aocalypse

Wednesday, October 29, 2014

Lipkin's anellovirus findings in CFS may just be more evidence that AIDS and CFS are part of the same epidemic

Lipkin, Anellovirus and CFS:
The Anellovirus was found in 75% of ME cases and evidence of Retroviruses were found in 85% of cases, in research conducted by Dr. Hornig and Dr. Lipkins study in September 2013.
http://www.cfs-ireland.com/diag/2.htm 

Anellovirus is found in a significant percentage of healthy controls as well. If Lipkin found a much higher viral load in ME/CFS patients this could be a very important finding because the Stanford study suggests that the anellovirus load is a good proxy for overall immune status.

Read more: The Lipkin Study, The Vagus Nerve Infection Hypothesis and HHV-6: Kristin Loomis of the HHV-6 Foundation Talks – Pt. I http://www.cortjohnson.org/blog/2014/01/09/lipkin-study-vagus-nerve-hhv-6-loomis-hhv-6-foundation/
Anellovirus is found in a significant percentage of healthy controls as well. If Lipkin found a much higher viral load in ME/CFS patients this could be a very important finding because the Stanford study suggests that the anellovirus load is a good proxy for overall immune status.

Read more: The Lipkin Study, The Vagus Nerve Infection Hypothesis and HHV-6: Kristin Loomis of the HHV-6 Foundation Talks – Pt. I http://www.cortjohnson.org/blog/2014/01/09/lipkin-study-vagus-nerve-hhv-6-loomis-hhv-6-foundation/
Anellovirus is found in a significant percentage of healthy controls as well. If Lipkin found a much higher viral load in ME/CFS patients this could be a very important finding because the Stanford study suggests that the anellovirus load is a good proxy for overall immune status.

Read more: The Lipkin Study, The Vagus Nerve Infection Hypothesis and HHV-6: Kristin Loomis of the HHV-6 Foundation Talks – Pt. I
http://www.cortjohnson.org/blog/2014/01/09/lipkin-study-vagus-nerve-hhv-6-loomis-hhv-6-foundation/
Anellovirus is found in a significant percentage of healthy controls as well. If Lipkin found a much higher viral load in ME/CFS patients this could be a very important finding because the Stanford study suggests that the anellovirus load is a good proxy for overall immune status.

Read more: The Lipkin Study, The Vagus Nerve Infection Hypothesis and HHV-6: Kristin Loomis of the HHV-6 Foundation Talks – Pt. I http://www.cortjohnson.org/blog/2014/01/09/lipkin-study-vagus-nerve-hhv-6-loomis-hhv-6-foundation/
Anellovirus and AIDS:
"We compared the plasma viromes of HIV-infected subjects with low versus high CD4+ T cell counts from the United States and Uganda by using deep sequencing and detected HIV, hepatitis C virus, hepatitis B virus, GB virus C, anellovirus, and human endogenous retrovirus (HERV) reads. An increase in the proportion of reads for anelloviruses, a family of highly prevalent and genetically diverse human viruses, was seen in subjects with AIDS from both countries. The proportion of endogenous human retrovirus reads was increased in AIDS subjects from Uganda but not the United States. Progression to AIDS is therefore associated with changes in the plasma concentration of commensal viruses."
 http://jvi.asm.org/content/87/19/10912.full

Anellovirus and Pigs
 Anelloviruses are small, single-stranded, circular DNA viruses that infect a wide range of animal species, from humans to domestic animals, including pigs (13, 34). Most recently, all human and other animal anelloviruses have been assigned to a newly established family, Anelloviridae, that includes nine genera (3). 

Human and porcine anelloviruses have the same genomic structure, which consists of at least four presumed open readingframes (ORFs), ORF1, ORF2, ORF1/1, and ORF2/2, as well as a short stretch with high GC content in the untranslated region (UTR) (5, 16, 36, 38).
 http://jvi.asm.org/content/86/11/6042.full

Do White Matter Integrity Issues Also Link AIDS to CFS and HHV-6?

Clinical contributors to cerebral white matter integrity in HIV-infected individuals.

 http://www.ncbi.nlm.nih.gov/pubmed/21965122

 

 "It seems wherever HHV-6 is going, you're bound to bump into HIV. It's like a cohabitation." --Robert Gallo http://www.aegis.com/news/newsday/1992/ND920206.html

cartoon, brain, hhv-6, egg

 

 

Damage to the anterior arcuate fasciculus predicts non-fluent speech production in aphasia

http://www.bioportfolio.com/resources/pmarticle/688740/Damage-to-the-anterior-arcuate-fasciculus-predicts-non-fluent-speech-production-in.html
cartoon, hhv-6, arcuate fasculitis, infection, hhv-7,

Findings of brain anomalies may shed light on chronic fatigue (Caused by HHV-6???)

 Radiology researchers have discovered that the brains of patients with chronic fatigue syndrome have diminished white matter and white matter abnormalities in the right hemisphere.

Three key findings

The analysis yielded three noteworthy results, the researchers said. First, an MRI showed that overall white-matter content of CFS patients’ brains, compared with that of healthy subjects’ brains, was reduced. The term “white matter” largely denotes the long, cablelike nerve tracts carrying signals among broadly dispersed concentrations of “gray matter.” The latter areas specialize in processing information, and the former in conveying the information from one part of the brain to another.
That finding wasn’t entirely unexpected, Zeineh said. CFS is thought to involve chronic inflammation, quite possibly as a protracted immunological response to an as-yet unspecified viral infection. Inflammation, meanwhile, is known to take a particular toll on white matter.

But a second finding was entirely unexpected. Using an advanced imaging technique — diffusion-tensor imaging, which is especially suited to assessing the integrity of white matter — Zeineh and his colleagues identified a consistent abnormality in a particular part of a nerve tract in the right hemisphere of CFS patients’ brains. This tract, which connects two parts of the brain called the frontal lobe and temporal lobe, is called the right arcuate fasciculus, and in CFS patients it assumed an abnormal appearance.

Furthermore, there was a fairly strong correlation between the degree of abnormality in a CFS patient’s right arcuate fasciculus and the severity of the patient’s condition, as assessed by performance on a standard psychometric test used to evaluate fatigue.

 http://med.stanford.edu/news/all-news/2014/10/study-finds-brain-abnormalities-in-chronic-fatigue-patients.html


 "The first, using magnetic resonance imaging that looked at overall size of certain types of brain matter, found that so-called white matter areas were smaller in the brains of chronic fatigue patients than in healthy subjects."


"Unexpected, however, was the discovery of abnormalities in a tract of the brain called the arcuate fasciculus, which connects the frontal and temporal lobes. Zeineh’s team uncovered these abnormalities using a scanning technique that looks at water displacement in the brain.
In the brain’s left hemisphere, the arcuate fasciculus connects areas devoted to language production and comprehension. But the chronic fatigue study found abnormalities only in the right hemisphere, and scientists aren’t sure what that part of the brain does on the right side. The team also found that in areas of the brain that were connected by the arcuate fasciculus, the gray matter was thicker.
Both findings involving the arcuate fasciculus suggest that the tract may be hyperactive in chronic fatigue patients, Zeineh said. But he noted that he’s only able make guesses for now."

http://www.sfgate.com/health/article/Findings-of-brain-anomalies-may-shed-light-on-5851844.php


Right Arcuate Fasciculus Abnormality in Chronic Fatigue Syndrome

"Bilateral white matter atrophy is present in CFS. No differences in perfusion were noted. Right hemispheric increased FA may reflect degeneration of crossing fibers or strengthening of short-range fibers. Right anterior arcuate FA may serve as a biomarker for CFS."
 http://pubs.rsna.org/doi/abs/10.1148/radiol.14141079?journalCode=radiology&

 


HHV-6 in Multiple Sclerosis

"Multiple sclerosis (MS) is a chronic, inflammatory, demyelinating disease of the white matter in the human central nervous system (CNS). The origin of MS is still unclear despite the many epidemiological, immunological, and neurological studies that have been conducted. Viruses have long been proposed to be either initiating factors for, or directly pathogenic in, the development of MS. These viruses may play a role both at the onset of the disease and during it and may trigger the exacerbations that are commonly seen with relapsing-remitting multiple sclerosis (RRMS). Although an etiological correlation has not been definitively proven, during the past few years many studies have focused on the relationship between human herpesvirus 6 (HHV-6) and MS. The virus is widely prevalent in the human population, and primary infection usually takes place in the first years of life. However, HHV-6 reactivates under certain conditions, and has been associated with RRMS and, specifically, with exacerbations. MS exacerbations (also known as a relapse, attack, or flare-up) cause new symptoms or the worsening of old symptoms. Relapses can be very mild or severe enough to interfere with a person’s ability to function on a day-to-day basis."
 http://www.coppelabs.com/about-hhv-6/hhv-6-in-ms

IN SEARCH OF HIV Analysis of the value of the tests used for 'HIV infection' By Fabio Franchi

http://www.virusmyth.com/aids/hiv/ffsearch.htm

Moronic AIDS Researchers Still Not Focused on HHV-6

http://aidsinfo.nih.gov/news/1508/nih-led-study-explores-prevention-of-heart-disease-in-hiv-infected-people

cartoon, hhv-6, clowns, cdc, nih, science



"Is there a danger, in molecular biology, that the accumulation of data will get so far ahead of its assimilation into a conceptual framework that the data will eventually prove an encumbrance? Part of the trouble is that excitement of the chase leaves little time for reflection. And there are grants for producing data, but hardly any for standing back in contemplation".
-- John Maddox Finding wood among the trees. Nature 1988; 335:11. 
http://www.virusmyth.com/aids/hiv/ffsearch.htm

"The most consistently reported syndrome associated with HHV-6 infection among transplant patients is encephalitis. Patients can have mental status changes, behavioral disturbance, memory loss, and seizures. Other manifestations of HHV-6 in this patient population include: fever and rash, hepatitis, gastro-duodenitis, colitis, pneumonitis, and encephalitis. "

http://washuid.blogspot.com/

Tuesday, October 28, 2014

(HHV-6/7 & EBV) Viral load and T-helper-1-cell cytokines in myalgic encephalomyelitis

 "Objectives: Myalgic encephalomyelitis (ME) is a polymorphic clinical entity. In some patients, chronic infection with Epstein–Barr virus (EBV), human herpesvirus 6 (HHV-6), and human herpesvirus 7 (HHV-7) is regarded as an important pathogenetic factor that contributes to chronic neuroinflammation. We determined a relationship between EBV, HHV-6 and HHV-7 viral load in the saliva and serum levels of pro-inflammatory cytokines (IFNalpha, IFNgamma, IL-1, IL-2) in a group of ME patients."

http://www.jni-journal.com/article/S0165-5728%2814%2900441-X/abstract

HHV-6-HERV-K18 as the Cause/Trigger (Whatever You Want To Call It) of Serious Digestive Disorders in AIDS/CFS/etc.

Human herpesvirus 6B infection of the large intestine of patients with diarrhea.

http://www.ncbi.nlm.nih.gov/pubmed/12491213

Colitis in a renal transplant patient with human herpesvirus-6 infection.

http://www.ncbi.nlm.nih.gov/pubmed/17116137 

Case report: severe gastrointestinal inflammation and persistent HHV-6B infection in a paediatric cancer patient.

 http://www.ncbi.nlm.nih.gov/pubmed/17939902

Case report: human herpesvirus 6 reactivation associated with colitis in a lung transplant recipient.

 http://www.ncbi.nlm.nih.gov/pubmed/18712834

HHV-6B is frequently found in the gastrointestinal tract in kidney transplantation patients.

http://www.ncbi.nlm.nih.gov/pubmed/22616807

Possible interference of human beta-herpesviruses-6 and -7 in gastrointestinal cancer development.

http://www.ncbi.nlm.nih.gov/pubmed/23828382

 

HHV-6 antigen and HHV-6 DNA expression in sporadic adenomatous polyps of the colon. 

http://www.ncbi.nlm.nih.gov/pubmed/24099308

 

Detection and quantification of EBV, HHV-6 and CMV DNA in the gastrointestinal tract of HIV-positive patients.

 http://www.ncbi.nlm.nih.gov/pubmed/25326253

 

Monday, October 27, 2014

The search for the cause of CFS

CFS, cartoon, HHV-6, chronic fatigue syndrome, medical

Most ironic quote of our time

"His biggest fear was that he had ME (chronic fatigue syndrome) so he was amazed when they said it was leukaemia.”
http://www.examiner.co.uk/news/west-yorkshire-news/lasting-legacy-brave-examiner-journalist-8003730

HHV-6 and Natural Killer Cells




P.P. Banerjee on IFN-gamma-Dependent Demyelinating Activity by Natural Killer Cells is Regulated by HLA-G Upregulation on Oligodendrocytes During HHV-6 Infection.

HHV-6 Modulates Natural Killer Cells Via IL-15 Production

HHV-7 and Natural Killer Cells
The Human Herpesvirus-7 (HHV-7) U21 Immunoevasin Subverts NK-Mediated Cytoxicity through Modulation of MICA and MICB
Christine L. Schneider and Amy W. Hudson
Abstract
Herpesviruses have evolved numerous immune evasion strategies to facilitate establishment of lifelong persistent infections. Many herpesviruses encode gene products devoted to preventing viral antigen presentation as a means of escaping detection by cytotoxic T lymphocytes. The human herpesvirus-7 (HHV-7) U21 gene product, for example, is an immunoevasin that binds to class I major histocompatibility complex molecules and redirects them to the lysosomal compartment. Virus infection can also induce the upregulation of surface ligands that activate NK cells. Accordingly, the herpesviruses have evolved a diverse array of mechanisms to prevent NK cell engagement of NK-activating ligands on virus-infected cells. Here we demonstrate that the HHV-7 U21 gene product interferes with NK recognition. U21 can bind to the NK activating ligand ULBP1 and reroute it to the lysosomal compartment. In addition, U21 downregulates the surface expression of the NK activating ligands MICA and MICB, resulting in a reduction in NK-mediated cytotoxicity. These results suggest that this single viral protein may interfere both with CTL-mediated recognition through the downregulation of class I MHC molecules as well as NK-mediated recognition through downregulation of NK activating ligands.

The Human Herpesvirus-7 (HHV-7) U21 Immunoevasin Subverts NK-Mediated Cytoxicity through Modulation of MICA and MICB
Christine L. Schneider, Amy W. Hudson
Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America
Abstract
Herpesviruses have evolved numerous immune evasion strategies to facilitate establishment of lifelong persistent infections. Many herpesviruses encode gene products devoted to preventing viral antigen presentation as a means of escaping detection by cytotoxic T lymphocytes. The human herpesvirus-7 (HHV-7) U21 gene product, for example, is an immunoevasin that binds to class I major histocompatibility complex molecules and redirects them to the lysosomal compartment. Virus infection can also induce the upregulation of surface ligands that activate NK cells. Accordingly, the herpesviruses have evolved a diverse array of mechanisms to prevent NK cell engagement of NK-activating ligands on virus-infected cells. Here we demonstrate that the HHV-7 U21 gene product interferes with NK recognition. U21 can bind to the NK activating ligand ULBP1 and reroute it to the lysosomal compartment. In addition, U21 downregulates the surface expression of the NK activating ligands MICA and MICB, resulting in a reduction in NK-mediated cytotoxicity. These results suggest that this single viral protein may interfere both with CTL-mediated recognition through the downregulation of class I MHC molecules as well as NK-mediated recognition through downregulation of NK activating ligands.

Friday, October 24, 2014

One thing you'll never see Tony Fauci doing with a HHV-6/CFS patient

http://www.vox.com/2014/10/24/7059743/why-is-ebola-virus-outbreak-american-africa-nina-pham

Detection and quantification of EBV, HHV-6 and CMV DNA in the gastrointestinal tract of HIV-positive patients

"Falasca F, et al. – In the present study, the detection rate and viral load of Epstein Barr virus (EBV), HHV–6 and Cytomegalovirus (CMV) were assessed in the GI tract of human immunodeficiency virus (HIV) positive patients and of uninfected patients. Therefore, the data suggest that the HIV infection status may increase the persistence of these viruses in the GI compartment. Intriguingly, CMV DNA was undetectable in all biopsy specimens analyzed."
http://www.mdlinx.com/infectious-disease/news-article.cfm/5664495/?xml

Thursday, October 23, 2014

HHV-6 and Glioblastoma

 

What is a glioblastoma and how is it treated?

 

http://www.cduma.com/blog/what-is-a-glioblastoma-and-how-is-it-treated/

Glioblastoma risk factors:
Like most tumors, there is no known cause of brain tumors like glioblastomas, however, some people believe there is a link between alcohol consumption, ionizing radiation, and the viruses HHV-6, SV40, and cytomegalovirus. More common risk factors include:
  • Age, particularly for those over 50
  • Gender, with a slight skew towards men than women.
  • Being diagnosed with a low-grade astrocytoma (brain tumor), which can develop into a higher-grade tumor.
  • If you are Caucasian, Hispanic, or asian.
  • Having a diagnosis of neurofibromatosis, Von Hippel-Lindau disease, Turcot syndrome, tuberous sclerosis, or Li-Fraumeni syndrome

GASTROINTESTINAL HHV-6 INFECTION IN KIDNEY TRANSPLANTATION PATIENTS AND PATIENTS WITH END-STAGE KIDNEY DISEASE COMPLICATIONS - INFECTIONS

http://65.54.113.26/Publication/29710825/gastrointestinal-hhv-6-infection-in-kidney-transplantation-patients-and-patients-with-end-stage

Sunday, October 19, 2014

Is there, in all likelihood, an undetected epidemic of *internal* Kaposi's sarcoma in Chronic Fatigue Syndrome patients?

http://www.name-us.org/ResearchPages/ResearchArticlesAbstracts/ImmuneArticles/Levine2001SpinalFluid%20infectAbs.pdf

HHV-8 and Chronic Fatigue Syndrome


Prevalence in the cerebrospinal fluid of the following infectious agents in a cohort of 12 CFS subjects: human herpes virus-6 and 8; chlamydia species; mycoplasma species; EBV; CMV; and Coxsackievirus.

Levine, S. Journal of Chronic Fatigue Syndrome, 2001, 9, 1/2, 41-51.
Abstract: Over the last decade a wide variety of infectious agents have been associated with the CFS as potential etiologies for this disorder. Many of these agents are neurotrophic and have been linked previously to other diseases involving the central nervous system (CNS). Human herpes virus-6 (HHV-6), especially the B variant, has been found in autopsy specimens of patients who suffered from MS. Because patients with CFS manifest a wide range of symptoms involving the CNS as shown by abnormalities on brain MRIs, SPECT scans of the brain and results of tilt table testing we sought to determine the prevalence of HHV-6, HHV-8, Epstein-Barr Virus (EBV), cytomegalovirus (CMV), mycoplasma species, chlamydia species, and Coxsackie virus in the spinal fluid of a group of 12 patients with CFS (CDC criteria '94).
We found evidence of HHV-6, HHV-8, chlamydia species, CMV and Coxsackie virus in 6/12 samples. Plasma tests were negative. It was surprising to obtain such a relatively high yield of infectious agents in cell free specimens of spinal fluid that had not been centrifuged. Future research in spinal fluid analysis, in addition to testing tissue samples by polymerase chain reaction (PCR) and other direct viral isolation techniques will be important in characterizing subpopulations of CFS patients, especially those with involvement of the CNS.
The low rate of isolation of HHV-6 may be related to the lack of gross neurological findings in the patients at the time of testing.

Kaposi's sarcoma-associated herpesvirus (HHV-8)

http://en.wikipedia.org/wiki/Kaposi%27s_sarcoma-associated_herpesvirus

Human herpesvirus-6A/B binds to spermatozoa acrosome and is the most prevalent herpesvirus in semen from sperm donors.

 http://www.ncbi.nlm.nih.gov/pubmed/23144982

PLoS One. 2012;7(11):e48810. doi: 10.1371/journal.pone.0048810. Epub 2012 Nov 7.

Abstract

An analysis of all known human herpesviruses has not previously been reported on sperm from normal donors. Using an array-based detection method, we determined the cross-sectional frequency of human herpesviruses in semen from 198 Danish sperm donors. Fifty-five of the donors had at least one ejaculate that was positive for one or more human herpesvirus. Of these 27.3% (n = 15) had a double herpesvirus infection. If corrected for the presence of multiple ejaculates from some donors, the adjusted frequency of herpesviruses in semen was 27.2% with HSV-1 in 0.4%; HSV-2 in 0.1%; EBV in 6.3%; HCMV in 2.7%; HHV-6A/B in 13.5%; HHV-7 in 4.2%, whereas none of the samples had detectable VZV or HHV-8. Subsequently, we examined longitudinally data on ejaculates from 11 herpesvirus-positive donors. Serial analyses revealed that a donor who tested positive for herpesvirus at one time point did not necessarily remain positive over time. For the most frequently found herpesvirus, HHV-6A/B, we examined its association with sperm. For HHV-6A/B PCR-positive semen samples, HHV-6A/B could be detected on the sperm by flow cytometry. Conversely, PCR-negative semen samples were negative by flow cytometry. HHV-6B was shown to associate with sperm within minutes in a concentration dependent manner. Confocal microscopy demonstrated that HHV-6B associated with the sperm head, but only to sperm with an intact acrosome. Taken together, our data suggest that HHV-6A/B could be transported to the uterus via binding to the sperm acrosome. Moreover, we find a 10 times higher frequency of HHV-7 in semen from healthy individuals than previously detected. Further research is required to determine the potential risk of using herpesvirus-positive donor semen. Longitudinally analyses of ejaculate series indicate that implementation of quarantine for a donor shown to shed a herpesvirus is not a tenable solution.

Monday, October 13, 2014

cdc, cfs, chronic fatigue syndrome, cartoon, epidemiology

Ad Blames GOP Budget Cuts For Ebola Outbreak

Defreitas, CFS and HHV-6-induced HERV-K18: Putting it all together

Connecting all of these may ultimately explain the retroviral involvement in CFS (as well as HIV-positive and HIV-negative AIDS).


Konnie Knox was looking into the HTLV connection to HHV-6:
The goals of the proposed studies are:
  • to use contemporary molecular diagnostic techniques in an attempt to confirm the findings of Dr. DeFreitas with respect to the presence of HTLV-2 DNA sequences in the white blood cells of patients with CFS
  • To correlate the presence of HTLV-2 DNA sequences with the presence of active infections with human herpesvirus six (HHV-6) or Epstein-Barr virus (EBV), two viruses that have been implicated in CFS

Role of the Human Endogenous Retrovirus HERV-K18 in Autoimmune Disease Susceptibility: Study in the Spanish Population and Meta-Analysis 

Conclusion

Association of the HERV-K18.3 haplotype in chromosome 1 with autoimmune-disease susceptibility was confirmed through meta-analysis.
 http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0062090


HHV-6A infection induces expression of HERV-K18-encoded superantigen.

CONCLUSION:

These results imply that HHV-6A, either in latent form or during acute infection, directly transactivates HERV-K18. This HERV-K18 induction may be mediated through IFN-alpha that is produced by the HHV-6A-infected cells. The functional implications of superantigen expression are discussed.
 http://www.ncbi.nlm.nih.gov/pubmed/19505843

Friday, October 10, 2014

Mollaret's meningitis due to human herpesvirus 6 in an adolescent

"We report the first pediatric case of Mollaret meningitis in an adolescent female with acute lymphoblastic leukemia in remission. This patient had signs and symptoms consistent with meningitis, with three episodes over a 3-month period. Human herpesvirus 6 (HHV-6) was identified during her last episode from polymerase chain reaction assay of a cerebrospinal fluid specimen. She was treated successfully with foscarnet, after which HHV-6 was undetectable in her cerebrospinal fluid."
https://www.readbyqxmd.com/read/17041177

Serum cytokines in patients with moderate and severe Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME)

http://www.sciencedirect.com/science/article/pii/S1043466614002919

Wednesday, October 08, 2014

Use of anti HHV-6 transfer factor for the treatment of two patients with chronic fatigue syndrome (CFS). Two case reports.

http://www.ncbi.nlm.nih.gov/pubmed/8993763



A show-stopping Gallo flashback

"Another way of doing it would be to find an animal model not infected with a parallel virus to HHV-6 which can be infected by SIV [simian immunodeficiency virus]. SIV can induce some immune deficiency not the acute sort but there are monkeys in which SIV induces nothing, there are monkeys in which some strains of SIV induce an acute AIDS, and there are monkeys where some strains of SIV induce a disease more similar to the human disease, where it takes time. We used such a system. This is not published data. With the SIV alone, there was a little immune deficiency, and with the HHV-6 alone nothing, but with the two together they got it. I think we have proven the point with that rhesus virus and that we can publish that soon. So, I believe human herpesvirus-6 is a factor in AIDS progression"
http://history.nih.gov/NIHInOwnWords/docs/gallo3_01.html

Gallo on HHV-6

Here's what Robert Gallo had to say about HHV-6 in an NIH interview in 1995:

Have we ever argued for a possible cofactor? Yes, with the qualification I just told you, that it is obvious that some things will promote progression and some things will inhibit progression. One of those things may be the genetics of me versus you. We can say dose is a factor that can lead to progression, or lack of it, and at a greater or lesser rate. But we have argued for certain herpesviruses as possibly being a factor in promoting AIDS progression. Several groups have argued for cytomegalovirus because it does do things and it does activate more HIV in some subtle settings.
In the middle of the 1980s, we became aware that the lymphomas that were associated with HIV infection were perhaps one-third of the time EBV-positive. Epstein-Barr virus, as you know, can immortalize some B cells and, when you have EBV-positive lymphomas, generally they are the kind of lymphomas that, more or less... If they do not require EBV, EBV makes the probability of getting a lymphoma much greater, because the cell cannot die easily. It is immortalized. Other genetic events are needed to develop the lymphoma, but the immortalization of the cell is perhaps a key factor that makes it probable that it will be an EBV-containing cell that is the one that will become a lymphoma.
What about the two-thirds of lymphomas in HIV-infected persons that were not EBV-positive? We wondered if there were herpesviruses yet to be discovered. We looked in the B-cell lymphomas of patients with AIDS who were negative for EBV and we discovered the first new herpesvirus in 25 years, and the first herpesvirus of man that targeted predominantly the T cell.
We had a new herpesvirus, but it was not involved in the lymphoma, at least not as far as anybody knows, even today. We even misnamed it. We called it HBLV, because we found it in a B-cell lymphoma. Then we studied it more intensively and determined that it primarily infected T cells, not B cells, which was an unexpected finding. We learned that it killed T cells when it replicated. Then we learned that it infected natural killer cells and, when it did so, it made those cells attack other natural killer cells. We learned that it could infect the same cell as HIV and activate HIV expression. Next we learned that it infected CD8 cells and activated the gene for CD4, the only known biological agent I am aware of that activates the gene for CD4. Now, the CD4+/CD8+ cells could be targets for HIV.
It was at that stage we proposed that the herpesvirus might be a cofactor for progression of AIDS. It was then that I started to be careful of the use of these words and called it a catalyst for progression, that is, a nonessential cofactor, but something that makes disease progression go faster and also makes it more probable that immune deficiency will develop.
We put that idea out and it got a little bit of a reception by [Dr. Larry] Corey in Seattle, and by [Dr. Donald] Don Carrigan at Wisconsin. But then [Dr. Harold] Jaffe published a paper, the data of which we already had in hand. I think that paper by Jaffe and his colleagues at the CDC [Centers for Disease Control and Prevention] was not a sophisticated look at the problem. Namely, they said, Look, everybody has antibody, so how can it be a factor in progression? That is like saying a cytokine like TNF [tumor necrosis factor] is not important in disease pathogenesis because everybody has it. The question is, if 90 percent of the human population has it, they also have EBV, but EBV can cause Burkitt's lymphoma under certain settings. The question is, does it get activated in an immune-suppressed individual?
We put the problem aside for a while because we did not have a quantitative assay to measure the amount of herpesvirus; only this antibody that indicated a previous exposure to the virus, which everybody showed. We argued, however, when we presented it, that we needed to have a quantitative assay for virus in blood and the amount of human herpesvirus-6 [HHV-6] DNA in lymphocytes circulating around.
At this time we learned of Carrigan's work. He reported in a few clinical papers, that sometimes in immune-suppressed people, following transplantations, he saw an enormous amount of human herpesvirus-6 replication and that he believed it was responsible for some of the bone marrow abnormalities in such people. He showed a lot of virus in bone marrow. Second, he pointed out and emphasized that interstitial pneumonia is the cause of death in 10 percent of the deaths of HIV-positive people. No one knows the cause of that interstitial pneumonia, and he found the lungs of those who died loaded with human HHV-6. He presented at our laboratory meeting that he thought it was very likely that HHV-6 was the cause of those deaths.
Meanwhile, before this, Japanese workers had shown that HHV-6 was the cause of roseola infantum, also known as exanthem subitum, a disease of infants, with fever and rash, but usually with not much more.
So now what is new? I have discussed with my colleague [Dr.] Paolo Russo that the only way we are going to get any proof of this, or get stronger support, is if we get a specific inhibitor that does not inhibit HIV, inhibits HHV-6, and as far as we know does not inhibit anything else, is relatively non-toxic, and then show that patients do better rather than worse.
Another way of doing it would be to find an animal model not infected with a parallel virus to HHV-6 which can be infected by SIV [simian immunodeficiency virus]. SIV can induce some immune deficiency not the acute sort but there are monkeys in which SIV induces nothing, there are monkeys in which some strains of SIV induce an acute AIDS, and there are monkeys where some strains of SIV induce a disease more similar to the human disease, where it takes time.
We used such a system. This is not published data. With the SIV alone, there was a little immune deficiency, and with the HHV-6 alone nothing, but with the two together they got it. I think we have proven the point with that rhesus virus and that we can publish that soon. So, I believe human herpesvirus-6 is a factor in AIDS progression.
http://history.nih.gov/NIHInOwnWords/docs/gallo3_01.html

Dr. Konstance Knox explains why HHV-6 may be the key to dealing with AIDS.

by Neenyah Ostrom
New York Native, issue #678, April 15, 1996
Konstance Knox, Ph.D., is an HHV-6 researcher who has just published a study with extraordinary implications for AIDS research and treatment strategies. Along with colleague Donald R. Carrigan, Ph.D., Knox demonstrated that 100 percent of HIV-infected patients studied (ten out of ten) had active Human Herpes Virus 6 Variant A infections in their lymph nodes early in the course of their disease. Seventy-five percent of these patients, in fact, had CD4 cell counts higher than 200 (the cut-off for receiving a diagnosis of AIDS), up to as high a CD4 count as 700. This finding led Knox and Carrigan to conclude that "active HHV-6 infections appear relatively early in the course of HIV disease and in vitro studies suggest that the A variant of HHV-6 is capable of breaking HIV latency, with the potential for helping to catalyze the progression of HIV infection to AIDS." This new study, in other words, presents data further implicating HHV-6, particularly Variant A (HHV-6A), as a cofactor (at the very least) in the development of AIDS. (The report is "Active HHV-6 Infection in the Lymph Nodes of HIV Infected Patients: In Vitro Evidence That HHV-6 Can Break HIV Latency," published in the Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology," April 1, 1996.) Knox, who has a Ph.D. in Experimental Pathology from the Medical College of Wisconsin, is currently conducting cancer research in the Immunotherapy Program at St. Luke's Medical Center in Milwaukee, Wisconsin. She spoke to the Native on the day following publication of the new study.
Neenyah Ostrom: What is the bottom line, with respect to your new findings? Is it that Human Herpes Virus 6 (HHV-6) is present from the beginning of what we define as AIDS?
Dr. Konstance Knox: HHV-6 is present from very early in HIV infection. So we're not talking about waiting until people have opportunistic infections, and CD4 counts between 100 and 200. We're finding HHV-6 in the lymph nodes early-active infection; this virus is replicating. This is unheard of for any other opportunistic infection, even TB. The only opportunistic infections that you see in AIDS patients with CD4 counts above even 100 are TB and Herpes simplex and Herpes zoster. And all three of those, of course, also infect healthy people and cause disease. So, what we found, when we examined the lymph node biopsies of HIV-infected patients, was HHV-6. We found both variants of HHV-6-HHV-6A and HHV-6B-but the predominant virus was HHV-6A. And we're talking about finding the virus in lymph nodes of patients with CD4 counts of over 700. The mean CD4 count of 75 percent of the patients we examined was approximately 300. (There was a total of ten patients in this study just published, and we had CD4 counts on eight of them.) That's a unique finding. And one of the patients had a CD4 count of 711. So why is that virus, HHV-6A, there? My personal impression, because of where we find HHV-6A-we find a predominance of infection in the germinal center of the lymph node, which is where we know HIV hangs out-is that the tat protein of HIV stimulates HHV-6A replication. And in the study that we have just published, the one that came out yesterday [April 1], we showed that HHV-6A causes an increase in HIV production. These findings are not based solely on this one study. We have done subsequent studies, and there is another already-published study by Charles Wood from Miami also demonstrating that tat protein from HIV induced more HHV-6A production. So the theory-what seems reasonable to us-is, because these viruses hang out in the same place, and they infect the same cells, that it's not an accident that they co-localize-where you find HIV, you find HHV-6A. I think that there is a mutual enhancement and potentially almost a mutual dependency for efficient replication. My impression is that HIV kind of acts as a wet nurse to HHV-6A, because in all the other immunocompromised patients that we have looked at-and primarily, these are bone marrow transplant patients-we don't find the A variant of the virus. We don't find it, and the best guestimates of how many people are infected with type A-well, the numbers are sketchy. Because of the blood tests previously available, we only know about type B. You know, the classic numbers are that 90 percent of people by the age of two are infected with HHV-6. But that's the B variant, not the A variant. And the best estimate, up to about the age of 12, is that about five to 15 percent of people are infected with variant A. The epidemiology of HHV-6A infection has not been done. Now, it's kind of curious to me why the studies have not been done. You know, there's been a lot of sort of pooh-poohing about the role of HHV-6 in AIDS. I think that's because people look at it, and they say, well, everybody's infected with HHV-6 by the age of two. Yes, everybody's infected with the B variant. But we don't know how many people are infected with the A variant. We've just completed a study that we have submitted in which we examined 22 HIV-positive and AIDS patients. Every one of them has active replication of HHV-6A and it doesn't matter what stage of disease they're in, from frank AIDS, to autopsies, all the way up to people with CD4 cell counts of over 700. We believe there is a special interaction between HIV and HHV-6A.
N. Ostrom: How different are variants B and A from each other?
K. Knox: Do you mean biologically?
N. Ostrom: Yes. I've heard speculation that they should have been classified as two different viruses, or that, conversely, HHV-7 is no more different from the two HHV-6 variants than they are from each other.
K. Knox: HHV-7 is probably more akin to HHV-6B. There was an interesting study-and it was a PCR [polymerase chain reaction, i.e. "DNA amplification"] study-which basically showed that, if you were to analyze peripheral lymphocytes, you can find HHV-7 and HHV-6B in about 83 percent and 25 percent of healthy people, respectively. HHV-6A is found much, much less frequently. We're talking about a very small percent-five percent of people. HHV-6A is different. Probably a general rule of thumb is that HHV-6A can do everything that B can do, and more. And it's also much more destructive. It is a very destructive virus. It's more similar to what people think of when they think of a herpes virus. It is very lytic-it kills very well, and it destroys tissue very well. It can infect the brain, the lungs, the lymphoid organs, and the bone marrow. In all the dozens to hundreds of transplant patients we've looked at, if we find HHV-6 disease, it's variant B. We have only seen HHV-6A in, I think, five different individuals, from whom we've isolated it or stained it in tissues. These are not HIV-positive individuals. So, we found HHV-6A in five out of 100 or so patients. Four of those patients were dead. It is very destructive.
N. Ostrom: The question then becomes, in my mind, can HHV-6A do everything that HIV can do?
K. Knox: As far as immunologic damage? Oh, HHV-6A does it much more efficiently than HIV. And these are data from many people's laboratory studies, and that includes Paolo Lusso and Robert Gallo, as well as our own. Where we have seen HHV-6A in tissue, we see dead tissue. And where you see HIV-you know, you can have HIV alone, and you may see some reactive changes, like the immune system reacting to a viral infection as if you have flu or something like that. But you don't see dead tissue. You don't see destroyed organs and scar formation, and that's what you see when you see HHV-6A. We find replacement of the normal architecture of the lymph nodes with scar tissue. HHV-6A kills it. It kills the lymph node tissue. If I were to place my bets-I do think the viruses HIV and HHV-6A are interactive. I think one of the reasons why you almost always find both of them is that there are viral products, some of the gene products that they make, that enhance each other's replication. I think they're a team. And, when the two of them are present, they induce the production of more of each other. It's a mutually enhancing relationship. It's our feeling that if you could interrupt or limit or suppress the HHV-6A infection, the levels of HIV would go down tremendously and HIV would become just a chronic viral infection. And, potentially, the antiviral agents that are out there would be able to manage that. We don't have any evidence, looking in the tissue, that HIV is responsible for any of the destruction. And, if you think about it, HIV infects patients for years-a decade or more-without progressing to AIDS. When you look in their tissues, you have to ask how you can have such a long-term viral infection and have no damage? Then something seems to happen somewhere in their course of disease. In some people, it happens earlier; in some people, it happens later; and there's that small percentage of people in whom it never seems to happen at all. Our hypothesis would be that, if we were to look in the lymph nodes of the long-term non-progressors, we would not find HHV-6A.
N. Ostrom: Do you have plans to do that study?
K. Knox: Well, last December I contacted Giuseppe Pantaleo-he's with Tony Fauci's group [at the National Institutes of Health], who had published the New England Journal of Medicine paper just about a year ago on the progressors and long-term non-progressors and the difference in the lymphoid organs between the two. The basic difference is, in the non-progressors, even though they have replication-competent HIV, they don't have any evidence of degeneration or destruction of their tissue, even though HIV is there. So the hypothesis would be that those few percentage of HIV-infected patients that are long-term non-progressors don't have HHV-6A replicating in their lymph node tissues. Pantaleo has agreed to send us what the NIH has in the way of tissues from that study. Now, I've been waiting-you know, they had the furlough, and all this other kind of stuff. And then I met with Dr. Pantaleo, actually, about the middle of February, and he again reiterated that he would be sending those tissues to me. Thus, he has personally assured me, but, until I have the tissues, we can't do the direct test of the hypothesis.
N. Ostrom: Why can't we get more funding for this research?
K. Knox: Well, I don't know if you've been tracking the kinds of exposes that Science magazine and others have published, that 80 percent of AIDS research monies are retained within the federal government programs on AIDS research. I think the science is very inbred. And I think there's been a real resistance to entertaining hypotheses or directions of AIDS research that aren't looking specifically at HIV, and that is the basic problem. Our studies themselves have been enthusiastically received, but the funding hasn't followed. And that is funding through the federal agencies-like the NIH-and I think one of the things that has stopped that has been the confusion with HHV-6B. People think, well, if everybody's infected with HHV-6, why doesn't everybody have AIDS? Well, we're all infected with HHV-6B, but there's probably only a very small percentage of people infected with HHV-6A. And there's a very unique relationship between A and HIV-when we examine HHV-6B and HIV together, we don't see the same effects. They don't have the same interaction. So, we're talking about two different viruses, essentially, A and B. And people have merged the two into just HHV-6 and have not appreciated the biologic differences between the two viruses. And actually, in our own research, this has only been clarified in the last year. In our earlier studies, we only had reagents to look at HHV-6. We did not have the specific reagents to separate the two when we looked in the tissue; we could not tell if it was A or B. It's only been in the past year that we have developed the technologies to be able to distinguish between the two.
N. Ostrom: So you now have very reliable testing that will distinguish between Variant A and Variant B?
K. Knox: Yes.
N. Ostrom: Is it antibody testing, or DNA testing?
K. Knox: It is antibody testing. You could do both, but we use antibody testing.
N. Ostrom: And you test blood? Or do you look only at tissues?
K. Knox: We do tissue biopsies. We look in the tissue itself. And it is very difficult for people to dismiss the idea of HHV6-A because, frankly, nobody knows what the epidemiology is, how many healthy people are infected, how it's transmitted, those kinds of things. We don't know. And there is a unique kind of collaboration between HHV-6A and HIV that HHV-6B does not have. HHV-6B does cause disease. It kills immunocompromised patients. It kills transplant patients. But, with respect to AIDS and HIV infection, we believe that the A variant is what is important, because it has this special interaction with HIV. And variant A is in all the AIDS patients. You don't find it, even in other immunocompromised patients, like bone marrow transplant patients. There is something special about the interaction of the two viruses, HIV and HHV-6A.
N. Ostrom: Do you think they might have evolved together?
K. Knox: Actually, that is a very interesting thing to think about. Yes, I think that they have evolved together, and I think they really like hanging out together. There seems to be a selective advantage to the two viruses being in close proximity-and the tat protein of HIV is something HHV-6A seems to like. There's something that HHV-6A makes as well that, in our laboratories, gets HIV really revved up. If there's an advantage, viruses evolve together. If selective pressures are put on them, they will respond to make their environment more compatible. Viruses want to make more of themselves. They don't destroy things on purpose, because it's actually not to their advantage. It wouldn't surprise me, in their natural histories, if HHV-6A and HIV evolved together, because there's such an enhancement of the two viruses when they're together. Although in vitro (laboratory) studies published over the last eight or ten years have suggested a synergy between HIV and HHV-6A, in vivo (in the body) evidence has been lacking. Finally, we have examined the tissue of HIV-infected patients and asked, why do all these people have HHV-6A replicating in their tissues when they're still healthy, and we can't even find it in other immunocompromised patients? It's a very provocative finding. There's also a study you'll find interesting, that was performed by Italian researcher Dario Diluca, published in the Journal of Clinical Microbiology, I think. Dario has also been doing HHV-6A and HIV research. What he just published last summer is a PCR study of HHV-6 in Chronic Fatigue Syndrome patients. The unique finding concerned HHV-6A. Whereas you can find it in the peripheral lymphocytes of about four percent of healthy people, you see it in 22 percent of Chronic Fatigue Syndrome patients. There's no difference in the levels of HHV-7 and HHV-6B in healthy people and CFS patients, but the A variant was seen at four percent in healthy people and 22 percent in CFS patients, which is very significant.
N. Ostrom: In their natural killer cell paper, Lusso and Gallo showed that HHV-6 was infecting and killing NK cells in both AIDS and CFS patients. They identified the problem in both sets of patients, so it makes sense that HHV-6A would also be a problem in Chronic Fatigue Syndrome.
K. Knox: Yes, it's a very disregulating virus. Variant B is not benign, but variant A is especially destructive. This is not only when we look at tissues, but also in the test tube-variant A is especially destructive. Which antiviral drugs do you know have effectiveness against HHV6-A? We know that foscarnet does; we know that ganciclovir does; and we have treated patients with those agents. Actually, with foscarnet, we have treated specifically HHV-6A infections and seen very nice reversals of clinical syndromes. We don't always know which variant we're treating when we're treating HHV-6. Also, if you look in the literature, there are three major studies looking at acyclovir in AIDS patients. These were patients with CD4s of less than 150. There was one study in particular that I'm recollecting in which there were about 300 patients. They treated half with AZT alone, and half with AZT plus acyclovir. What they wanted to do was to look to see if acyclovir could suppress CMV reactivation. Well, what they found was that it had no effect on CMV infection, but there was a curious, significant prolongation of life in the patients who had AZT and acyclovir, as opposed to AZT alone. There are three major studies in the literature like that, and the speculation as to why that is? They don't know. And they don't address it, because they haven't got a clue as to why it might be. Now, we have never treated HHV-6 infections with acyclovir, because the B variant of the virus is resistant, and that's usually the virus that we see in transplant patients. But in laboratory testing, HHV-6A is sensitive to acyclovir. So we have a curiosity as well. I mean, that would be pretty dandy, because certainly acyclovir has less toxicity than ganciclovir, and if you're talking about treating healthy people in a clinical trial, you're looking for something that people can take orally. You don't want them to have to come in for IV infusions, and foscarnet would require that. So I would say that acyclovir and its analogs and ganciclovir would be very interesting.
N. Ostrom: So, what you have discovered should be viewed as good news?
K. Knox: Oh, I think it's tremendously good news. I think it offers the best hope that we've seen in 15 years of this epidemic. That's because it's the first new approach. And the difference is that we believe that actually what destroys the immune organs, the lymph nodes, is HHV-6A. It is not HIV. HIV keeps it going, and HHV-6A keeps goosing HIV, and together they keep secreting products that each other love. They stroke each other. And that's a hard team to break up. You can't do it just by targeting HIV.
N. Ostrom: Is there anything else you'd like people to know about your research?
K Knox: Now that we've made the distinction between the two HHV-6 viruses, A and B, we're really hoping that funding is loosened up and the abuses of how AIDS research has been managed by the government agencies, by NIH-certainly, we've been caught in that trap. I just hope that they loosen up soon enough that we don't have to abort our program. And it's getting pretty close. It's pretty close. http://www.chronicillnet.org/online/Knox.html

Tuesday, October 07, 2014

Innate Immune Changes in the Peripheral Blood of Chronic Fatigue Syndrome Patients: Risk Factors for Disease Progression and Management

Authors:  (Deborah L.S Goetz, Judy A. Mikovits, Jamie Deckoff-Jones, Francis W. Ruscetti, LANDRES Management Consultant, MAR Consulting Inc., Private CFS Practice, and others)

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Breaking News

Co-Reactivation of Human Herpesvirus 6 (HHV-6) and Cytomegalovirus (CMV) is Associated with Worse Clinical Outcome in Critically Ill Immunocompetent Adults


The CDC's CFS Clown Car Act

http://www.washingtonpost.com/national/health-science/how-the-definition-of-chronic-fatigue-syndrome-keeps-changing/2014/10/06/def05db4-0d1c-11e4-b8e5-d0de80767fc2_story.html

http://www.washingtonpost.com/national/health-science/what-is-chronic-fatigue-syndrome-and-why-arent-we-doing-more-to-treat-the-illness/2014/10/06/4cfff312-d458-11e3-8a78-8fe50322a72c_story.html

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