Kutapressin

[Guest guest]

Kutapressin for Chronic Fatigue Syndrome

ImmuneSupport.com

04-26-2002

D.V. Ablashi, Z. Berneman, C. Lawyer and A. Komaroff National Cancer

Institute, Bethesda, land; town University School of

Medicine, Washington, DC; Private Practice, Mequon, Wisconsin; Div

General Medicine, Brigham and Woman's Hospital and Harvard University,

Boston, Massachusetts

Clinical Infectious Diseases 1994; 18 (S-1):S113

Kutapressin (KU: Schwarz Pharma, Milwaukee, WI) is a prescription drug

consisting of processed extract from porcine livers that contains

peptides; it has been used in the treatment of patients with herpes

zoster, keloids, seborrhea, other skin diseases and neurasthenia.

More recently, results of uncontrolled studies have indicated that

treatment with KU results in abatement of symptoms of many patients

with chronic fatigue syndrome (CFS). One large study found evidence of

reactivation of human herpesvirus type 6 (HHV-6) in many patients with

CFS. Moreover, HHV-6 DNA was detected by southern blot analysis in

lymphocytes from patients with CFS. Because treatments with KU may

have positive clinical effects on patients with CFS and the evidence

that CFS is associated with reactivation of HHV-6, we investigated the

possibility that KU might have direct activity against HHV-6.

KU that was free of phenol was dissolved in tissue culture medium

(RPMI 1640 supplemented with 10% fetal calf serum and antibiotics) for

in vitro studies. A human T lymphocyte cell line (HSB-2) was infected

with HHV-6.

KU blocked HHV-6 (variant A, GS strain) infection of HSB-2 cells most

effectively at doses of 300 and 500 ug/mL. These doses of the drug

were not toxic to the cells. Inhibition of HHV-6 infection (1,000

TCID50) was most effective (>95%) when cells (>106/mL) were pretreated

with KU overnight, prior to viral infection, and then were maintained

in the presence of KU throughout the experiment (14 days after infection).

In addition, inhibition (>80%) of HHV-6 infection was observed when

HSB-2 cells were first infected with 1,000 TCID50 of HHV-6 and were

then maintained in the presence of 300- and 500- ug doses of KU. When

300 and 500 ug/mL doses of KU were added to cells 3 days after the

start of infection with HHV-6, it inhibited only 22% and 33% of viral

infection, respectively. When the cells were simultaneously treated

with virus and 300 and 500 ug/mL of KU, ~90% of HHV-6 infection was

inhibited.

These data show that KU is a potent inhibitor of HHV-6 infection.

Although the mechanism of HHV-6 inhibition by KU is under

investigation, electron microscopic examination of cells treated with

KU prior to HHV-6 infection revealed abundant extracellular virus

particles, which suggests inhibition of viral attachment and penetration.