No Evidence for Human T-cell Leukemia Virus Type I or Human T-cell Leukemia Virus Type II Infection in Patients With Multiple Sclerosis

Perl, András; Nagy, K.; Pazmany, Tamas; Isaacs, Cary; Baraczka, Krisztina; Szabó, T; Fehér, János

doi:10.1001/archneur.1990.00530100023007

Cited by 7 publications

(3 citation statements)

References 21 publications

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“…Although some of the first serological and gene amplification reports suggested a role for a virus similar to HTLV-I 10 the consensus is that these observations are not reproducible." 15 The failure to identify retroviral genes in the tissues of ALS patients is in keeping with the negative serological studies published to date. 1 A virus etiology for ALS is still possible.…”

Section: Discussionmentioning

confidence: 84%

Absence of HTLV-I and HTLV-II Proviral Genome in the Brains of Patients with Multiple Sclerosis and Amyotrophic Lateral Sclerosis

Dekaban

Hudson²,

Rice³

1992

Can. j. neurol. sci.

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ABSTRACT:Previous studies have failed to provide serological evidence to incriminate a retroviral infection in the cause of multiple sclerosis. Gene amplification techniques have also failed to identify retroviral footprints in DNA from peripheral blood leukocytes. Here we provide evidence that proviral DNA of HTLV-I and HTLV-II is not found in the central nervous system tissues of patients with multiple sclerosis, patients with amyotrophic lateral sclerosis and controls.

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Section: Discussionmentioning

confidence: 84%

Absence of HTLV-I and HTLV-II Proviral Genome in the Brains of Patients with Multiple Sclerosis and Amyotrophic Lateral Sclerosis

Dekaban

Hudson²,

Rice³

1992

Can. j. neurol. sci.

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“…This is in accordance with earlier data showing similar frequency of HTLV-I gag p24-reactive antibodies in patients with MS (7)(8)(9). Antibodies to all characteristic HTLV-I virion proteins, using Western blot analysis and prototype HTLV-I DNA based on polymerase chain reaction, were absent in these patients (10)(11)(12)(13). However, 9 of the HTLV-I gag p24-reactive patients had antibodies to both of the HRES-1 peptides.…”

Section: Discussionmentioning

confidence: 96%

“…Antibodies reacting with gag proteins ofhuman T-cell lymphotropic virus I (HTLV-I) were described in patients with systemic lupus erythematosus (SLE) (6) and multiple sclerosis (MS) (7)(8)(9). However, the presence of HTLV-I, HTLV-II, or related exogenous retroviruses could not be conclusively associated with these diseases (10)(11)(12)(13). This raised the possibility that the natural targets of HTLV-I-reactive antibodies of patients with autoimmune disease may correspond to endogenous retroviral sequences (ERSs).…”

mentioning

confidence: 99%

Human T-cell lymphotropic virus (HTLV)-related endogenous sequence, HRES-1, encodes a 28-kDa protein: a possible autoantigen for HTLV-I gag-reactive autoantibodies.

Bánki

Maceda

Hurley

et al. 1992

Proc. Natl. Acad. Sci. U.S.A.

142

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The presence of a human T-cell lymphotropic virus (HTLV)-related endogenous sequence, HRES-1, in the human genome has been documented. The HRES-1 genomic locus is transcriptionally active and contains open reading frames. Antibodies 232 and 233, specific for synthetic peptides pepl4-24 and pepll7-127, corresponding to two nonoverlapping HTLV-related regions in the longer open reading frame of HRES-1, recognize an identical 28-kDa protein in H9 human T cells. Thus, HRES-1 is a human endogenous retroviral sequence capable of protein expression. HRES-l/p28 is localized to the cytoplasm and nuclear bodies. While HTLV-I-specific antibodies react with HRES-1 peptides, antibody 233 crossreacts with HTLV

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Polymorphic genotypes of the HRES-1 human endogenous retrovirus locus correlate with systemic lupus erythematosus and autoreactivity

Magistrelli

Samoilova²,

Agarwal³

et al. 1999

Immunogenetics

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Antinuclear autoantibodies are a hallmark of systemic lupus erythematosus (SLE). Autoantibodies to HRES-1/p28, a 28 000 M(r) nuclear protein, commonly occur in patients with SLE. HRES-1 is a single-copy endogenous retroviral element mapped to human Chromosome 1 at q42. A polymorphic Hin dIII site defines two different allelic forms of the genomic locus. The HRES-1/1 probe [5.5 kilobases (kb)] anneals to three polymorphic fragments and three genotypes can be differentiated: I, 5.5 kb fragment only; II, 3.7 kb and 1.8 kb fragments only; and III, all three polymorphic fragments. By cloning of the HRES-1 locus from homozygous type I and type II human DNA samples, the polymorphic Hin dIII site was identified as a G to C transition at position 653 of the long terminal repeat region. Family studies showed that Hin dIII genotypes of the HRES-1 locus are inherited in a Mendelian pattern. The relative frequency of genotype I with respect to genotype III was 3.1-fold lower in patients with SLE (14:40=0.35) in comparison to 100 ethnically matched control donors (47:43=1.09; P=0.0084). Frequency of genotype I vs genotype II alleles was lower in SLE (68/52) than in normal donors (137/63; P=0.033), suggesting that a genotype I allele of the HRES-1 locus may be protective against SLE. Western blot seroreactivity with recombinant HRES-1/p28 was noted in 4/14 (29%) of genotype I patients and 13/19 (68%) of genotype III patients (P<0.025). These data raise the possibility that the HRES-1 element or a gene in linkage disequilibrium with this genomic locus may influence autoimmunity in SLE.

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No Evidence for Human T-cell Leukemia Virus Type I or Human T-cell Leukemia Virus Type II Infection in Patients With Multiple Sclerosis

Cited by 7 publications

References 21 publications

Absence of HTLV-I and HTLV-II Proviral Genome in the Brains of Patients with Multiple Sclerosis and Amyotrophic Lateral Sclerosis

Absence of HTLV-I and HTLV-II Proviral Genome in the Brains of Patients with Multiple Sclerosis and Amyotrophic Lateral Sclerosis

Human T-cell lymphotropic virus (HTLV)-related endogenous sequence, HRES-1, encodes a 28-kDa protein: a possible autoantigen for HTLV-I gag-reactive autoantibodies.

Polymorphic genotypes of the HRES-1 human endogenous retrovirus locus correlate with systemic lupus erythematosus and autoreactivity

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