin,-eliminates-SARS-CoV-2-in-cells-in-48-hours
+|Laboratory experiment shows Ivermectin can kill the virus within 48 hours in cell culture]]   (({{pmid>long:32251768}}))
+[[https://www.monash.edu/discovery-institute/news-and-events/news/2020-articles/Lab-experiments-show-anti-parasitic-drug,-Ivermectin,-eliminates-SARS-CoV-2-in-cells-in-48-hours|48-hours to eliminate SARS-CoV-2 in cell culture]] "The next steps are to determine the correct human dosage – ensuring the doses shown to effectively treat the virus in vitro are safe for humans."
+[[https://www.drugs.com/pro/stromectol.html|Ivermectin studied in humans]]
+[[https://www.wionews.com/south-asia/bangladesh-doctors-claim-to-have-found-effective-drug-combination-to-cure-covid-19-patients-299247|Bangladeshi doctors report curing Coronavirus by a single dose of a frequently used antiprotozoal medicine called Ivermectin, in combination with Doxycycline, an antibiotic. ]]
+[[https://www.newsmax.com/us/ivermectin-drug-virus/2020/05/22/id/968688/|drug already approved by the FDA to treat parasitic infections is showing “astounding” results]]
+Physicians who participated in the study report that patients’ viral loads began declining almost immediately after they began administering ivermectin, a widely available prescription drug approved to combat parasites, scabies and head lice.
+[[https://www.uu.nl/en/news/researchers-report-discovery-of-antibody-that-blocks-infection-by-the-novel-coronavirus-sars-cov-2|A fully human monoclonal antibody that prevents the SARS-CoV-2 (COVID-19) virus from infecting cultured cells is identified by research at Erasmus Medical Center and Harbour BioMed, Utrecht Univ.  ]]
+<relatedarticle> [[home:starting:usingforum:home_help_using_forums:a_a_href#new_information|5 key elements of MP#new information]] </article>
 ==== Bacteria ====
-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.
+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.(({{pmid>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.
+Expanding on this work, Trost //et al.// performed a pentapeptide and hexapeptide analyses of sequence similarities between bacterial and human DNA.(({{pmid>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.(({{pmid>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}}))
+Surveys of protein-protein interactions have also been completed for //Salmonella//,(({{pmid>long:22750305}})) (({{pmid>long:22589098}})) //Clostridium difficile//, and //Mycobacterium tuberculosis//.(({{pmid>long:22587966}}))
@@ Line 42: / Line 130: @@
 //**Trevor Marshall, PhD**//</blockquote>
-Researchers are increasingly highlighting the intracellular activities of microbes such as //Staphylococcus aureus// once thought to be exclusively extracellular and what this means for medicine.(({{pubmed>long:21297670}}))
+Researchers are increasingly highlighting the intracellular activities of microbes such as //Staphylococcus aureus// once thought to be exclusively extracellular and what this means for medicine.(({{pmid>long:21297670}}))
-The Marshall Pathogenesis describes how microbes persist intraphagocytically – that is, inside the phagocytes. For example, //Enterobacter hormaechei// can infect skin cells,(({{pubmed>long:17957161}})) but where it can really wreak havoc is in infecting the very cells charged with ingesting bacteria. As Kozarov //et al.// explain, infection of phagocytes by  //E. hormaechei// "can be especially aggravating for an existing inflammation as phagocyte recruitment to the site would actually exacerbate the inflammation by delivering additional pathogens."(({{pubmed>long:20972353}})) In other words, not only do intraphagocytic microbes remain alive but they have evolved a way to deliver themselves to the site of infection so that they may spread further. Kozarov //et al.// conclude, "the key step [towards systemic infection] is the persistence of intracellular bacteria in phagocytes."
+The Marshall Pathogenesis describes how microbes persist intraphagocytically – that is, inside the phagocytes. For example, //Enterobacter hormaechei// can infect skin cells,(({{pmid>long:17957161}})) but where it can really wreak havoc is in infecting the very cells charged with ingesting bacteria. As Kozarov //et al.// explain, infection of phagocytes by  //E. hormaechei// "can be especially aggravating for an existing inflammation as phagocyte recruitment to the site would actually exacerbate the inflammation by delivering additional pathogens."(({{pmid>long:20972353}})) In other words, not only do intraphagocytic microbes remain alive but they have evolved a way to deliver themselves to the site of infection so that they may spread further. Kozarov //et al.// conclude, "the key step [towards systemic infection] is the persistence of intracellular bacteria in phagocytes."
-Such an adaptation may further account for the resistance of chronic diseases to antibiotic treatment.(({{pubmed>long:20972353}})) This may explain why several large randomized placebo-controlled clinical trials using antibiotics for the secondary prevention (strategies attempting to diagnose and treat an existing disease in its early stages before it results in significant morbidity) of cardiovascular events have failed to show a benefit.(({{pubmed>long:15749042}}))
+Such an adaptation may further account for the resistance of chronic diseases to antibiotic treatment.(({{pmid>long:20972353}})) This may explain why several large randomized placebo-controlled clinical trials using antibiotics for the secondary prevention (strategies attempting to diagnose and treat an existing disease in its early stages before it results in significant morbidity) of cardiovascular events have failed to show a benefit.(({{pmid>long:15749042}}))
 ===== Bacteria affect host-cell pathways =====
-Bacterial pathogens operate by attacking crucial intracellular pathways in their hosts. These pathogens usually target more than one intracellular pathway and often interact at several points in each of these pathways to commandeer them fully.(({{pubmed>long:17943119}})) These well-documented strategies include, to cite just several among many examples:
+Bacterial pathogens operate by attacking crucial intracellular pathways in their hosts. These pathogens usually target more than one intracellular pathway and often interact at several points in each of these pathways to commandeer them fully.(({{pmid>long:17943119}})) These well-documented strategies include, to cite just several among many examples:
-  * modulation of programmed host-cell death, known as apoptosis, to facilitate survival in the host;(({{pubmed>long:11137044}})) (({{pubmed>long:12819104}})) (({{pubmed>long:16086183}})) delayed apoptosis is a common feature of chronic inflammatory diseases; for more, see discussion of [[home:diseases:sarcoidosis#granuloma|granuloma]]
+  * modulation of programmed host-cell death, known as apoptosis, to facilitate survival in the host;(({{pmid>long:11137044}})) (({{pmid>long:12819104}})) (({{pmid>long:16086183}})) delayed apoptosis is a common feature of chronic inflammatory diseases; for more, see discussion of [[home:diseases:sarcoidosis#granuloma|granuloma]]
-  * modulation of vesicular traffic, a strategy which provides a protective niche within host cells, including in macrophages and neutrophils, which normally kill bacteria(({{pubmed>long:10560000}}))
+  * modulation of vesicular traffic, a strategy which provides a protective niche within host cells, including in macrophages and neutrophils, which normally kill bacteria(({{pmid>long:10560000}}))
-  * modulation of membrane traffic as is the case with the Legionnaire's bacterium //Legionella pneumophila// (({{pubmed>long:20651120}}))
+  * modulation of membrane traffic as is the case with the Legionnaire's bacterium //Legionella pneumophila// (({{pmid>long:20651120}}))
-  * modulation of macrophage cytokine production(({{pubmed>long:19231999}}))
+  * modulation of macrophage cytokine production(({{pmid>long:19231999}}))
-  * secretion of proteins, which are similar in effect to substances known to be toxic to humans(({{pubmed>long:16497587}}))
+  * secretion of proteins, which are similar in effect to substances known to be toxic to humans(({{pmid>long:16497587}}))
-  * creation of virulence factors which suppress MAMPs (Microbial Associated Molecular Patterns)(({{pubmed>long:18639458}}))
+  * creation of virulence factors which suppress MAMPs (Microbial Associated Molecular Patterns)(({{pmid>long:18639458}}))
-  * Ehrlichia/anaplasma (EA) are an obscure group of obligate parasitic intracellular pathogens that intracellularly excrete a substance called host transcriptional protein, which can alter transcription in cell division. Infection with EA may lead to changes in transcription in proliferating cells, and contribute to illnesses such as leukemia, systemic lupus erythematosus, myelodysplastic disease, multiple sclerosis, amyotrophic lateral sclerosis, and rheumatoid arthritis.(({{pubmed>long:21669495}}))
+  * Ehrlichia/anaplasma (EA) are an obscure group of obligate parasitic intracellular pathogens that intracellularly excrete a substance called host transcriptional protein, which can alter transcription in cell division. Infection with EA may lead to changes in transcription in proliferating cells, and contribute to illnesses such as leukemia, systemic lupus erythematosus, myelodysplastic disease, multiple sclerosis, amyotrophic lateral sclerosis, and rheumatoid arthritis.(({{pmid>long:21669495}}))
-  * [[home:pathogenesis:vitamind:metabolism#bacteria_disable_the_vdr|creation of ligands]] such as Capnine which bind, block, and downregulate the Vitamin D Receptor;(({{pubmed>long:18200565}})) Alzheimer's may be a case where bacteria stimulate the body's production of the antimicrobial peptide amyloid-beta to dramatically suppress VDR activity(({{pubmed>long:20966550}}))
+  * [[home:pathogenesis:vitamind:metabolism#bacteria_disable_the_vdr|creation of ligands]] such as Capnine which bind, block, and downregulate the Vitamin D Receptor;(({{pmid>long:18200565}})) Alzheimer's may be a case where bacteria stimulate the body's production of the antimicrobial peptide amyloid-beta to dramatically suppress VDR activity(({{pmid>long:20966550}}))
@@ Line 67: / Line 155: @@
-<blockquote>Conversely, harmful bacteria may deregulate genes mediating energy metabolism, and can produce toxins that mutate DNA, affecting the nervous and immune systems. The outcome is various forms of chronic disease, including obesity, diabetes and even cancers.(({{pubmed>long:17210919}})) (({{pubmed>long:17456850}})) (({{pubmed>long:20176062}}))
+<blockquote>Conversely, harmful bacteria may deregulate genes mediating energy metabolism, and can produce toxins that mutate DNA, affecting the nervous and immune systems. The outcome is various forms of chronic disease, including obesity, diabetes and even cancers.(({{pmid>long:17210919}})) (({{pmid>long:17456850}})) (({{pmid>long:20176062}}))
 //**Liping Zhao**//</blockquote>
@@ Line 74: / Line 162: @@
-[{{ :home:pathogenesis:imgp0910-cleaned.jpg?350|**Using electron microscopy, William Wirostko, M.D. //et al// [[http://www.ncbi.nlm.nih.gov/pubmed/2600945|identified]] cell wall deficient bacteria within immune cells of patients with juvenile rheumatoid arthritis and uveitis.** This image suggests that pathogens have access to the human cell's transcriptional machinery.}}]
+[{{ :home:pathogenesis:imgp0910-cleaned.jpg?350|**Using electron microscopy, William Wirostko, M.D. //et al// [[https://www.ncbi.nlm.nih.gov/pubmed/2600945|identified]] cell wall deficient bacteria within immune cells of patients with juvenile rheumatoid arthritis and uveitis.** This image suggests that pathogens have access to the human cell's transcriptional machinery.}}]
-According to one analysis, 463 human genes are changed during an infection with //Mycobacterium tuberculosis//.(({{pubmed>long:12890386}})) Of the 463 genes whose expression were changed. 366 of them were known genes. The other genes were unknown – mutations. Of the 366 human genes affected, 25 were upregulated and 341 were downregulated. Two more significant effects were the downregulation of the CD14 receptor which was downregulated 2.3-fold, and the VDR receptor which was downregulated 3.3-fold. The mutated genes function in various cellular processes including intracellular signalling, cytoskeletal rearrangement, apoptosis, transcriptional regulation, cell surface receptors, cell-mediated immunity and cellular metabolic pathways.
+According to one analysis, 463 human genes are changed during an infection with //Mycobacterium tuberculosis//.(({{pmid>long:12890386}})) Of the 463 genes whose expression were changed. 366 of them were known genes. The other genes were unknown – mutations. Of the 366 human genes affected, 25 were upregulated and 341 were downregulated. Two more significant effects were the downregulation of the CD14 receptor which was downregulated 2.3-fold, and the VDR receptor which was downregulated 3.3-fold. The mutated genes function in various cellular processes including intracellular signalling, cytoskeletal rearrangement, apoptosis, transcriptional regulation, cell surface receptors, cell-mediated immunity and cellular metabolic pathways.
 It is quite plausible that "autoimmunity," in which it is believed that the body is attacking itself, is caused by bacterial-induced alteration of human genes. All a bacterium would need to do in order to generate an apparent "autoimmune" reaction would be to interfere with the genes necessary for the production of proteins against which autoantibodies are produced.
@@ Line 95: / Line 183: @@
+{{tag>pathogenesis  Microbes_in_the_human_body}}
+<nodisp>
 ===== Notes and comments =====
-===== References =====
+===== References =====</nodisp>

home/pathogenesis/microbiota/interaction.1348439571.txt.gz · Last modified: 09.23.2012 by paulalbert