Marshall Protocol Knowledge Base - home:pathogenesis:microbiota

Acute infections

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:53 +0000

Biofilm bacteria

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:53 +0000

Detecting bacteria

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Effects of bacteria and viruses on their human host

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L-form bacteria

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 20:53:53 +0000

10.27.2019		current
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	====== L-form bacteria ======		====== L-form bacteria ======

-	As a part of their natural life cycle, bacteria can transform into a variety of forms. One of those phases is the L-form. L-form bacteria, also known as cell wall deficient bacteria, are a phase of bacteria that are very small and lack cell walls.	+	As a part of their natural life cycle, bacteria can transform into a variety of forms. One of those phases is the L-form.
		+
		+	L-form bacteria, also known as cell wall deficient bacteria, are a phase of bacteria that are very small and lack cell walls.

	Though the subject of a great deal of research over the last 100 years and implicated in a variety of diseases, L-forms remain largely misunderstood - or at the very least, underappreciated - by the medical research community. According to the Marshall Pathogenesis, L-forms are part of a metagenomic microbiota responsible for chronic disease.		Though the subject of a great deal of research over the last 100 years and implicated in a variety of diseases, L-forms remain largely misunderstood - or at the very least, underappreciated - by the medical research community. According to the Marshall Pathogenesis, L-forms are part of a metagenomic microbiota responsible for chronic disease.
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	===== Species capable of L-form transformation =====		===== Species capable of L-form transformation =====

-	Thus far, researchers have identified over 50 different species of bacteria capable of transforming into the L-form and it is likely that more species will be found in the coming years. “Probably most bacterial species can be converted into L-forms if treated with the antibiotics that inhibit cell wall synthesis,” states researcher Josep Casadesus. (({{pubmed>long:18008373}}))	+	Thus far, researchers have identified over 50 different species of bacteria capable of transforming into the L-form and it is likely that more species will be found in the coming years. “Probably most bacterial species can be converted into L-forms if treated with the antibiotics that inhibit cell wall synthesis,” states researcher Josep Casadesus. (({{pmid>long:18008373}}))

	Some of the species of L-form bacteria that have been implicated in chronic disease include //Bacillus anthracis, Treponema pallidum, Mycobacterium tuberculosis, Helicobacter pylori, Rickettsia prowazekii,// and //Borrelia burgdorferi//. Not all species cause disease.		Some of the species of L-form bacteria that have been implicated in chronic disease include //Bacillus anthracis, Treponema pallidum, Mycobacterium tuberculosis, Helicobacter pylori, Rickettsia prowazekii,// and //Borrelia burgdorferi//. Not all species cause disease.
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	===== Resistance to certain antibiotics =====		===== Resistance to certain antibiotics =====

-	Cell wall deficient variants of bacteria cannot be killed by many commonly used antibiotics. Multiple studies, from many years ago(({{pubmed>long:13475673}})) to the present, have also shown that when one of the [[home:othertreatments:antibacterials:betalactams\|Beta-lactam antibiotics]], a class of antibiotics that includes penicillin, are applied to wild-type bacteria in a Petri dish, small colonies of L-form bacteria form on the edges of the plate. According to Casadesus:(({{pubmed>long:18008373}}))	+	Cell wall deficient variants of bacteria cannot be killed by many commonly used antibiotics. Multiple studies, from many years ago(({{pmid>long:13475673}})) to the present, have also shown that when one of the [[home:othertreatments:antibacterials:betalactams\|Beta-lactam antibiotics]], a class of antibiotics that includes penicillin, are applied to wild-type bacteria in a Petri dish, small colonies of L-form bacteria form on the edges of the plate. According to Casadesus:(({{pmid>long:18008373}}))

	<blockquote>Treatment with penicillin does not merely select for L-forms (which are penicillin resistant) but actually induces L-form growth.\\		<blockquote>Treatment with penicillin does not merely select for L-forms (which are penicillin resistant) but actually induces L-form growth.\\
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	Classical forms of most bacterial species can be found in the bloodstream. However L-form bacteria have figured out how to successfully infect and live inside the very cells of the immune system whose role is to kill bacteria. Once inside these cells, they can no longer be detected by the immune system and are able to persist in the body over long periods of time. L-form bacteria can infect many types of cells but prefer to infect white blood cells called macrophages.		Classical forms of most bacterial species can be found in the bloodstream. However L-form bacteria have figured out how to successfully infect and live inside the very cells of the immune system whose role is to kill bacteria. Once inside these cells, they can no longer be detected by the immune system and are able to persist in the body over long periods of time. L-form bacteria can infect many types of cells but prefer to infect white blood cells called macrophages.

-	Several very recent studies have confirmed the fact that bacteria can live inside the cells of the immune system. In a paper published in the Journal of Immunology by a team at the University of Michigan Medical School, Gabreil Nunez, senior author of the 2007 paper, stated “In our study, the presence of bacterial microbes inside the cell is what triggers the immune response.”(({{pubmed>long:17433728}}))	+	Several very recent studies have confirmed the fact that bacteria can live inside the cells of the immune system. In a paper published in the Journal of Immunology by a team at the University of Michigan Medical School, Gabreil Nunez, senior author of the 2007 paper, stated “In our study, the presence of bacterial microbes inside the cell is what triggers the immune response.”(({{pmid>long:17433728}}))

	Similarly, a team of researchers at the Bacterienne Institute in France released a paper detailing how the bacteria //E. coli// is able to live inside the cells of the immune system.		Similarly, a team of researchers at the Bacterienne Institute in France released a paper detailing how the bacteria //E. coli// is able to live inside the cells of the immune system.
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	<blockquote>[//E. coli// are] true invasive pathogens, able to invade intestinal epithelial cells and replicate intracellularly. Strains also survive and replicate within the macrophages.		<blockquote>[//E. coli// are] true invasive pathogens, able to invade intestinal epithelial cells and replicate intracellularly. Strains also survive and replicate within the macrophages.

-	//Nathalie Rolhion et al.// (({{pubmed>long:17476674}}))</blockquote>	+	//Nathalie Rolhion et al.// (({{pmid>long:17476674}}))</blockquote>

-	Markova has provided evidence that //E. coli// can survive lethal treatments such as boiling or autoclaving (subjecting equipment to high pressure steam at 121 °C or more) by transitioning into the L-form.((Markova N, Slavchev G, Michailova L, Jourdanova M. [[http://www.biolsci.org/v06p0303.htm\|Survival of Escherichia coli under lethal heat stress by L-form conversion]]. //Int J Biol Sci// 2010; 6:303-315.))	+	Markova has provided evidence that //E. coli// can survive lethal treatments such as boiling or autoclaving (subjecting equipment to high pressure steam at 121 °C or more) by transitioning into the L-form.((Markova N, Slavchev G, Michailova L, Jourdanova M. [[https://www.biolsci.org/v06p0303.htm\|Survival of Escherichia coli under lethal heat stress by L-form conversion]]. //Int J Biol Sci// 2010; 6:303-315.))


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	===== Images of L-forms =====		===== Images of L-forms =====

-	L-form bacteria have been photographed by a wide variety of researchers including Gerald Domingue (({{pubmed>long:9105757}})) and Nadya Markova. (({{pubmed>long:10959728}}))	+	L-form bacteria have been photographed by a wide variety of researchers including Gerald Domingue (({{pmid>long:9105757}})) and Nadya Markova. (({{pmid>long:10959728}}))

	Here are various images of L-forms. (Click for a larger image and description.)		Here are various images of L-forms. (Click for a larger image and description.)
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	{{gallery>home:pathogenesis:microbiota?showtitle&onlyflame&150x150&3&lightbox&nodirect }}		{{gallery>home:pathogenesis:microbiota?showtitle&onlyflame&150x150&3&lightbox&nodirect }}

-	[{{ :home:pathogenesis:imgp0910-cleaned.jpg?350\|Using electron microscopy, Dr. William Wirostko //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, Dr. William Wirostko //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.}}]

	--></html>		--></html>
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	Several studies have shown that once inside a macrophage, L-form bacteria are able to delay the process of apoptosis, or programmed cell death, allowing them to thrive inside the cell for a period of time even longer than 45 days.		Several studies have shown that once inside a macrophage, L-form bacteria are able to delay the process of apoptosis, or programmed cell death, allowing them to thrive inside the cell for a period of time even longer than 45 days.

-	Life without a wall or division machine in Bacillus subtilis. (({{pubmed>long:19212404}}))	+	Life without a wall or division machine in Bacillus subtilis. (({{pmid>long:19212404}}))


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-	In 1915, Löhnis authored a [[http://naldc.nal.usda.gov/download/IND43965684/PDF\|paper]] entitled "Life cycles of the bacteria" in which they marveled at the complexity of the bacterial life cycle but also his failure to recognize its potential significance earlier:	+	In 1915, Löhnis authored a [[https://naldc.nal.usda.gov/download/IND43965684/PDF\|paper]] entitled "Life cycles of the bacteria" in which they marveled at the complexity of the bacterial life cycle but also his failure to recognize its potential significance earlier:

	<blockquote>The senior author also did not know that for more than 11 years he had in his collection, patiently waiting to be photographed, that fine prepárate now shown in figure 6 (PI. A) until, as stated before, he decided to take down his "theoretical blinders." We have already mentioned that a careful study of the illustrations contained in our daily used textbooks will now reveal several things which we were so very well trained not to see. Certainly the German philosopher Lichtenberg made a very wise remark when he said: //Was jederman für ausgemacht hält, verdient am meisten untersucht zu werden.// [What everyone thinks identified deserves to be studied the most]		<blockquote>The senior author also did not know that for more than 11 years he had in his collection, patiently waiting to be photographed, that fine prepárate now shown in figure 6 (PI. A) until, as stated before, he decided to take down his "theoretical blinders." We have already mentioned that a careful study of the illustrations contained in our daily used textbooks will now reveal several things which we were so very well trained not to see. Certainly the German philosopher Lichtenberg made a very wise remark when he said: //Was jederman für ausgemacht hält, verdient am meisten untersucht zu werden.// [What everyone thinks identified deserves to be studied the most]
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	//Gerald Domingue, professor emeritus, Tulane University School of Medicine// </blockquote>		//Gerald Domingue, professor emeritus, Tulane University School of Medicine// </blockquote>

-	“Features of a number of important but poorly explained human clinical syndromes strongly indicate a microbial etiology,” states Relman. “In these syndromes, the failure of cultivation-dependent microbial detection methods reveals our ignorance of microbial growth requirements.” (({{pubmed>long:9716951}}))	+	“Features of a number of important but poorly explained human clinical syndromes strongly indicate a microbial etiology,” states Relman. “In these syndromes, the failure of cultivation-dependent microbial detection methods reveals our ignorance of microbial growth requirements.” (({{pmid>long:9716951}}))


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	==== Select diseases linked to l-forms ====		==== Select diseases linked to l-forms ====

-	* psoriasis – In a 2009 study, Wang investigated the carriage rate of cell wall deficient bacteria in the tonsil or pharynx of psoriasis patients. CWDB were isolated from 74.2% of psoriasis patients, 23.5% of chronic tonsillitis patients and only 6.3% of controls. Meanwhile, our study showed that CWDB and wide-type bacteria significantly enhanced the production of IFN-gamma, in vitro, and peripheral blood mononuclear cells proliferation.(({{pubmed>long:20137493}}))	+	* psoriasis – In a 2009 study, Wang investigated the carriage rate of cell wall deficient bacteria in the tonsil or pharynx of psoriasis patients. CWDB were isolated from 74.2% of psoriasis patients, 23.5% of chronic tonsillitis patients and only 6.3% of controls. Meanwhile, our study showed that CWDB and wide-type bacteria significantly enhanced the production of IFN-gamma, in vitro, and peripheral blood mononuclear cells proliferation.(({{pmid>long:20137493}}))


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	People are exposed to L-form bacteria in many places. Because they cannot be killed by pasteurization or chlorination, L-form bacteria can be found in milk, food, and water. They can be transmitted via sperm, intimate contact, and can be passed from mother to child during childbirth. Since they are too small to be filtered during the purification processes used in pharmaceutical manufacturing procedures, they can be transmitted through injectable medicines. They have even been cultured from dry soil.		People are exposed to L-form bacteria in many places. Because they cannot be killed by pasteurization or chlorination, L-form bacteria can be found in milk, food, and water. They can be transmitted via sperm, intimate contact, and can be passed from mother to child during childbirth. Since they are too small to be filtered during the purification processes used in pharmaceutical manufacturing procedures, they can be transmitted through injectable medicines. They have even been cultured from dry soil.

-	One [[http://www.reuters.com/article/healthNews/idUSN1362317620071113?feedType=RSS&feedName=healthNews\|2007 trial]] for an AIDS vaccine had to be abruptly discontinued when scientists realized that the vaccine somehow raised the risk of infection. The researchers administering the trial stressed that the vaccine could not itself cause the infection. Although it was not mentioned in the news story about the incident, one very plausible hypothesis is that the vaccines were infected with L-form bacteria.	+	One [[https://www.reuters.com/article/healthNews/idUSN1362317620071113?feedType=RSS&feedName=healthNews\|2007 trial]] for an AIDS vaccine had to be abruptly discontinued when scientists realized that the vaccine somehow raised the risk of infection. The researchers administering the trial stressed that the vaccine could not itself cause the infection. Although it was not mentioned in the news story about the incident, one very plausible hypothesis is that the vaccines were infected with L-form bacteria.

	Once macrophages and other cells have been infected with L-form bacteria, the bacteria circulate in the blood and tissues. In some cases they cluster together in clumps called granulomas. In other cases, they accumulate in regions such as the joints.		Once macrophages and other cells have been infected with L-form bacteria, the bacteria circulate in the blood and tissues. In some cases they cluster together in clumps called granulomas. In other cases, they accumulate in regions such as the joints.
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	===== Recent research =====		===== Recent research =====

-	L-form bacteria cohabitants in human blood: significance for health and diseases. (({{pubmed>long:28715646}}))	+	L-form bacteria cohabitants in human blood: significance for health and diseases. (({{pmid>long:28715646}}))

-	Possible role of L-form switching in recurrent urinary tract infection (({{pubmed>long:31558767}}))	+	Possible role of L-form switching in recurrent urinary tract infection (({{pmid>long:31558767}}))

	==== Future research ====		==== Future research ====
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	{{tag>pathogenesis Microbes_in_the_human_body}}		{{tag>pathogenesis Microbes_in_the_human_body}}
		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====


-	Link removed [[http://www.cancer.med.umich.edu/news/immune07.shtml\|stated]]	+	Link removed [[https://www.cancer.med.umich.edu/news/immune07.shtml\|stated]]
	the cancer site keeps only VERY recent research		the cancer site keeps only VERY recent research

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	Listeria L-Forms: Discovery Of An Unusual Form Of Bacterial Life		Listeria L-Forms: Discovery Of An Unusual Form Of Bacterial Life

-	http://www.sciencedaily.com/releases/2009/09/090912145843.htm	+	https://www.sciencedaily.com/releases/2009/09/090912145843.htm
	</blockquote>		</blockquote>

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	<blockquote>The Foundation has now put Lida Mattman's second-to-last presentation on YouTube. This was filmed at our 2005 Chicago conference.		<blockquote>The Foundation has now put Lida Mattman's second-to-last presentation on YouTube. This was filmed at our 2005 Chicago conference.

-	http://www.youtube.com/watch?v=WozrCFW0mRM</blockquote>	+	https://www.youtube.com/watch?v=WozrCFW0mRM</blockquote>

-	http://www.discoverymedicine.com/Gerald-J-Domingue/2010/09/23/demystifying-pleomorphic-forms-in-persistence-and-expression-of-disease-are-they-bacteria-and-is-peptidoglycan-the-solution/	+	https://www.discoverymedicine.com/Gerald-J-Domingue/2010/09/23/demystifying-pleomorphic-forms-in-persistence-and-expression-of-disease-are-they-bacteria-and-is-peptidoglycan-the-solution/


	<blockquote>PLoS One. 2009 Oct 6;4(10):e7316.		<blockquote>PLoS One. 2009 Oct 6;4(10):e7316.
-	Insights into the molecular basis of L-form formation and survival in Escherichia coli.(({{pubmed>long:19806199}}))	+	Insights into the molecular basis of L-form formation and survival in Escherichia coli.(({{pmid>long:19806199}}))

	Glover WA, Yang Y, Zhang Y.		Glover WA, Yang Y, Zhang Y.
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	PMID: 19806199</blockquote>		PMID: 19806199</blockquote>

-	[[http://www.sciencedaily.com/releases/2009/09/090912145843.htm\|Listeria L-Forms: Discovery Of An Unusual Form Of Bacterial Life]]	+	[[https://www.sciencedaily.com/releases/2009/09/090912145843.htm\|Listeria L-Forms: Discovery Of An Unusual Form Of Bacterial Life]]
-	===== References =====	+	===== References =====</nodisp>

01.12.2020		current
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	<relatedarticles>		<relatedarticles>
-	[[home:othertreatments/antibacterials/takingnonmpantibiotics]], [[home:pathogenesis:successive_infection\|Successive infection and variability in disease]]	+	[[home:othertreatments/antibacterials/takingnonmpantibiotics]], [[home:pathogenesis/microbiota/interaction\|Effects of bacteria and viruses on their human host]], [[home:pathogenesis:successive_infection\|Successive infection and variability in disease]]
	</article>		</article>

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	The white blood cell count rises in cases of infection, steroid use and other conditions.		The white blood cell count rises in cases of infection, steroid use and other conditions.

-	The immune system responds to cues in the microenvironment to make acute and chronic adaptations in response to inflammation and injury. The therapeutic significance of adenosine-mediated effects on the immune system is discussed here. (({{pubmed>long:21586357 }}))	+	The immune system responds to cues in the microenvironment to make acute and chronic adaptations in response to inflammation and injury. The therapeutic significance of adenosine-mediated effects on the immune system is discussed here. (({{pmid>long:21586357 }}))

	The term acute infection is used to refer to microbe living inside a host for a limited period of time, typically less than six months. However, an abundance of research has emerged suggesting that acute infections have long-lasting effects, predisposing a person to later onset of chronic diseases.		The term acute infection is used to refer to microbe living inside a host for a limited period of time, typically less than six months. However, an abundance of research has emerged suggesting that acute infections have long-lasting effects, predisposing a person to later onset of chronic diseases.
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	\|Terms \|early, acute \|late, chronic, fastidious, latent; an important type of chronic infection is the l-form \|		\|Terms \|early, acute \|late, chronic, fastidious, latent; an important type of chronic infection is the l-form \|
	\|Duration \|lasts no more than six months (although, as we'll see below, the effects of acute infections can be long-lived) \|lasts more than six months \|		\|Duration \|lasts no more than six months (although, as we'll see below, the effects of acute infections can be long-lived) \|lasts more than six months \|
-	\|Rate of growth \|fast - reproduce over the course of days \|slow – may take several weeks to reproduce; build up over the course of decades (for example, the velocity of DNA replication fork progression for //Mycoplasma// reproduces ten times slower than //Escherichia coli//(({{pubmed>long:9440514}}))) \|	+	\|Rate of growth \|fast - reproduce over the course of days \|slow – may take several weeks to reproduce; build up over the course of decades (for example, the velocity of DNA replication fork progression for //Mycoplasma// reproduces ten times slower than //Escherichia coli//(({{pmid>long:9440514}}))) \|
	\|Ease of study \|present their own problems but more recognized and studied \|relatively difficult – fewer markers, more challenging to infer causation \|		\|Ease of study \|present their own problems but more recognized and studied \|relatively difficult – fewer markers, more challenging to infer causation \|

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	===== Acute infections predispose to chronic diseases=====		===== Acute infections predispose to chronic diseases=====

-	There is broad support for the conclusion that early infections, especially acute infections, predispose a person to later onset of chronic diseases, diseases which are likely caused by chronic microbial infections. In a 2004 //Science// paper, Finch and Crimmins proposed that early infection burdened survivors with a "cohort morbidity phenotype," which they carry with them throughout their lives.(({{pubmed>long:15375259}}))	+	There is broad support for the conclusion that early infections, especially acute infections, predispose a person to later onset of chronic diseases, diseases which are likely caused by chronic microbial infections. In a 2004 //Science// paper, Finch and Crimmins proposed that early infection burdened survivors with a "cohort morbidity phenotype," which they carry with them throughout their lives.(({{pmid>long:15375259}}))

-	Microbial infections make the body a more hospitable environment for other infections via two primary means: affecting both [[home:pathogenesis:microbiota#bacteria_affect_host-cell_pathways\|human host-cell pathways]] and the [[home:pathogenesis:microbiota#bacteria_affect_human_genes_and_gene_expression\|expression of human genes]]. This effect has been documented in a range of clinical and laboratory-based studies. O'Connor and team at the Centers for Disease Control and Prevention state, "At least 13 of 39 recently described infectious agents induce chronic syndromes."(({{pubmed>long:16836820}})) The section [[home:pathogenesis:successive_infection#successive_infectionearly_infections_predispose_a_person_to_later_chronic_disease\|Successive infection: early infections predispose a person to later chronic disease]] lists at least a dozen such examples.	+	Microbial infections make the body a more hospitable environment for other infections via two primary means: affecting both [[home:pathogenesis:microbiota#bacteria_affect_host-cell_pathways\|human host-cell pathways]] and the [[home:pathogenesis:microbiota#bacteria_affect_human_genes_and_gene_expression\|expression of human genes]]. This effect has been documented in a range of clinical and laboratory-based studies. O'Connor and team at the Centers for Disease Control and Prevention state, "At least 13 of 39 recently described infectious agents induce chronic syndromes."(({{pmid>long:16836820}})) The section [[home:pathogenesis:successive_infection#successive_infectionearly_infections_predispose_a_person_to_later_chronic_disease\|Successive infection: early infections predispose a person to later chronic disease]] lists at least a dozen such examples.

	===== Certain treatments for acute infections can predispose to chronic disease=====		===== Certain treatments for acute infections can predispose to chronic disease=====

	A variety of conventional treatments address acute infections with no eye towards their effect on chronic microbes:		A variety of conventional treatments address acute infections with no eye towards their effect on chronic microbes:
-	* corticosteroids – In a 2011 //Lancet// study, Dutch researchers [[http://www.drugs.com/news/corticosteroids-may-speed-pneumonia-recovery-some-31677.html\|concluded]] that patients with community-acquired pneumonia appear to recovery quickly in the hospital when treated with dexamethasone, a corticosteroid, in addition to the standard regimen of antibiotics.(({{pubmed>long:21636122}})) The statistically significant benefit: approximately 24 hours. While the researchers concluded that "serious adverse events were rare," patients were observed for all of a week – certainly not long enough to measure the effect an immunosuppressant has on chronic microbes. A follow up study of sufficient time would surely show something different.	+	* corticosteroids – In a 2011 //Lancet// study, Dutch researchers [[https://www.drugs.com/news/corticosteroids-may-speed-pneumonia-recovery-some-31677.html\|concluded]] that patients with community-acquired pneumonia appear to recovery quickly in the hospital when treated with dexamethasone, a corticosteroid, in addition to the standard regimen of antibiotics.(({{pmid>long:21636122}})) The statistically significant benefit: approximately 24 hours. While the researchers concluded that "serious adverse events were rare," patients were observed for all of a week – certainly not long enough to measure the effect an immunosuppressant has on chronic microbes. A follow up study of sufficient time would surely show something different.
-	* beta-lactam antibiotics – Beta-lactam antibiotics such as ceftazidime for //Psuedomonas aeruginosa// induce microbes to shed their cell walls, producing "viable monsters."((Mattman, L.H. (2000). //Cell wall deficient forms.// Third edition, [[http://books.google.com/books?id=mincr2Hi81UC&pg=PA23&vq=penicillin&dq=beta-lactam+lida+mattman+cell+wall+deficient&source=gbs_search_s&cad=0#PPA82,M1\|p. 84]].))	+	* beta-lactam antibiotics – Beta-lactam antibiotics such as ceftazidime for //Psuedomonas aeruginosa// induce microbes to shed their cell walls, producing "viable monsters."((Mattman, L.H. (2000). //Cell wall deficient forms.// Third edition, [[https://books.google.com/books?id=mincr2Hi81UC&pg=PA23&vq=penicillin&dq=beta-lactam+lida+mattman+cell+wall+deficient&source=gbs_search_s&cad=0#PPA82,M1\|p. 84]].))
	* antibiotics – High-dose antibiotics used to control inflammation would likewise show a short-term benefit and long-term harm. Note that the Marshall Protocol uses pulsed low-dose antibiotics so as to avoid this problem.		* antibiotics – High-dose antibiotics used to control inflammation would likewise show a short-term benefit and long-term harm. Note that the Marshall Protocol uses pulsed low-dose antibiotics so as to avoid this problem.

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	Some have speculated that vitamin D is protective against acute infections, but this has not been supported by the evidence.		Some have speculated that vitamin D is protective against acute infections, but this has not been supported by the evidence.
-	* A 2009 systematic review examined 13 studies examining vitamin D for treatment or prevention of infectious diseases in humans. The authors concluded (in the euphemistic fashion characteristic of many pro-vitamin D studies) that vitamin D was ineffective: "On the basis of studies reviewed to date, the strongest evidence supports further research into adjunctive vitamin D therapy for tuberculosis, influenza, and viral upper respiratory tract illnesses."(({{pubmed>long: 19491064}}))	+	* A 2009 systematic review examined 13 studies examining vitamin D for treatment or prevention of infectious diseases in humans. The authors concluded (in the euphemistic fashion characteristic of many pro-vitamin D studies) that vitamin D was ineffective: "On the basis of studies reviewed to date, the strongest evidence supports further research into adjunctive vitamin D therapy for tuberculosis, influenza, and viral upper respiratory tract illnesses."(({{pmid>long: 19491064}}))
-	* Shaman //et al.// found that they could not use serum concentration of the vitamin D metabolite 25-D in a model for seasonal changes in infection.(({{pubmed>long:21677774}}))	+	* Shaman //et al.// found that they could not use serum concentration of the vitamin D metabolite 25-D in a model for seasonal changes in infection.(({{pmid>long:21677774}}))


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	{{tag>acute_infections Pathogenesis Microbes_in_the_human_body}}		{{tag>acute_infections Pathogenesis Microbes_in_the_human_body}}

		+	<nodisp>
	===== Notes and comments =====		===== Notes and comments =====

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	* Legacy content		* Legacy content
-	* http://www.marshallprotocol.com/view_topic.php?id=3837&forum_id=32&jump_to=86100#p86100 f170	+	* https://www.marshallprotocol.com/view_topic.php?id=3837&forum_id=32&jump_to=86100#p86100 f170
	*		*


-	<blockquote>There is also very little evidence that vitamin D affects the course of human TB infection. Experiments have not been done in cells, mice or humans to evaluate the effect of vitamin D on influenza virus. At this time it would be premature to claim that vitamin D has an effect on TB, influenza or any other infection.(({{pubmed>long:20660091}}))	+	<blockquote>There is also very little evidence that vitamin D affects the course of human TB infection. Experiments have not been done in cells, mice or humans to evaluate the effect of vitamin D on influenza virus. At this time it would be premature to claim that vitamin D has an effect on TB, influenza or any other infection.(({{pmid>long:20660091}}))

	</blockquote>		</blockquote>
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	Measles may protect kids against allergies		Measles may protect kids against allergies

-	http://www.reuters.com/article/healthNews/idUSTRE5236HS20090304	+	https://www.reuters.com/article/healthNews/idUSTRE5236HS20090304

	There was no correlation with immunization, just with catching the actual disease. Kids who had been immunized and still caught measles (about 11% of the them) received the same benefit as kids who had never been immunized. The disease was what modified the allergies		There was no correlation with immunization, just with catching the actual disease. Kids who had been immunized and still caught measles (about 11% of the them) received the same benefit as kids who had never been immunized. The disease was what modified the allergies
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-	(({{pubmed>long:8008534}}))	+	(({{pmid>long:8008534}}))

	Measles makes the cells more susceptible to a secondary infection		Measles makes the cells more susceptible to a secondary infection

-	[[http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=pmd&part=A2876#A2876\|Measles Virus-induced Immunosuppression]]	+	[[https://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=pmd&part=A2876#A2876\|Measles Virus-induced Immunosuppression]]

	"MV infection, while inducing lifelong immunity, also suppresses the immune system leading to an increase in susceptibility to other, secondary infections (24, 67, 91). In vitro research has shown that MV infection of cell cultures makes the cells more susceptible to a secondary bacterial invasion (13) "		"MV infection, while inducing lifelong immunity, also suppresses the immune system leading to an increase in susceptibility to other, secondary infections (24, 67, 91). In vitro research has shown that MV infection of cell cultures makes the cells more susceptible to a secondary bacterial invasion (13) "

	<blockquote>PLoS One. 2009 Dec 31;4(12):e8540.		<blockquote>PLoS One. 2009 Dec 31;4(12):e8540.
-	Streptococcus pneumoniae coinfection is correlated with the severity of H1N1 pandemic influenza.(({{pubmed>long:20046873}}))	+	Streptococcus pneumoniae coinfection is correlated with the severity of H1N1 pandemic influenza.(({{pmid>long:20046873}}))


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-	===== References =====	+	===== References =====</nodisp>

01.11.2019		current
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	====== Biofilm bacteria ======		====== Biofilm bacteria ======

-	Biofilms are densely packed communities of microbial cells that grow on living or inert surfaces and surround themselves with secreted polymers. Many bacterial species form biofilms, and their study has revealed them to be complex and diverse. The structural and physiological complexity of biofilms has led to the idea that they are coordinated and cooperative groups, analogous to multicellular organisms.(({{pubmed>long:19067751}}))	+	Biofilms are densely packed communities of microbial cells that grow on living or inert surfaces and surround themselves with secreted polymers. Many bacterial species form biofilms, and their study has revealed them to be complex and diverse. The structural and physiological complexity of biofilms has led to the idea that they are coordinated and cooperative groups, analogous to multicellular organisms.(({{pmid>long:19067751}}))

	Researchers have estimated that 60-80 percent of microbial infections in the body are caused by bacteria growing as a biofilm – as opposed to planktonic (free-floating) bacteria.		Researchers have estimated that 60-80 percent of microbial infections in the body are caused by bacteria growing as a biofilm – as opposed to planktonic (free-floating) bacteria.
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-	Biofilm-related disease. (({{pubmed>long:29235402}}))	+	Biofilm-related disease. (({{pmid>long:29235402}}))


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-	In the years which followed, researchers have concentrated primarily on planktonic (free-floating) bacteria, the kinds of microbes studied by the likes of Louis Pasteur and Robert Koch. It was not until the 1970s that scientists began to appreciate that bacteria in the biofilm mode of existence constitute such a major component of the bacterial biomass in most environments. In the 1980s and 1990s, scientists began to understand how elaborately organized a bacterial biofilm community can be.(({{pubmed>long:10334980}}))	+	In the years which followed, researchers have concentrated primarily on planktonic (free-floating) bacteria, the kinds of microbes studied by the likes of Louis Pasteur and Robert Koch. It was not until the 1970s that scientists began to appreciate that bacteria in the biofilm mode of existence constitute such a major component of the bacterial biomass in most environments. In the 1980s and 1990s, scientists began to understand how elaborately organized a bacterial biofilm community can be.(({{pmid>long:10334980}}))

-	Paul Stoodley of the Center for Biofilm Engineering at Montana State University, attributes much of the lag in studying biofilms to the difficulties of working with heterogeneous biofilms compared with homogeneous planktonic populations. In a 2004 paper in //Nature Reviews//, the molecular biologist describes many reasons why biofilms are extremely difficult to culture, such as the fact that the diffusion of liquid through a biofilm and the fluid forces acting on a biofilm must be carefully calculated if it is to be cultured correctly. According to Stoodley, the need to master such difficult laboratory techniques has deterred many scientists from attempting to work with biofilms.(({{pubmed>long:15040259}}))	+	Paul Stoodley of the Center for Biofilm Engineering at Montana State University, attributes much of the lag in studying biofilms to the difficulties of working with heterogeneous biofilms compared with homogeneous planktonic populations. In a 2004 paper in //Nature Reviews//, the molecular biologist describes many reasons why biofilms are extremely difficult to culture, such as the fact that the diffusion of liquid through a biofilm and the fluid forces acting on a biofilm must be carefully calculated if it is to be cultured correctly. According to Stoodley, the need to master such difficult laboratory techniques has deterred many scientists from attempting to work with biofilms.(({{pmid>long:15040259}}))


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	<blockquote>According to a recent public statement from the National Institutes of Health, more than 65% of all microbial infections are caused by biofilms.... If one recalls that such common infections as urinary tract infections (caused by //E. coli// and other pathogens), catheter infections (caused by //Staphylococcus aureus// and other gram-positive pathogens), child middle-ear infections (caused by //Haemophilus influenzae//, for example), common dental plaque formation, and gingivitis, all of which are caused by biofilms, are hard to treat or frequently relapsing, this figure appears realistic.		<blockquote>According to a recent public statement from the National Institutes of Health, more than 65% of all microbial infections are caused by biofilms.... If one recalls that such common infections as urinary tract infections (caused by //E. coli// and other pathogens), catheter infections (caused by //Staphylococcus aureus// and other gram-positive pathogens), child middle-ear infections (caused by //Haemophilus influenzae//, for example), common dental plaque formation, and gingivitis, all of which are caused by biofilms, are hard to treat or frequently relapsing, this figure appears realistic.

-	//Kim Lewis// (({{pubmed>long:11257008}}))</blockquote>	+	//Kim Lewis// (({{pmid>long:11257008}}))</blockquote>
	==== Diseases for which biofilm have been implicated ====		==== Diseases for which biofilm have been implicated ====

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	In just a short period of time, researchers studying internal biofilms have already determined they cause a number of chronic infections and diseases. Notable diseases include:		In just a short period of time, researchers studying internal biofilms have already determined they cause a number of chronic infections and diseases. Notable diseases include:
-	* atherosclerosis – Biofilm //may// contribute to the development of atherosclerosis. Ott //et al.//'s work showed a diverse groups of bacterial "signatures" in atherosclerotic lesions of patients with coronary heart disease.(({{pubmed>long:16490835}})) In a commentary following Ott's paper, Katz and Shannon concluded that his work suggested that atherosclerotic plaques are composed of "functional biofilm." The team noted that the characteristics of a "mature" arterial wall make it well-suited for biofilm formation and explains the inefficacy of antibiotics, such as macrolides or fluoroquinolones, in clinical trials.(({{pubmed>long:16490832}}))	+	* atherosclerosis – Biofilm //may// contribute to the development of atherosclerosis. Ott //et al.//'s work showed a diverse groups of bacterial "signatures" in atherosclerotic lesions of patients with coronary heart disease.(({{pmid>long:16490835}})) In a commentary following Ott's paper, Katz and Shannon concluded that his work suggested that atherosclerotic plaques are composed of "functional biofilm." The team noted that the characteristics of a "mature" arterial wall make it well-suited for biofilm formation and explains the inefficacy of antibiotics, such as macrolides or fluoroquinolones, in clinical trials.(({{pmid>long:16490832}}))
-	* chronic sinusitis – One study found that biofilms are present on the removed tissue of two-thirds of patients undergoing surgery for chronic inflammation of the sinuses.(({{pubmed>long:16730544}}))	+	* chronic sinusitis – One study found that biofilms are present on the removed tissue of two-thirds of patients undergoing surgery for chronic inflammation of the sinuses.(({{pmid>long:16730544}}))
-	* chronic wounds – Biofilm have been implicated in chronic wounds. Dr. Randall Wolcott has published work offering strategies for managing wounds.(({{pubmed>long:19418781}}))	+	* chronic wounds – Biofilm have been implicated in chronic wounds. Dr. Randall Wolcott has published work offering strategies for managing wounds.(({{pmid>long:19418781}}))

	<blockquote>Molecular analyses of chronic wound specimens revealed diverse polymicrobial communities and the presence of bacteria, including strictly anaerobic bacteria, not revealed by culture. Bacterial biofilm prevalence in specimens from chronic wounds relative to acute wounds observed in this study provides evidence that biofilms may be abundant in chronic wounds.		<blockquote>Molecular analyses of chronic wound specimens revealed diverse polymicrobial communities and the presence of bacteria, including strictly anaerobic bacteria, not revealed by culture. Bacterial biofilm prevalence in specimens from chronic wounds relative to acute wounds observed in this study provides evidence that biofilms may be abundant in chronic wounds.

-	//GA James et al.// (({{pubmed>long:18086294}}))</blockquote>	+	//GA James et al.// (({{pmid>long:18086294}}))</blockquote>


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	[{{ :home:pathogenesis:microbiota:biofilm:otitis_media.jpg?300\|Otitis media, or inflammation of the inner ear, is caused by biofilm.}}]		[{{ :home:pathogenesis:microbiota:biofilm:otitis_media.jpg?300\|Otitis media, or inflammation of the inner ear, is caused by biofilm.}}]

10.13.2018		current
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-	It has been called one of the greatest false prophecies in the history of medicine. In 1821, Sir John Forbes concluded that the newly invented stethoscope was “ludicrous” and would never be generally adopted by physicians.(({{pubmed>long:7026784}})) However, this honor might better be bestowed upon many members of the microbiology community, who before the advent of molecular technology, deemed the body to be largely sterile.	+	It has been called one of the greatest false prophecies in the history of medicine. In 1821, Sir John Forbes concluded that the newly invented stethoscope was “ludicrous” and would never be generally adopted by physicians.(({{pmid>long:7026784}})) However, this honor might better be bestowed upon many members of the microbiology community, who before the advent of molecular technology, deemed the body to be largely sterile.


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	<relatedarticle> [[home:pathogenesis:kochs_postulates\|Koch's postulates]] </article>		<relatedarticle> [[home:pathogenesis:kochs_postulates\|Koch's postulates]] </article>

-	Until very recently, efforts to detect and identify microorganisms have depended on //in vitro// studies – research in which bacteria were grown in culture in a laboratory setting. Because at least a fraction of microorganisms are not particular in their growth requirements, these efforts have yielded an array of diverse microbial cultivation techniques. Microbial cultivation methods opened up an unsuspected world of microscopic life and presumed causative agents of human illness.(({{pubmed>long:9716951}}))	+	Until very recently, efforts to detect and identify microorganisms have depended on //in vitro// studies – research in which bacteria were grown in culture in a laboratory setting. Because at least a fraction of microorganisms are not particular in their growth requirements, these efforts have yielded an array of diverse microbial cultivation techniques. Microbial cultivation methods opened up an unsuspected world of microscopic life and presumed causative agents of human illness.(({{pmid>long:9716951}}))

	Koch's postulates is a set of ground rules to determine whether a given organism can cause a given disease. One of its dictates is that a bacterium must be shown to grow outside the body in culture in order to prove that the bacterium causes disease. For at least a century, Koch's postulates have held sway.		Koch's postulates is a set of ground rules to determine whether a given organism can cause a given disease. One of its dictates is that a bacterium must be shown to grow outside the body in culture in order to prove that the bacterium causes disease. For at least a century, Koch's postulates have held sway.

-	According to Robert Koch, or at least the ideas since attributed to him, there were no cultivation-resistant microbes. Over the years, varied researchers had difficulty consistently culturing bacteria found in disease. As a result, many researchers began to assume that chronic diseases were not caused by microbes. The net effect of all this was that the understanding of pathogens in disease was driven by the study of well-known, easy-to-culture microbes(({{pubmed>long:19040704}})) – which, as it turns out, represents the vast minority of bacteria in the human body.	+	According to Robert Koch, or at least the ideas since attributed to him, there were no cultivation-resistant microbes. Over the years, varied researchers had difficulty consistently culturing bacteria found in disease. As a result, many researchers began to assume that chronic diseases were not caused by microbes. The net effect of all this was that the understanding of pathogens in disease was driven by the study of well-known, easy-to-culture microbes(({{pmid>long:19040704}})) – which, as it turns out, represents the vast minority of bacteria in the human body.

	===== A history of discounting culture-independent methods of microbe identification =====		===== A history of discounting culture-independent methods of microbe identification =====
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	The case for uncultured organisms even existing let alone remaining uncultured has not been proven and repetitive uncontrolled observations do not serve the scientific community well and may mislead the unwary.		The case for uncultured organisms even existing let alone remaining uncultured has not been proven and repetitive uncontrolled observations do not serve the scientific community well and may mislead the unwary.

-	//Anonymous Lancet editorial// (({{pubmed>long:1970375}}))	+	//Anonymous Lancet editorial// (({{pmid>long:1970375}}))
	</blockquote>		</blockquote>

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	Researchers have long known that traditional methods for culturing bacteria are effective at identifying only a fraction of the bacteria in a given sample. One of the first reports of this came from Razumov((Razumov, A. S. 1932. //Mikrobiologija//, 1:131-46 116.)) who noted in 1932 that a large discrepancy between the viable plate count and total direct microscopic count of bacteria taken from aquatic habitats. Razumov found higher numbers (by several orders of magnitude) by direct microscopic counting than by the plating procedure.		Researchers have long known that traditional methods for culturing bacteria are effective at identifying only a fraction of the bacteria in a given sample. One of the first reports of this came from Razumov((Razumov, A. S. 1932. //Mikrobiologija//, 1:131-46 116.)) who noted in 1932 that a large discrepancy between the viable plate count and total direct microscopic count of bacteria taken from aquatic habitats. Razumov found higher numbers (by several orders of magnitude) by direct microscopic counting than by the plating procedure.

-	In 1949, Winogradsky confirmed Razumov's assessment also noted that many microbes are not satisfied with laboratory cultivation conditions. He remarked that readily cultivated bacteria in natural microbial communities "draw importance to themselves, whereas the other forms, being less docile, or even resistant, escape attention."(({{pubmed>long:9716951}}))	+	In 1949, Winogradsky confirmed Razumov's assessment also noted that many microbes are not satisfied with laboratory cultivation conditions. He remarked that readily cultivated bacteria in natural microbial communities "draw importance to themselves, whereas the other forms, being less docile, or even resistant, escape attention."(({{pmid>long:9716951}}))

-	In 1985, Staley and Konopka pointed to Razumov's discrepancy and called it "the Great Plate Count Anomaly."(({{pubmed>long:18502944}})) Their review describes work in which the researchers took hundreds, perhaps even thousands, of water samples from Lake Washington and performed two methods for counting bacteria.	+	In 1985, Staley and Konopka pointed to Razumov's discrepancy and called it "the Great Plate Count Anomaly."(({{pmid>long:18502944}})) Their review describes work in which the researchers took hundreds, perhaps even thousands, of water samples from Lake Washington and performed two methods for counting bacteria.

	Figure 1 shows the number of bacteria identified using a fluorescent dye, acridine orange. Acridine orange counts bacteria by interacting with bacterial DNA and RNA.		Figure 1 shows the number of bacteria identified using a fluorescent dye, acridine orange. Acridine orange counts bacteria by interacting with bacterial DNA and RNA.
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	As it is plainly evident, the genomic method for detecting bacteria (Figure 1) was orders of magnitude more sensitive than a method based on viability in a culture (Figure 2). The shortcomings of the cultivation method is striking and suggests that this traditional method for cultivation is only effective in identifying a fraction of all bacteria.		As it is plainly evident, the genomic method for detecting bacteria (Figure 1) was orders of magnitude more sensitive than a method based on viability in a culture (Figure 2). The shortcomings of the cultivation method is striking and suggests that this traditional method for cultivation is only effective in identifying a fraction of all bacteria.

-	The author's conclusions have been used even very recently to apply to cells everywhere including in the human body:(({{pubmed>long:18502944}}))	+	The author's conclusions have been used even very recently to apply to cells everywhere including in the human body:(({{pmid>long:18502944}}))

	<blockquote>		<blockquote>
	As the figures illustrate, only approximately 0.1-1.0% of the total bacteria can be enumerated by the plating procedure. Indeed, as a general rule we have found that the maximum recovery of heterotrophic bacteria [bacteria that don't use photosynthesis] is 1% of the total direct count using plating procedures or other viable enumeration methods.... From a microbiological perspective, only a few percent of the bacterial cells enumerated by direct microscopic count can be cultured and identified (see previous section on plate counts). No breakthrough in determining species diversity seems likely in the near future.		As the figures illustrate, only approximately 0.1-1.0% of the total bacteria can be enumerated by the plating procedure. Indeed, as a general rule we have found that the maximum recovery of heterotrophic bacteria [bacteria that don't use photosynthesis] is 1% of the total direct count using plating procedures or other viable enumeration methods.... From a microbiological perspective, only a few percent of the bacterial cells enumerated by direct microscopic count can be cultured and identified (see previous section on plate counts). No breakthrough in determining species diversity seems likely in the near future.

-	//James T. Staley and Allan Konopka, PhD// (({{pubmed>long:3904603}}))</blockquote>	+	//James T. Staley and Allan Konopka, PhD// (({{pmid>long:3904603}}))</blockquote>

05.23.2020		current
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-	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.}}]		[{{ :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 ====		==== 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}}))	+	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).(({{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.	+	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 ====		==== Coronavirus ====
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	[[https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(20)30132-8/fulltext\|3 Antiviral and anti-inflammatory treatments compared]]		[[https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(20)30132-8/fulltext\|3 Antiviral and anti-inflammatory treatments compared]]

-	[[http://www.koreabiomed.com/news/articleView.html?idxno=7428\|Treatment guidelines for coronavirus (Korea 2020)]]	+	[[https://www.koreabiomed.com/news/articleView.html?idxno=7428\|Treatment guidelines for coronavirus (Korea 2020)]]

-	[[http://www.koreabiomed.com/news/articleView.html?idxno=7718\|Fewer new cases 20/3/2020 (Korea) ]]	+	[[https://www.koreabiomed.com/news/articleView.html?idxno=7718\|Fewer new cases 20/3/2020 (Korea) ]]

-	current evidence(({{pubmed>long: 32096567}}))	+	current evidence(({{pmid>long: 32096567}}))

-	chloroquine (({{pubmed>long: 32147496}}))	+	chloroquine (({{pmid>long: 32147496}}))

-	neuroinvasive potential(({{pubmed>long: 32104915}}))	+	neuroinvasive potential(({{pmid>long: 32104915}}))

-	Unique epidemiological and clinical features(({{pubmed>long: 32134116}}))	+	Unique epidemiological and clinical features(({{pmid>long: 32134116}}))

-	Presumed Asymptomatic Carrier Transmission(({{pubmed>long: 32083643}}))	+	Presumed Asymptomatic Carrier Transmission(({{pmid>long: 32083643}}))

-	Discovering drugs(({{pubmed>long: 32147628}}))	+	Discovering drugs(({{pmid>long: 32147628}}))

-	breakthrough(({{pubmed>long: 32074550}}))	+	breakthrough(({{pmid>long: 32074550}}))