Absence of HTLV‐1 related sequences in MS from high prevalence areas in Western Norway

In Western Norway, long‐term follow up epidemiological studies have revealed significant increases in the incidence and prevalence rates of multiple sclerosis (MS) in stable populations, indicating the impact of exogenous factors. In this study 183 MS patients and 102 controls from high prevalence areas in Western Norway were investigated for human T‐lymphotropic virus type I (HTLV‐1) related sequences by polymerase chain reaction. Using primers targeting the gag, pol and env genes in the HTLV‐1 provirus genome, no amplification products were detected in the 183 MS patients or 102 controls. The results strongly suggest that neither HTLV‐1 nor a closely related retrovirus participate in the aetiology of MS.

[1]  Rice Gp.  Virus-induced demyelination in man: models for multiple sclerosis. , 1992 .

[2]  A. Sadovnick,et al.  Epidemiology and genetics of multiple sclerosis. , 1992, Current opinion in neurology and neurosurgery.

[3]  M. Giacca,et al.  Lack of detectable human T‐cell lymphotropic virus type I sequences in samples from multiple sclerosis patients , 1992, Journal of medical virology.

[4]  G. Rice.  Virus-induced demyelination in man: models for multiple sclerosis. , 1992, Current opinion in neurology and neurosurgery.

[5]  E. Wattel,et al.  No evidence of HTLV-I infection in French patients with multiple sclerosis using the polymerase chain reaction. , 1991, Journal of clinical pathology.

[6]  P. Rudge,et al.  Multiple sclerosis, tropical spastic paraparesis and HTLV-1 infection in Afro-Caribbean patients in the United Kingdom. , 1991, Journal of neurology, neurosurgery, and psychiatry.

[7]  L. Pease,et al.  Human T-cell lymphotropic virus type I sequences detected by nested polymerase chain reactions are not associated with multiple sclerosis. , 1991, Mayo Clinic proceedings.

[8]  T. Riise,et al.  Epidemiologic trends in multiple sclerosis in Møre and Romsdal, Norway , 1991, Neurology.

[9]  D. Gambi,et al.  Amplifications of multiple regions of the HTLV-I genome from DNA of an Italian spastic paraparesis patient but not from DNA of multiple sclerosis patients , 1991, Journal of the Neurological Sciences.

[10]  H. Hansen,et al.  Just another dubious virus in cells from a patient with multiple sclerosis? , 1991, The Lancet.

[11]  C. Geny,et al.  Isolation of retrovirus from patients with multiple sclerosis , 1991, The Lancet.

[12]  T. Waldmann,et al.  Multiple sclerosis, retroviruses, and PCR , 1991, Neurology.

[13]  R. Murray,et al.  Multiple sclerosis, human T‐lymphotropic virus type I, and human endogenous retrovirus sequences , 1991, Annals of neurology.

[14]  P. Lebon,et al.  Analysis of retroviral sequences in the spinal form of multiple sclerosis , 1991, Annals of neurology.

[15]  T. Miyatake,et al.  Absence of highly homologous sequence to HTLV‐I in Japanese multiple sclerosis , 1991, Neurology.

[16]  T. Riise,et al.  Incidence of multiple sclerosis in Hordaland, western Norway: a fluctuating pattern. , 1991, Neuroepidemiology.

[17]  J. Olesen,et al.  Absence of HTLV-I DNA in blood from patients with multiple sclerosis. , 1990, AIDS research and human retroviruses.

[18]  J. Merrill,et al.  Failure to detect human T-cell leukemia virus-related sequences in multiple sclerosis blood. , 1990, Archives of neurology.

[19]  J. Féher,et al.  No evidence for human T-cell leukemia virus type I or human T-cell leukemia virus type II infection in patients with multiple sclerosis. , 1990, Archives of neurology.

[20]  L. Steinman,et al.  HTLV‐I sequences are not detected in peripheral blood genomic DNA or in brain cDNA of multiple sclerosis patients , 1990, Annals of neurology.

[21]  G. Rice,et al.  Retroviruses and multiple sclerosis. II. , 1990, Neurology.

[22]  L. Fugger,et al.  Failure to demonstrate human T cell lymphotropic virus type I in multiple sclerosis patients. , 1990, The Journal of general virology.

[23]  R. Moriuchi,et al.  Amplification of HTLV‐1‐related Sequences among Patients with Neurological Disorders in Highly Endemic Nagasaki: Lack of Evidence for Association of HTLV‐1 with Multiple Sclerosis , 1990, Japanese journal of cancer research : Gann.

[24]  D. Hafler,et al.  PCR Analysis of DNA from Multiple Sclerosis Patients for the Presence of HTLV-I , 1989, Science.

[25]  J. Cruickshank,et al.  PCR analysis of DNA from multiple sclerosis patients for the presence of HTLV-I , 1989 .

[26]  M. Sandberg‐Wollheim,et al.  Amplification and molecular cloning of HTLV-I sequences from DNA of multiple sclerosis patients. , 1989, Science.

[27]  L. Haaheim,et al.  Antibodies in sera from Norwegian multiple sclerosis patients and the general population reacting with HTLV‐I , 1989 .

[28]  S. Kwok,et al.  Avoiding false positives with PCR , 1989, Nature.

[29]  T. Waldmann,et al.  Detection of sequences homologous to human retroviral DNA in multiple sclerosis by gene amplification. , 1989, Proceedings of the National Academy of Sciences of the United States of America.

[30]  E. Reddy,et al.  PCR analysis of DNA from multiple sclerosis patients for the presence of HTLV-I. , 1989, Science.

[31]  M. Feinberg,et al.  Multiple sclerosis and human T-cell lymphotropic retroviruses , 1985, Nature.

[32]  A. Dilella,et al.  Nucleotide sequence of a full-length complementary DNA clone and amino acid sequence of human phenylalanine hydroxylase. , 1985, Biochemistry.

[33]  M. Yoshida,et al.  Human adult T-cell leukemia virus: complete nucleotide sequence of the provirus genome integrated in leukemia cell DNA. , 1983, Proceedings of the National Academy of Sciences of the United States of America.

[34]  H. Bauer.  IMAB-Enquête Concerning the Diagnostic Criteria for MS , 1980 .