Anthony Komaroff

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Anthony L. Komaroff, MD, is an Internal Medicine physician and since 1993, a professor at Harvard Medical School in the United States, holding the title of the Steven P. Simcox, Patrick A. Clifford and James H. Higby Distinguished Professor of Medicine.[1][2]

He was quoted in a Rolling Stone article in 1987, written by Hillary Johnson, stating that he did not agree the illness was a "yuppie disease", which became the derogatory label that became commonly used later, Yuppie Flu.[3] He is featured in Ryan Prior's documentary, Forgotten Plague.

He served as past President of the Board of Directors of the International Association for Chronic Fatigue Syndrome/Myalgic Encephalomyelitis from 1991-1992.[4]


  • 1963 – 1967, M.D., University of Washington
  • 1959 – 1963, A.B., History, Pre-Med, Stanford University

Awards and Honors[edit]

  • 2001, Rudy Perpich Senior Lectureship Award, presented to a distinguished CFS/FM scientist, physician or healthcare worker awarded by IACFS/ME[5]
  • Fellow of the American Association for the Advancement of Science, the American College of Physicians, and the Association for Health Services Research.
  • Served on advisory committees for the U.S. Department of Health and Human Services, the Surgeon General of the United States, the Centers for Disease Control and Prevention, and the Institute of Medicine/National Academy of Sciences.
  • Member of the Scientific Advisory Board of the HHV-6 Foundation.[6]

Medscape Continuing Medicine Education[edit]


Notable studies[edit]

  • 2017, Fecal metagenomic profiles in subgroups of patients with myalgic encephalomyelitis/chronic fatigue syndrome (FULL TEXT)
    Abstract - Background: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is characterized by unexplained persistent fatigue, commonly accompanied by cognitive dysfunction, sleeping disturbances, orthostatic intolerance, fever, lymphadenopathy, and irritable bowel syndrome (IBS). The extent to which the gastrointestinal microbiome and peripheral inflammation are associated with ME/CFS remains unclear. We pursued rigorous clinical characterization, fecal bacterial metagenomics, and plasma immune molecule analyses in 50 ME/CFS patients and 50 healthy controls frequency-matched for age, sex, race/ethnicity, geographic site, and season of sampling. Results: Topological analysis revealed associations between IBS co-morbidity, body mass index, fecal bacterial composition, and bacterial metabolic pathways but not plasma immune molecules. IBS co-morbidity was the strongest driving factor in the separation of topological networks based on bacterial profiles and metabolic pathways. Predictive selection models based on bacterial profiles supported findings from topological analyses indicating that ME/CFS subgroups, defined by IBS status, could be distinguished from control subjects with high predictive accuracy. Bacterial taxa predictive of ME/CFS patients with IBS were distinct from taxa associated with ME/CFS patients without IBS. Increased abundance of unclassified Alistipes and decreased Faecalibacterium emerged as the top biomarkers of ME/CFS with IBS; while increased unclassified Bacteroides abundance and decreased Bacteroides vulgatus were the top biomarkers of ME/CFS without IBS. Despite findings of differences in bacterial taxa and metabolic pathways defining ME/CFS subgroups, decreased metabolic pathways associated with unsaturated fatty acid biosynthesis and increased atrazine degradation pathways were independent of IBS co-morbidity. Increased vitamin B6 biosynthesis/salvage and pyrimidine ribonucleoside degradation were the top metabolic pathways in ME/CFS without IBS as well as in the total ME/CFS cohort. In ME/CFS subgroups, symptom severity measures including pain, fatigue, and reduced motivation were correlated with the abundance of distinct bacterial taxa and metabolic pathways. Conclusions: Independent of IBS, ME/CFS is associated with dysbiosis and distinct bacterial metabolic disturbances that may influence disease severity. However, our findings indicate that dysbiotic features that are uniquely ME/CFS-associated may be masked by disturbances arising from the high prevalence of IBS co-morbidity in ME/CFS. These insights may enable more accurate diagnosis and lead to insights that inform the development of specific therapeutic strategies in ME/CFS subgroups.[8]
  • 2016, CDC Grand Rounds: Chronic Fatigue Syndrome — Advancing Research and Clinical Education. Morbidity and Mortality Weekly Report[9]
  • 2015, Findings from a clinical and laboratory database developed for discovery of pathogenic mechanisms in myalgic encephalomyelitis/chronic fatigue syndrome. Abstract[10]
  • 2015, Distinct plasma immune signatures in ME/CFS are present early in the course of illness FULL TEXT
    "Abstract: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is an unexplained incapacitating illness that may affect up to 4 million people in the United States alone. There are no validated laboratory tests for diagnosis or management despite global efforts to find biomarkers of disease. We considered the possibility that inability to identify such biomarkers reflected variations in diagnostic criteria and laboratory methods as well as the timing of sample collection during the course of the illness. Accordingly, we leveraged two large, multicenter cohort studies of ME/CFS to assess the relationship of immune signatures with diagnosis, illness duration, and other clinical variables. Controls were frequency-matched on key variables known to affect immune status, including season of sampling and geographic site, in addition to age and sex. We report here distinct alterations in plasma immune signatures early in the course of ME/CFS (n = 52) relative to healthy controls (n = 348) that are not present in subjects with longer duration of illness (n = 246). Analyses based on disease duration revealed that early ME/CFS cases had a prominent activation of both pro- and anti-inflammatory cytokines as well as dissociation of intercytokine regulatory networks. We found a stronger correlation of cytokine alterations with illness duration than with measures of illness severity, suggesting that the immunopathology of ME/CFS is not static. These findings have critical implications for discovery of interventional strategies and early diagnosis of ME/CFS."[11]
  • 2007, Changes in Functional Status in Chronic Fatigue Syndrome Over a Decade: Do Age and Gender Matter?
    "Abstract - Objective: Patients with chronic fatigue syndrome (CFS) have substantial deficits in functional capacity, but the course of these deficits over time has not often been studied. This study measured functional capacity on three occasions over a decade, in patients with CFS. Methods: The study was a longitudinal cohort study, and employed the Medical Outcomes Study Short Form-36 (SF-36) instrument to assess physical and mental/emotional functional status. Results: Physical function, as reflected in several different scales, improved modestly but significantly over time, particularly for patients aged 18-60 years and for women. Mental/emotional function was not substantially impaired at the outset of the study, and did not change over time. Conclusion: This study found that physical function tended to improve formany patients over time, despite the fact that they were aging. Physical function did not deteriorate with time."[12]
  • 2001, Increased Eosinophil Protein X Levels in Chronic Fatigue Syndrome
    "Abstract - Chronic fatigue syndrome is a condition of unknown etiology characterized by severe fatigue and accompanied by symptoms including cognitive difficulties, myalgias, and headaches. Studies of this illness have found chronic activation of the immune system, including one reporting elevated levels of eosinophil cationic protein, considered an eosinophil activation marker. The aim of this study was to measure serum levels of eosinophil protein X, a cationic protein not measured previously in this illness. Measurements are reported on serum samples from 29 patients meeting the Centers for Disease Control and Prevention criteria for chronic fatigue syndrome, and 30 healthy controls of similar age and gender. The median serum eosinophil protein X level in patients was higher than controls: 37.9 vs. 25.3μg/L (p = 0.037). Forty-eight percent of patients versus 23% of controls had levels above the normal range. The marked increase in serum levels of eosinophil protein X in chronic fatigue syndrome patients could reflect eosinophil activation in this illness."[13]
  • 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."[14]
  • 1992, A chronic illness characterized by fatigue, neurologic and immunologic disorders, and active human herpesvirus type 6 infection[15]

Talks & interviews[edit]

Online presence[edit]

Learn more[edit]

See also[edit]


  3. Journey Into Fear: Part Two
  8. Nagy-Szakal, Dorottya; Williams, Brent L.; Mishra, Nischay; Che, Xiaoyu; Lee, Bohyun; Bateman, Lucinda; Klimas, Nancy G.; Komaroff, Anthony L.; Levine, Susan; Montoya, Jose G.; Peterson, Daniel L.; Ramanan, Devi; Jain, Komal; Eddy, Meredith L.; Hornig, Mady; Lipkin, W. Ian (2017), "Fecal metagenomic profiles in subgroups of patients with myalgic encephalomyelitis/chronic fatigue syndrome", Microbiome, 5 (44), doi:10.1186/s40168-017-0261-y 
  9. Unger, ER; Lin, JS; Brimmer, DJ; Lapp, CW; Komaroff, AL; Nath, A; Laird, S; Iskander, J (2016), "CDC Grand Rounds: Chronic Fatigue Syndrome — Advancing Research and Clinical Education", Morbidity and Mortality Weekly Report, 65 (5051): 1434–1438, doi:10.15585/mmwr.mm655051a4 
  10. Klimas, N.G.; Ironson, G.; Carter, A.; Balbin, E.; Bateman, L.; Felsenstein, D.; Levine, S.; Peterson, D.; Chiu, K.; Allen, A.; Cunningham, K.; Gottschalk, C.G.; Fletcher, M; Hornig, M.; Canning, C.; Komaroff, A.L. (2015), "Findings from a clinical and laboratory database developed for discovery of pathogenic mechanisms in myalgic encephalomyelitis/chronic fatigue syndrome", Fatigue: Biomedicine, Health & Behavior, 3 (2): 75-96, doi:10.1080/21641846.2015.1023652 
  11. Hornig, M; Montoya, JG; Klimas, NG; Levine, SM; Felsenstein, D; Bateman, L; Peterson, DL; Gottschalk, CG; Schultz, AF; Che, X; Eddy, ML; Komaroff, AL; Lipkin, WI (2015), "Distinct plasma immune signatures in ME/CFS are present early in the course of illness", Science Advances, 1 (1), doi:10.1126/sciadv.1400121 
  12. Rosalind M. Matthews & Anthony L. Komaroff. (2007). Changes in Functional Status in Chronic Fatigue Syndrome Over a Decade: Do Age and Gender Matter? Journal of Chronic Fatigue Syndrome, Vol. 14, Iss. 1, pp. 33-42.
  13. Richard S. Schacterle, Fabrizio Conti, Laura Magrini, Anthony L. Komaroff & Guido Valesini. (2001). Increased Eosinophil Protein X Levels in Chronic Fatigue Syndrome. Journal of Chronic Fatigue Syndrome, Vol. 9, Iss. 1-2, pp. 21-30.
  14. Ablashi DV, Berneman ZN, Williams M, Strayer DR, Kramarsky B, Suhadolnik RJ, Reichenbach N, Hiltzges P, Komaroff AL. (1994). Ampligen inhibits human herpesvirus-6 in vitro. In Vivo, 8 (4):587-91. Retrieved from
  15. Buchwald, Dedra; Cheney, Paul R.; Peterson, Daniel L.; Henry, Berch; Wormsley, Susan B.; Geiger, Ann; Ablashi, Dharam V.; Salahuddin, S. Zaki; Saxinger, Carl; Biddle, Royce; Kikinis, Ron; Jolesz, Ferenc A.; Folks, Thomas; Balachandran, N.; Peter, James B.; Gallo, Robert C.; Komaroff, Anthony L. (1992), "A chronic illness characterized by fatigue, neurologic and immunologic disorders, and active human herpesvirus type 6 infection", Annals of Internal Medicine, 116 (2): 103-113, PMID 1309285 

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From MEpedia, a crowd-sourced encyclopedia of ME and CFS science and history