quote:Proc Natl Acad Sci U S A. 2005 Aug 23;102:11993-8 16040799 (P,S,E,B) Cited:2 Toward a live microbial microbicide for HIV: commensal bacteria secreting an HIV fusion inhibitor peptide.
[My paper] Srinivas Rao, Stella Hu, Louise McHugh, Kira Lueders, Ken Henry, Qi Zhao, Richard A Fekete, Sudeshna Kar, Sankar Adhya, Dean H Hamer Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. Most HIV transmission occurs on the mucosal surfaces of the gastrointestinal and cervicovaginal tracts, both of which are normally coated by a biofilm of nonpathogenic commensal bacteria. We propose to genetically engineer such naturally occurring bacteria to protect against HIV infection by secreting antiviral peptides. Here we describe the development and characterization of Nissle 1917, a highly colonizing probiotic strain of Escherichia coli, secreting HIV-gp41-hemolysin A hybrid peptides that block HIV fusion and entry into target cells. By using an appropriate combination of cis- and transacting secretory and regulatory signals, micromolar secretion levels of the anti-HIV peptides were achieved. The genetically engineered Nissle 1917 were capable of colonizing mice for periods of weeks to months, predominantly in the colon and cecum, with lower concentrations of bacteria present in the rectum, vagina, and small intestine. Histological and immunocytochemical examination of the colon revealed bacterial growth and peptide secretion throughout the luminal mucosa and in association with epithelial surfaces. The use of genetically engineered live microbes as anti-HIV microbicides has important potential advantages in economy, efficacy, and durability. Mesh-terms: Animals; Anti-HIV Agents :: metabolism; Anti-HIV Agents :: pharmacology; Cecum :: microbiology; Colon :: microbiology; Comparative Study; Escherichia coli :: genetics; Escherichia coli :: metabolism; Female; Genetic Engineering :: methods; HIV :: drug effects; HIV :: metabolism; HIV Envelope Protein gp41 :: metabolism; HIV Infections :: prevention & control; Hemolysins :: metabolism; Humans; Intestinal Mucosa :: microbiology; Mice; Models, Biological; Peptides :: pharmacology; Peptides :: secretion; Vagina :: microbiology;
-------------------- Bob Posts: 2150 | From Maryland | Registered: Dec 2007
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This is a good point. So how do we disrupt bad biofilms without inhibiting good ones? This seems very complicated to me.
Wrotek, please edit your post to make that long url into a tiny url, so that the page does not go wide and people can read it without scrolling. Thanks.
Posts: 8430 | From Not available | Registered: Oct 2000
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lymie_in_md
Frequent Contributor (1K+ posts)
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Lou, I don't think they are constructed with the same materials, but this is even newer science then biofilm from pathogenic bacteria.
If we could increase the strength of positive biofilm it might give rise to super probiotics. Where our good friends are better protected in our bodies especially if we're taking ABX.
-------------------- Bob Posts: 2150 | From Maryland | Registered: Dec 2007
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huh. this is really interesting. i got well and never used heparin or any other product to thin blood, but did do allot of diet/alternative treatments that would have the same effect.
btw, how many llmd's are now using fry (officially)? ..for either treatment progress or documentation of the organisms?
what are the other conditions that heparin is used to treat?
mo
Posts: 8337 | From the other shore | Registered: Jul 2002
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