| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
From the Centre of Virology (Drs. Steele and Garson), Department of Infection, University College London, and Department of Neurology (Dr. Al-Chalabi), Institute of Psychiatry, King’s College London, UK; and Department of Neurology (Drs. Cudkowicz and Brown, K. Ferrante), Massachusetts General Hospital, Boston, MA.
Address correspondence and reprint requests to Dr. J.A. Garson, Centre of Virology, University College London, Windeyer Institute, 46, Cleveland St., London, W1T 4JF, UK; e-mail: j.garson{at}ucl.ac.uk
Background: Retroviral involvement in the etiology of sporadic ALS has been suspected for several years since the recognition that both murine and human retroviruses can cause motor neuron disease–like syndromes. In a pilot study, an increased prevalence of a retroviral marker (reverse transcriptase [RT] activity) was demonstrated in the serum of British patients with ALS. The current investigation was designed to confirm and extend these findings in a geographically distinct patient cohort under blinded testing conditions.
Methods: A highly sensitive product-enhanced RT assay was employed to test coded sera obtained from 30 American patients with sporadic ALS and from 14 of their blood relatives, 16 of their spouses, and 28 nonrelated, nonspousal control subjects.
Results: Serum RT activity was detected in a higher proportion of ALS patients (47%) than in non-blood-related controls (18%; p = 0.008). The prevalence of RT activity in the serum of spousal controls (13%) was similar to that in other non-blood-related controls. Unexpectedly, the prevalence of serum RT activity in blood relatives of ALS patients (43%) approached that in the ALS patients themselves.
Conclusions: These results confirm that patients with ALS have a significantly higher prevalence of serum reverse transcriptase (RT) activity than that seen in unrelated control subjects. The finding of a similarly increased prevalence in blood relatives of ALS patients raises the possibility that the observed RT activity might be due to an inherited endogenous retrovirus.
See also page 410
Supported by Project A.L.S. (New York); and by the Angel Fund, National Institute for Neurologic Disease and Stroke, Al-Athel ALS Research Foundation, and ALS Association (R.H.B.). At the time of this work, Dr. Al-Chalabi was a Medical Research Council (UK) Clinician Scientist Fellow.
Received July 8, 2004. Accepted in final form October 1, 2004.
Related articles in Neurology:
This article has been cited by other articles:
|
|
 |
|
  A. L. McCormick, R. H. Brown Jr, M. E. Cudkowicz, A. Al-Chalabi, and J. A. Garson Quantification of reverse transcriptase in ALS and elimination of a novel retroviral candidate Neurology, January 22, 2008; 70(4): 278 - 283. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D.J.L. MacGowan, S. N. Scelsa, T. E. Imperato, K.-N Liu, P. Baron, and B. Polsky A controlled study of reverse transcriptase in serum and CSF of HIV-negative patients with ALS Neurology, May 29, 2007; 68(22): 1944 - 1946. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. G. Weisskopf, M. L. McCullough, N. Morozova, E. E. Calle, M. J. Thun, and A. Ascherio Prospective Study of Occupation and Amyotrophic Lateral Sclerosis Mortality Am. J. Epidemiol., December 15, 2005; 162(12): 1146 - 1152. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. Robberecht and B. Jubelt Reverse transcriptase takes ALS back to viruses Neurology, February 8, 2005; 64(3): 410 - 411. [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
