Dharam Ablashi

Dharam V. Ablashi, (b. 1931), DVM, MS, Dip. Bact. (Diploma in Bacteriology), Research Microbiologist, Head of DNA Viruses Section and Coordinator of DNA Viruses, National Cancer Institute.

He co-discovered HHV-6 in 1986, while working at the National Cancer Institute at National Institutes of Health and is the Scientific Director of the HHV-6 Foundation and Chair of the Scientific Advisory Committee.

Ablashi co-founded the American Association of CFS with Orvalene Prewitt, in 1990. The organization has been renamed as the International Association for Chronic Fatigue Syndrome/Myalgic Encephalomyelitis with Ablashi serving as a past President of the Board of Directors from 2003-2004.

Awards

 * 2007, Rudy Perpich Senior Lectureship Award, presented to a distinguished CFS/FM scientist, physician or healthcare worker awarded by IACFS/ME
 * 2007, Achievement Award from New Jersey CFS Association Inc.

CFSAC Testimony

 * Written presentation at October 29, 2009:"It is imperative that the CDC study biopsy samples from the gut, and brain as well as heart tissues, and that they look at spinal fluid. Most of the studies done by the CDC have been on serum. However, many pathogens cannot be found in the serum because they do not circulate in the peripheral blood after the initial infection."

Open Letter to The Lancet
Two open letters to the editor of The Lancet urged the editor to commission a fully independent review of the PACE trial, which the journal had published in 2011. In 2016, Dr. Ablashi, along with 41 colleagues in the ME/CFS field, signed the second letter.
 * 10 February 2016, An open letter to The Lancet, again - Virology blog

Notable Studies

 * 2010, Serum Cytokine Levels in Postinfective Fatigue Syndrome FULL TEXT
 * 1996, Chronic Fatigue Syndrome (CFS): A Critical Evaluation of Testing for Active Human Herpesvirus-6 (HHV-6) Infection, Review of Data of 107 Cases"Abstract: 'Aim: To conduct a virologic study in patients with chronic fatigue syndrome (CFS, ICD-10: G 93.3) for identification of reactivated human herpesvirus-6 (HHV-6) infection. Patients and Method: One hundred seven patients (60 women, 47 men, f/m ratio: 1.27/1; age: between 7 and 76 years, medium 41.8 years) with clinical CFS were studied with follow-up periods from 10 months to 7.5 years. Patients were recruited for the study by answering a standard questionnaire and by matching the Holmes' criteria for CFS. This was followed by physical examination, conventional hematological and chemistry testing, lymphocyte phenotyping, and control of other immunologic parameters. Testing for HHV-6 infection included indirect immunofluorescence assays (IFA), antigen capture enzyme linked immunosorbent assay (antigen capture ELISA, ACE), nested polymerase chain reaction (nPCR) on peripheral blood cells, and virus isolation. Results: HHV-6 seroprevalence in CFS patients was 97%. Seventy-two percent of the CFS patients had elevated serum anti-HHV-6 IgG titers, but active HHV-6 infection was detected in only 38.6% of the cases as identified by ACE, nPCR, and virus isolation. In absence of anti-HHV-6-IgM, anti-HHV-6-IgG titers were less reliable for monitoring virus activity. Among other infections EBV was seen in 19.6% of the cases and, less frequently, HSV, Chlamydia, Campylobacter, coxsackie, CMV, Yersinia or Candida. In 46% of the patients there were evident signs of immune deficiency. In additional 20% evidence was less clear (e.g., decreased lymphocyte stimulation: PHA/ConA 46%; low NK cell levels: 35%; and low CD4/CD8 cell ratio: 21%). Conclusion: Active HHV-6 infection was prevalent in one third of our CFS patients, much less than expected. Additional testing besides routine IFA is necessary for confirminig virus activity."
 * 1995, Viruses and Chronic Fatigue Syndrome "Abstract: 'Because of the sudden onset of 'flu-like' symptoms in he vast majority of cases, followed by persistent illness and fatigue over several years, bolh RNA (retroviruses) and DNA (herpesviruses and enteroviruses) viruses have been suspected to be implicated in the pathogenesis of CFS. In recent years, evidence of the association of some viruses wilh CFS has progressed, whereas, with some others it has weakened considerably. Thus far, no single virus has been found to be the causative agent of CFS. Reactivation, however, of latent virus or viruses could contribute to the symptomatology of CFS by damaging the immune system either directly or indirectly. In this report we have provided a comprehensive review of the status of research on viral agents which have been investigated for their role in the pathogenesis of CFS.'"
 * 1995, Long Term Improvements in Patients with Chronic Fatigue Syndrome Treated with Ampligen"Abstract: 'Fifteen patients who fit the CDC definition of chronic fatigue syndrome (CFS) and had evidence of severe reduction in performance levels by low Karnofsky performance scores (KPS) of 20-60 were treated with Ampligen. At baseline most patients showed evidence of cerebral dysfunction by neuropsychological testing, were antigen positive by cell culture assay for human herpesvirus-6 (HHV-6), and displayed reduced performance during exercise tolerance testing, as measured by oxygen consumption. These patients represented a subset of CFS patients with especially severe and sustained symptomatology. Following 1248 weeks of Ampligen therapy, sustained improvements were noted in KPS (p < 0.01). Cognitive function improved including IQ and memory. Oxygen uptake and treadmill duration during exercise tolerance testing was also improved after 24 weeks of treatment (p < 0.01). Reduction in HHV-6 expression as measured by the giant cell assay was significant (p < 0.001). Patients continued to show significant improvement late in therapy, taking 8 to 12 weeks as baseline. It was concluded that while receiving Ampligen, the severely afflicted patients studied here derived long-lasting clinical benefit from the Ampligen therapy.'"
 * 1994, Ampligen inhibits human herpesvirus-6 in vitro."Abstract: 'The recently discovered human herpesvirus-6 (HHV-6) is being associated with an increasing number of conditions in which there is evidence of immunologic dysfunction. A number of widely available antiviral agents have shown little or no activity against the virus. We found that Ampligen [Poly (1): Poly (C12U), a synthetic, mismatched, double-stranded RNA, has potent, previously unexpected antiviral effects. Cells known to allow replication of HHV-6 were infected with the virus and treated with Ampligen under various conditions. When cells were pretreated with Ampligen (concentrations of 100 or 200 micrograms/ml) prior to infection or treated shortly after infection, viral replication was inhibited by 46-98%. At 100 and 200 micrograms/ml, Ampligen also inhibited the DNA polymerase activity of HHV-6 by 42-98%. When lower concentrations of Ampligen (10 and 50 micrograms/ml) were used, only pretreatment of cells, with Ampligen, followed by virus infection and carrying the infected cells with Ampligen, significantly inhibited HHV-6 infection (83.7 and 89.1% respectively). Indirect evidence suggests that Ampligen may inhibit viral attachment to cellular receptors and/or inhibit intracellular maturation of the virus. The above concentrations of Ampligen were not toxic to the cells used in the study. Given these in vitro findings, and the low frequency of toxicity reported with the use of Ampligen, clinical trials of this drug in patients with evidence of reactivated HHV-6 infection would seem to be warranted.'"
 * 1992, A chronic illness characterized by fatigue, neurologic and immunologic disorders, and active human herpesvirus type 6 infection

Learn More

 * HHV-6 Foundation Website