Lähettäjä: Soijuv Lähetetty: 15.11.2006 8:47
Kroonista borrelioosia sairastavilla esiintyy usein lisäksi lukuisia lisäinfektioita, esim. mykoplasma, keuhkoklamydia ja erilaisia herpes-viruksia kuten sytomegalovirus ja HHV-6. Jokainen näistä mikrobeista saattaa aiheuttaa tulehduksen esim. sydämessä.
Seuraavassa kertomuksessa "Traaginen kuolema" Casey Fero kuoli HHV-6 -viruksen aiheuttamaan sydänlihastulehdukseen. Hänellä diagnosoitiin krooninen väsymysoireyhtymä jo 9-vuotiaana ja uudelleen 15-vuotiaana.
Caseyllä oli päänsärkyä, muisti-/ajatteluvaikeuksia, lihasheikkoutta ja väsymystä. Sen lisäksi että poika sai kärsiä vaikeista oireista, hänen täytyi kestää lääkäreiden mielipiteet, joiden mukaan hän ei ole "oikeasti" sairas. Opettajien mielestä hän oli "koulupinnaaja".
Casey Fero oli kuollessaan 23-vuotias. Hänen sydämensä pysähtyi hänen nukkuessaan. Patologi oli järkyttynyt nähdessään pojan sydämessä olevat vauriot. Sydän oli infektoitunut kokonaan. Siinä oli myös sidekudosta, joka oli muodostunut vuosia kestäneen infektion seurauksena.
TRAGIC DEATH
http://phoenix-cfs.org/Tragic%20death%2 ... eitzer.htm
This testimony was given to the CFSAC (The Chronic Fatigue Syndrome Advisory Committee of the U.S. Department of Health and Human Services) on Monday, September 12, 2005 by Mary Schweitzer Ph.D.
On July 4, 2005, sometime between 2:30 am when his mother kissed him good night, and 6:30 am when his father came downstairs, Casey Fero died in his sleep. His heart simply stopped.
Casey Fero was 23.
Casey was a charming, friendly kid with blue-green eyes. He was first diagnosed with CFS at the age of 9, then again at 15. He was plagued by headaches, cognitive difficulties, muscle weakness, and exhaustion. In addition to the symptoms of a serious illness, he had to endure doctors who did not "believe" he was "really" sick, and teachers who saw in him only a shirker. By the end of his short life, however, he was happy. He
had just completed two years of community college and was looking forward to beginning courses at the University of Wisconsin. He had acquired a summer job. He had many friends, who came to his home for days after he slipped away to mourn the loss together. The family and Wisconsin CFS Association will honor Casey with a blood and tissue bank for CFS/M.E. victims.
The flyer was posted to Co-Cure yesterday, and can be found at http://www.co-cure.org/flyer_WI.pdf . To contribute to the Casey Fero ME/CFS Tissue and Blood Bank go to <www.wicfs-me.org>]
In his mother's words, "Casey had bull dog determination. In his mind he had overcome all illness and if he just worked harder he could do anything.... Interesting, how he died so well, with so much enthusiasm to live."
Casey's mother, Pat Fero, President of the Wisconsin CFS Association testified before this Committee about a year and a half ago. Pat has had CFS since before Casey was born. She and Bruce sought diagnosis and treatment for Casey, but as he passed into adulthood, he no longer had a doctor of his own. Even at the University of Wisconsin,there were no doctors who "believed in" the disease or, for that matter, really believed Casey was sick. Casey carved his own therapy out of over-the-counter and mail-order supplements such as powdered whey protein and Co-Q-10.
Seeing the supplements, the coroner originally told Pat that this would be their first "steroid" death. Even in death, the first response was that it could not be CFS, because CFS is not a serious disease.
Last Thursday, September 8, Pat received the coroner's report. The University of Wisconsin forensic pathologist found that: **Casey died of myocarditis that is, his heart was infected with disease. There was inflammation, and the tissue was full of viral infection. Casey also had old fibrosis, indicating that the viral infection was not of a new onset.**
The pathologist was "shocked" at this finding.
Casey Fero died of Chronic Fatigue Syndrome.
Why?
Specialists on NMH said they knew of no cases where someone died from that condition nor had there been reason to suspect carditis was involved in NMH.
Using an ultra-sensitive type of electrocardiogram, Dr. A. Martin Lerner of Wayne State University has found evidence that EBV and cytomegaloviruses in CFS patients has caused heart damage. I do not know whether this research has been replicated, but under the circumstances, it takes on a new importance.
There is evidence that HHV-6 can infect the heart. Other possible culprits include Lyme Disease, mycoplasma, and Chlamydia. In 2003, Arnold Peckerman, Benjamin Natelson and others published their research finding that most CFS patients suffer from cardiac abnormalities "Abnormal Impedance Cardiography Predicts Symptom Severity in Chronic Fatigue Syndrome," in The American Journal of the Medical Sciences 326:2 (2003): 55-60].
The cause was left to further studies, but Dr. Paul Cheney has suggested viral infection. Clearly this research could lead to an answer to Casey's death, but it has no federal funding.
The harsh reality is that research on CFS, viruses, and cardiac abnormalities is under-funded, ignored, and at times outright dismissed by those charged with informing the public of the dangers of diseases.
However, if you turn to the Myalgic Encephalomyelitis (M.E.) literature in Great Britain, there is evidence of deaths in both adults and teenagers from sudden heart stoppage. Ramsay wrote about such cases, and in correspondence with Dr. Malcolm Hooper I was informed that he, too, was aware of premature deaths from heart failure. Dr. Hooper has long been studying the hypothesis that M.E. is caused by an enterovirus (such as polio and coxsackie). There is no comparable research on enteroviruses in the United States (unless you count the sparse literature on post-polio syndrome)
Is this the price we have paid because in 1988 we rejected, instead of embracing, the robust research programs and existing literature in the M.E. community? Had we built on these studies, instead of squandering our time on measures of "fatigue" and a plethora of studies of CFS as a "somaticizing" disorder, where might we be today? For the past twenty years, had we been looking at this as a disease rather than a psychological disorder, would we now know enough to have prevented Casey's death?
And if we hadn't hidden what we already know from the public, would Casey have had a doctor of his own, perhaps even one that would have looked into the condition of his heart?
Pat Fero came down with CFS before her son Casey was born. His entire life was lived under the shadow of this disease a shadow of widespread ignorance.
Why?
The pathologist was shocked to find heart damage.
Why?
What is the virus that the pathologists found? HHV-6? Mycoplasma? Anenterovirus? Cytomegalovirus? EBV? Something completely new? Why is there no money for researchers studying these very questions?
We need the public to be told NOW that there is a serious disease out there, and that nearly a million people in the United States have it. They need to be told of the uncertainty about cause, prognosis, and cure. They need to be told what they should be tested for to rule out other diseases.
And they need to know that patients die.
Two months after Casey's tragic, untimely death, most primary care physicians know little more about the disease than they did on the day Casey was born. That is criminal.
One year after this committee sent a list of suggestions (as is its task), to the Secretary of the DHHS, there has been no [effective] response. That is also criminal.
What does it take to impart a sense of urgency to this task?
Does it take the tragedy of a young man's senseless death?
Hold Casey's memory high, like a banner. Take him to Congress, to the press, to the appropriate medical specialties. Let this be a turning point.
Casey Fero died too young. Do not let his death be in vain.
----------------------
To contribute to the Casey Fero ME/CFS Tissue and Blood Bank go to
www.wicfs-me.org or you may also send a check to:
The Wisconsin CFS Association
747 Lois Drive
Sun Prairie, WI 53590
Be sure to specify "CASEY'S FUND" on the check.
LISÄINFEKTIO: HERPESVIRUKSET - KROONINEN VÄSYMYS
Valvojat: Jatta1001, Borrelioosiyhdistys, Bb
LISÄINFEKTIO: HERPESVIRUKSET - KROONINEN VÄSYMYS
Viimeksi muokannut Bb, Pe Huhti 16, 2010 22:43. Yhteensä muokattu 3 kertaa.
Lähettäjä: Soijuv Lähetetty: 15.11.2006 9:52
Krooninen aktiivinen HHV 6 infektio: J.Brewer MD
Asikloviiri (zovirax), famsikloviiri (famvir) ja valasikloviiri (valtrex) näyttäisivät olevan melko tehottomia HHV-6 infektion hoidossa. Gansikloviiri (cytovene) ja foscarnet (foscavir) ovat olleet jonkin verran tehokkaampia.
MS-ja/tai kroonista fatiikkia sairastavat saivat selkeästi apua gansikloviirista. Toisen tutkimuksen mukaan myös asikloviirirista oli apua. MS-tautia sairastavien oireiden pahenemiskaudet vähenivät antiviraalisen hoidon aikana. Oireet kuitenkin palasivat kun hoito lopetettiin (joillakin hoito oli kestänyt jopa 6 kk). Immuunipuolustus; tappajasolujen toiminta, ei parantunut hoidon aikana, mikä saattaa selittää oireiden uusiutumisen.
Immuunijärjestelmän modulointi on eräs varteenotettava hoitokeino. Beta Interferoni vähentää tutkimusten mukaan MS -relapseja ja aivoleesioiden määrää. On mahdollista että positiiviset tulokset johtuvat nimenomaan interferonin antiviraalisesta vaikutuksesta.
Eräs immuunijärjestelmää moduloiva valmiste "transfer factor (TF)" saattaa osoittautua lupaavaksi virustautien hoidossa. Sen on toistamiseen osoitettu estäneen virusinfektioita. Se on osoittautunut erittäin turvalliseksi eikä sillä ole havaittu sivuvaikutuksia.
Muita mahdollisia hoitoja: Suonensisäisesti annettava gammaglobuliini on parantanut joidenkin MS-ja kroonista väsymysoireyhtymää sairastavien oireita.
Veren hyytymiseen vaikuttava lääkitys on myös osoittautunut mielenkiintoiseksi hoitomahdollisuudeksi.Veren hyytymistä vähentävät lääkkeet saattavat lisätä hapen kulkeutumista kudoksiin ja vähentää näin oireita. Yhden tutkimuksen mukaan väsymysoireyhtymää sairastavat, hepariinihoitoa saaneiden henkilöiden oireet paranivat hoidon aikana. Hepariinilla saattaa lisäksi olla antiviraalisia vaikutuksia.
Chronic Active Human Herpesvirus-6 (HHV-6) Infection: A ew Disease Paradigm
by Joseph H. Brewer, M.D.
Koko artikkeli:
http://www.plazamedicine.com/hhv6/hhv6_6.html
Treatment
Treatment of HHV-6 infection has not received much attention in the literature. The obvious initial consideration for a treatment strategy would be antiviral therapy. Several antiviral agents are now available for the prevention and treatment of the herpes viruses (HSV 1 and 2, VZV, and CMV) (82). The role of these agents in the treatment of HHV-6 infections is not well established due to limited data. In vitro studies with HHV-6 have shown that the virus is resistant to acyclovir (Zovirax) at achievable serum levels (83, 84, 85). Although not specifically studied, the other oral agents, famciclovir (Famvir) and valacyclovir (Valtrex) are likely to be ineffective as well.
The parenteral antiviral drugs that have activity against cytomegalovirus (CMV) have been studied in vitro against HHV-6, with conflicting results (83, 84, 85). Albiet HHV-6 has been sensitive to ganciclovir (Cytovene) and foscarnet (Foscavir), some studies have shown resistance, especially with ganciclovir and the HHV-6A variant (85). Resistance may be strain dependent. Both agents have been used successfully to treat life threatening HHV-6 infections in transplant patients, including encephalitis (86, 87). Cidofovir (Visitide) would be an attractive consideration, given its broad antiviral activity, however it has not been studied with HHV-6. The toxicity of cidofovir may also be a problem, especially with more prolonged use. In acute HHV-6 infections, as is the case in the transplant patients, the anti-CMV agents may be very useful (86, 87). The role of the parenteral agents currently used for CMV infections in chronic active HHV-6 infection may be more limited. The reasons for this include: inconvenient route for chronic administration (intravenous), risk of catheter complications with chronic use, toxicity (particularly cumulative toxicity over time), and relapse of infection when therapy is discontinued. We have administered IV ganciclovir to several selected patients with MS or severe unrelenting CFS in which there was ongoing active HHV-6 infection of the bloodstream documented by repeatedly positive blood cultures. Analysis of this data has lead to several preliminary observations. The clinical and virologic responses have been variable.
A subset of patients with both MS and CFS clearly seemed to respond to ganciclovir. In the "responders", there appeared to be diminished viral activity (decreased number of positive viral blood cultures) but we rarely saw complete clearance of viremia. These patients also showed evidence of a clinical response (an example, is an MS case that we have previously reported, who had a marked decrease in MS relapses on therapy) (27). Also, in the group of patients who "responded" clinically and virologically, there was a tendency to relapse when antiviral therapy was discontinued (even after 6 months or more of therapy).
Immune function (low NK function) did not improve on ganciclovir therapy, which may partially explain the tendency to relapse. There was another group of patients that did not respond to the ganciclovir. Although the reason for this is unknown, we would postulate strain specific resistance as a likely explanation. We found that ganciclovir was well tolerated in these patients.
One study of CFS patients treated with IV ganciclovir (for 30 days) has been reported in the literature (88 ). Using functional status, there was improvement in 13 of 18 patients at 24 weeks after ganciclovir. The remainder of patients failed to improve. HHV-6 was not addressed in this study and long term follow up data was not provided. This type of data, at 24 weeks, would be generally consistent with our observations. We have given IV foscarnet to two patients with active HHV-6 infection. In both, therapy was discontinued by the fourth week due to toxicity.
Oral antiviral therapy may be more practical and amenable to long term maintenance therapy. Unfortunately, as noted above, none of the currently available agents appear to be particularly attractive based on their in vitro activity. Acyclovir (or valacyclovir) may have some limited, strain dependent activity. One study showed that acyclovir reduced the frequency of disease exacerbations in MS patients. Valganciclovir, an oral form of ganciclovir with serum levels similar to the IV formulation, is currently being evaluated in clinical trials of patients with CMV infections. Several drugs that have a very broad antiviral spectrum (including herpes viruses) are being evaluated as potential antiviral agents. Some of these agents (e.g. PMPA) may surface in the future as effective agents for HHV-6.
Given the immune deficiency that results from chronic active HHV-6 infection, immune modulation is another attractive avenue for consideration. Beta interferon has been shown to decrease MS relapses and decrease the number of active lesions on MRI head scans in controlled studies (both Beta 1a and Beta 1b types) (89). The proposed mechanism is an immune regulatory role (down regulation of CMI) by the interferon. Since interferon has known anti-viral properties, another explanation for the positive results could be an anti-viral effect on HHV-6. In our observations of MS patients with HHV-6 viremia, we have not seen a lower rate of positive HHV-6 blood cultures or higher NK function assay results in patients on either of the beta interferon preparations (unpublished data). However, this would not rule out an anti-viral effect of interferon, particularly a partial effect. Since the beta interferon studies included large numbers of patients, our observations in a small number of patients is likely too small of a sample to see a statistically significant difference. The anti-viral effects of the interferon preparations on HHV-6 have not been studied. Defining the effect of interferon on HHV-6 will be an important area of research. Intravenous gamma globulin has been given to both MS and CFS patients with improvement in clinical parameters, but results in the literature have varied (90, 91). Other immune modulators such as G-CSF and GM-CSF have not been studied.
Another immune modulator that may have substantial promise is transfer factor (TF). There are several reasons to consider TF. TF has consistently shown efficacy in the prevention and treatment of viral infections. Studies reporting efficacy of specific TF have been reported with HSV 1 and 2, VZV, EBV, and CMV (93, 94, 95, 96). TF has proven to be extremely safe with virtually no significant adverse effects (96). Since TF acts on CMI, this type of agent may improve the immune dysfunction that is a key feature of chronic active HHV-6 infection (97). Recent techniques obtaining TF from bovine colostrum provides a way to recover TF in large enough amounts for commercial preparation (98 ). We have done some preliminary studies in patients with CFS and chronic active HHV-6 infection using a TF preparation derived from bovine colostrum that has activity for HHV-6 included in its scope of TF activities. Albeit the data is still preliminary, this type of immune modulation appears to be very promising. We have seen significant symptom improvement, consistently negative HHV-6 blood cultures and marked improvement in NK function in patients taking this particular TF (unpublished data).
Another interesting treatment concept involves the use of anti-coagulants. Given the issue of activated coagulation pathways in these patients (endothelial cell tropism and vasculopathy), anti-coagulation may improve oxygen delivery and help with the symptoms that have been caused by a hypercoaguable state and fibrin deposition (99). One study has demonstrated symptom improvements in CFS patients treated with heparin (99). Several studies have shown that herpes viruses attach to cell surfaces via heparan sulfate receptors and that exogenous heparin can block this interaction and viral infectivity (100, 101). Thus, heparin may have some antiviral properties for herpes viruses. Patients with hereditary hypercoaguable syndromes (thrombophilia or hypofibrinolysis) may be at further risk for substantial hypercoaguable related problems and require anticoagulation. One evolving concept involves blocking viral activation (antiviral agents or immune modulation such as TF) combined with anticoagulants (heparin or coumadin). A model for a hypercoaguable state in patients with active HHV-6 infection and possible management strategies of the patient with a hypercoaguable state and associated active HHV-6 infection are outlined in Table 2 and 3.
Krooninen aktiivinen HHV 6 infektio: J.Brewer MD
Asikloviiri (zovirax), famsikloviiri (famvir) ja valasikloviiri (valtrex) näyttäisivät olevan melko tehottomia HHV-6 infektion hoidossa. Gansikloviiri (cytovene) ja foscarnet (foscavir) ovat olleet jonkin verran tehokkaampia.
MS-ja/tai kroonista fatiikkia sairastavat saivat selkeästi apua gansikloviirista. Toisen tutkimuksen mukaan myös asikloviirirista oli apua. MS-tautia sairastavien oireiden pahenemiskaudet vähenivät antiviraalisen hoidon aikana. Oireet kuitenkin palasivat kun hoito lopetettiin (joillakin hoito oli kestänyt jopa 6 kk). Immuunipuolustus; tappajasolujen toiminta, ei parantunut hoidon aikana, mikä saattaa selittää oireiden uusiutumisen.
Immuunijärjestelmän modulointi on eräs varteenotettava hoitokeino. Beta Interferoni vähentää tutkimusten mukaan MS -relapseja ja aivoleesioiden määrää. On mahdollista että positiiviset tulokset johtuvat nimenomaan interferonin antiviraalisesta vaikutuksesta.
Eräs immuunijärjestelmää moduloiva valmiste "transfer factor (TF)" saattaa osoittautua lupaavaksi virustautien hoidossa. Sen on toistamiseen osoitettu estäneen virusinfektioita. Se on osoittautunut erittäin turvalliseksi eikä sillä ole havaittu sivuvaikutuksia.
Muita mahdollisia hoitoja: Suonensisäisesti annettava gammaglobuliini on parantanut joidenkin MS-ja kroonista väsymysoireyhtymää sairastavien oireita.
Veren hyytymiseen vaikuttava lääkitys on myös osoittautunut mielenkiintoiseksi hoitomahdollisuudeksi.Veren hyytymistä vähentävät lääkkeet saattavat lisätä hapen kulkeutumista kudoksiin ja vähentää näin oireita. Yhden tutkimuksen mukaan väsymysoireyhtymää sairastavat, hepariinihoitoa saaneiden henkilöiden oireet paranivat hoidon aikana. Hepariinilla saattaa lisäksi olla antiviraalisia vaikutuksia.
Chronic Active Human Herpesvirus-6 (HHV-6) Infection: A ew Disease Paradigm
by Joseph H. Brewer, M.D.
Koko artikkeli:
http://www.plazamedicine.com/hhv6/hhv6_6.html
Treatment
Treatment of HHV-6 infection has not received much attention in the literature. The obvious initial consideration for a treatment strategy would be antiviral therapy. Several antiviral agents are now available for the prevention and treatment of the herpes viruses (HSV 1 and 2, VZV, and CMV) (82). The role of these agents in the treatment of HHV-6 infections is not well established due to limited data. In vitro studies with HHV-6 have shown that the virus is resistant to acyclovir (Zovirax) at achievable serum levels (83, 84, 85). Although not specifically studied, the other oral agents, famciclovir (Famvir) and valacyclovir (Valtrex) are likely to be ineffective as well.
The parenteral antiviral drugs that have activity against cytomegalovirus (CMV) have been studied in vitro against HHV-6, with conflicting results (83, 84, 85). Albiet HHV-6 has been sensitive to ganciclovir (Cytovene) and foscarnet (Foscavir), some studies have shown resistance, especially with ganciclovir and the HHV-6A variant (85). Resistance may be strain dependent. Both agents have been used successfully to treat life threatening HHV-6 infections in transplant patients, including encephalitis (86, 87). Cidofovir (Visitide) would be an attractive consideration, given its broad antiviral activity, however it has not been studied with HHV-6. The toxicity of cidofovir may also be a problem, especially with more prolonged use. In acute HHV-6 infections, as is the case in the transplant patients, the anti-CMV agents may be very useful (86, 87). The role of the parenteral agents currently used for CMV infections in chronic active HHV-6 infection may be more limited. The reasons for this include: inconvenient route for chronic administration (intravenous), risk of catheter complications with chronic use, toxicity (particularly cumulative toxicity over time), and relapse of infection when therapy is discontinued. We have administered IV ganciclovir to several selected patients with MS or severe unrelenting CFS in which there was ongoing active HHV-6 infection of the bloodstream documented by repeatedly positive blood cultures. Analysis of this data has lead to several preliminary observations. The clinical and virologic responses have been variable.
A subset of patients with both MS and CFS clearly seemed to respond to ganciclovir. In the "responders", there appeared to be diminished viral activity (decreased number of positive viral blood cultures) but we rarely saw complete clearance of viremia. These patients also showed evidence of a clinical response (an example, is an MS case that we have previously reported, who had a marked decrease in MS relapses on therapy) (27). Also, in the group of patients who "responded" clinically and virologically, there was a tendency to relapse when antiviral therapy was discontinued (even after 6 months or more of therapy).
Immune function (low NK function) did not improve on ganciclovir therapy, which may partially explain the tendency to relapse. There was another group of patients that did not respond to the ganciclovir. Although the reason for this is unknown, we would postulate strain specific resistance as a likely explanation. We found that ganciclovir was well tolerated in these patients.
One study of CFS patients treated with IV ganciclovir (for 30 days) has been reported in the literature (88 ). Using functional status, there was improvement in 13 of 18 patients at 24 weeks after ganciclovir. The remainder of patients failed to improve. HHV-6 was not addressed in this study and long term follow up data was not provided. This type of data, at 24 weeks, would be generally consistent with our observations. We have given IV foscarnet to two patients with active HHV-6 infection. In both, therapy was discontinued by the fourth week due to toxicity.
Oral antiviral therapy may be more practical and amenable to long term maintenance therapy. Unfortunately, as noted above, none of the currently available agents appear to be particularly attractive based on their in vitro activity. Acyclovir (or valacyclovir) may have some limited, strain dependent activity. One study showed that acyclovir reduced the frequency of disease exacerbations in MS patients. Valganciclovir, an oral form of ganciclovir with serum levels similar to the IV formulation, is currently being evaluated in clinical trials of patients with CMV infections. Several drugs that have a very broad antiviral spectrum (including herpes viruses) are being evaluated as potential antiviral agents. Some of these agents (e.g. PMPA) may surface in the future as effective agents for HHV-6.
Given the immune deficiency that results from chronic active HHV-6 infection, immune modulation is another attractive avenue for consideration. Beta interferon has been shown to decrease MS relapses and decrease the number of active lesions on MRI head scans in controlled studies (both Beta 1a and Beta 1b types) (89). The proposed mechanism is an immune regulatory role (down regulation of CMI) by the interferon. Since interferon has known anti-viral properties, another explanation for the positive results could be an anti-viral effect on HHV-6. In our observations of MS patients with HHV-6 viremia, we have not seen a lower rate of positive HHV-6 blood cultures or higher NK function assay results in patients on either of the beta interferon preparations (unpublished data). However, this would not rule out an anti-viral effect of interferon, particularly a partial effect. Since the beta interferon studies included large numbers of patients, our observations in a small number of patients is likely too small of a sample to see a statistically significant difference. The anti-viral effects of the interferon preparations on HHV-6 have not been studied. Defining the effect of interferon on HHV-6 will be an important area of research. Intravenous gamma globulin has been given to both MS and CFS patients with improvement in clinical parameters, but results in the literature have varied (90, 91). Other immune modulators such as G-CSF and GM-CSF have not been studied.
Another immune modulator that may have substantial promise is transfer factor (TF). There are several reasons to consider TF. TF has consistently shown efficacy in the prevention and treatment of viral infections. Studies reporting efficacy of specific TF have been reported with HSV 1 and 2, VZV, EBV, and CMV (93, 94, 95, 96). TF has proven to be extremely safe with virtually no significant adverse effects (96). Since TF acts on CMI, this type of agent may improve the immune dysfunction that is a key feature of chronic active HHV-6 infection (97). Recent techniques obtaining TF from bovine colostrum provides a way to recover TF in large enough amounts for commercial preparation (98 ). We have done some preliminary studies in patients with CFS and chronic active HHV-6 infection using a TF preparation derived from bovine colostrum that has activity for HHV-6 included in its scope of TF activities. Albeit the data is still preliminary, this type of immune modulation appears to be very promising. We have seen significant symptom improvement, consistently negative HHV-6 blood cultures and marked improvement in NK function in patients taking this particular TF (unpublished data).
Another interesting treatment concept involves the use of anti-coagulants. Given the issue of activated coagulation pathways in these patients (endothelial cell tropism and vasculopathy), anti-coagulation may improve oxygen delivery and help with the symptoms that have been caused by a hypercoaguable state and fibrin deposition (99). One study has demonstrated symptom improvements in CFS patients treated with heparin (99). Several studies have shown that herpes viruses attach to cell surfaces via heparan sulfate receptors and that exogenous heparin can block this interaction and viral infectivity (100, 101). Thus, heparin may have some antiviral properties for herpes viruses. Patients with hereditary hypercoaguable syndromes (thrombophilia or hypofibrinolysis) may be at further risk for substantial hypercoaguable related problems and require anticoagulation. One evolving concept involves blocking viral activation (antiviral agents or immune modulation such as TF) combined with anticoagulants (heparin or coumadin). A model for a hypercoaguable state in patients with active HHV-6 infection and possible management strategies of the patient with a hypercoaguable state and associated active HHV-6 infection are outlined in Table 2 and 3.