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WPI describes how Ampligen boosts NK cell activity in XMRV-positive CFS patients' cells

  [ 55 votes ]   [ 3 Comments ]
By Isabel Barao-Silvestre, et al. • • May 7, 2010

Following is the abstract of a research paper by a team of University of Nevada/Whittemore Peterson Institute researchers. The paper will be presented May 9 to immunologists gathered in Baltimore at Immunology 2010™ by UN/WPI lead author Isabel Barao-Silvestre.

[Note: Degranulation is release of microbe-toxic molecules from granules found inside some immune cells, including Natural Killer cells.] ______________________________________

Characterization of the therapeutic increases in Natural Killer (NK) activity of xenotropic murine leukemia virus-related virus (XMRV)-positive chronic fatigue syndrome (CFS) patients effected by poly (I): poly (C12U) (Ampligen) – Source: May 9 Presentation, Immunology 2010™

Chronic Fatigue Syndrome (CFS) is a debilitating disease of unknown etiology that affects ~17 million people worldwide. Patients suffer persistent viral infections and may develop hematopoietic malignancies. The patients have reduced Natural Killer (NK) cell activities which could contribute to the diseases, and, if restored, potentially reduce symptoms.

We characterized the in vitro effects on NK cells of the interferon inducer poly (I): poly (C12U) (Ampligen) which in some CFS patients abates disease symptoms.

The 30 CFS patients were infected with the gammaretrovirus xenotropic murine leukemia virus-related virus (XMRV).

We cultured their peripheral blood mononuclear cells with the drug for 24 hrs and monitor NK activity to K562 cells by flow cytometry, concurrently measuring degranulation by externalization of CD107a, and expression of Grz B and perforin.

Treatment markedly increased CD107a externalization in the NK cell population as indicated by 5-fold increases in CD107a-positive cell frequencies and 3-fold increases in their CD107a MFI, with slight positive shifts in intracellular Grz B and perforin.

In contrast, T cells showed little change in CD107a externalization.

Our results suggest that degranulation rates may be more affected than the levels of cytotoxic proteins, indicating a novel mechanism by which NK activity was affected by the drug.

The increase in degranulation per NK cell indicates a mechanism by which Ampligen treatment can improve NK cell function.

Source: Poster for May 9 presentation by Isabel Barao Silvestre at Immunology 2010™ in Baltimore, Maryland. Paper by Barao-Silvestre I, Marshall M, Hagen KS, Pfost MA, Strayer D, Peterson D, Hudig D, Mikovits JA. Whittemore Peterson Institute, Reno; University of Nevada, Reno, Nevada; Hemispherx Biopharma, Inc., Philadelphia, Pennsylvania, USA.

Please Discuss This Article:   Post a Comment 

Posted by: Mya Symons
May 9, 2010
Could someone explain this so a person without medical training could understand this?
Reply Reply

Posted by: jmkinsey
May 13, 2010
Ampligen has been in the works for years now. When is it ever going to be available? Or is it? I guess I'm getting a little impatient with the lack of availablitly of a promising treatment for a disease that has ruined 23 years of my life.
Reply Reply

LDN works too
Posted by: DiamonDie
May 14, 2010
You can also boost NK cell function with low dose naltrexone, which costs a tiny fraction of Ampligen's price tag, is much safer, doesn't require intravenous administration and is already available.
Reply Reply

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