Human T‐cell lymphotropic virus type II–associated myelopathy: Clinical and immunologic profiles

Lehky, Tanya; Flerlage, Nicholas; Katz, David A.; Houff, Sidney A.; Hall, William H.; Ishii, Kazuyoshi; Monken, Claude E.; Dhib‐Jalbut, Suhayl; McFarland, Henry F.; Jacobson, Steven

doi:10.1002/ana.410400507

Cited by 49 publications

(27 citation statements)

References 52 publications

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“…10 We have previously reported 4 cases of HAM among HTLV-II patients in the HOST cohort, 4 and there are a number of other HTLV-II HAM case reports in the literature. [28][29][30][31][32][33][34] These results, in addition to the spectrum of milder abnormalities found in our study, support the neuropathologic effects of this virus.…”

Section: Discussionsupporting

confidence: 86%

Neurologic abnormalities in HTLV-I– and HTLV-II–infected individuals without overt myelopathy

Biswas

Engstrom²,

Kaidarova³

et al. 2009

Neurology

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Section: Discussionsupporting

confidence: 86%

Neurologic abnormalities in HTLV-I– and HTLV-II–infected individuals without overt myelopathy

Biswas

Engstrom²,

Kaidarova³

et al. 2009

Neurology

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“…The mtDNA analyses showed that most of the Indians belonged to the A haplotype but representatives of the B, C and D haplotypes, 5 Highest grade level completed: GS = graduate school; C = 2 or more years of college; CC = 1 or more years of community college; HS = 2 or more years of high school; NS = no schooling. History of taking drugs -except alcohol -within the past 15 years, or current drug user.…”

Section: Resultsmentioning

confidence: 99%

HTLV-II Risk Factors in Native Americans in Florida

et al. 1998

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Earlier virologic studies established that human T-cell lymphotropic virus type II (HTLV-II) is the predominant retrovirus type found among Seminole Indians in southern Florida. We studied 46 members of the Seminole tribe living on 3 reservations to determine the risk factors for HTLV-II and to investigate disease association with the virus. The donors’ plasma samples were evaluated with the enzyme-linked immunosorbent and Western blot assays. DNA extracted from their peripheral blood mononuclear cells were analyzed by type-specific polymerase chain reaction amplification and detection of the HTLV pol gene using the primer pair SK110/SK111, and the probes SK112 or SK188. One of 46 (2%) subjects was identified as HTLV-I positive and 11 (24%) were identified as HTLV-II positive. Restriction fragment length polymorphism and sequence analyses indicated that all of the HTLV-II strains were subtype b. Mitochondrial DNA analyses indicated that all of the HTLV-II-positive subjects had an Amerindian haplotype. HTLV-II was more prevalent in Indians who were >45 years of age or female, had multiple sex partners or had received a blood transfusion. However, only the latter risk factor was statistically significant. Three of the HTLV-II-positive Indians demonstrated signs and symptoms of an ataxic neuropathy. The data support that HTLV-IIb is endemic among the Seminoles and that they will be a key population for further virologic studies.

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“…70% sequence homology with HTLV-1. To date, HTLV-2 infection has been rarely and controversially linked to the development of neurodegenerative diseases (2,30).…”

mentioning

confidence: 99%

Proinflammatory Cytokine Gene Induction by Human T-Cell Leukemia Virus Type 1 (HTLV-1) and HTLV-2 Tax in Primary Human Glial Cells

Banerjee¹,

Rochford²,

Antel

et al. 2007

J Virol

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Infection with human T-cell leukemia virus type 1 (HTLV-1) can result in the development of HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), a chronic inflammatory disease of the central nervous system (CNS). HTLV-2 is highly related to HTLV-1 at the genetic level and shares a high degree of sequence homology, but infection with HTLV-2 is relatively nonpathogenic compared to HTLV-1. Although the pathogenesis of HAM/TSP remains to be fully elucidated, previous evidence suggests that elevated levels of the proinflammatory cytokines in the CNS are associated with neuropathogenesis. We demonstrate that HTLV-1 infection in astrogliomas results in a robust induction of interleukin-1␤ (IL-1␤), IL-1␣, tumor necrosis factor alpha (TNF-␣), TNF-␤, and IL-6 expression. HTLV encodes for a viral transcriptional transactivator protein named Tax that also induces the transcription of cellular genes. To investigate and compare the effects of Tax1 and Tax2 expression on the dysregulation of proinflammatory cytokines, lentivirus vectors were used to transduce primary human astrocytomas and oligodendrogliomas. The expression of Tax1 in primary human astrocytomas and oligodendrogliomas resulted in significantly higher levels of proinflammatory cytokine gene expression compared to Tax2. Notably, Tax1 expression uniquely sensitized primary human astrocytomas to apoptosis. A Tax2/Tax1 chimera encoding the C-terminal 53 amino acids of the Tax1 fused to the Tax2 gene (Tax 221 ) demonstrated a phenotype that resembled Tax1, with respect to proinflammatory cytokine gene expression and sensitization to apoptosis. The patterns of differential cytokine induction and sensitization to apoptosis displayed by Tax1 and Tax2 may reflect differences relating to the heightened neuropathogenicity associated with HTLV-1 infection and the development of HAM/TSP.Human T-cell leukemia virus type 1 (HTLV-1) is the etiological agent of a slow progressive neurological disease, HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) (42). Although most HTLV-1-infected individuals remain asymptomatic carriers, an estimated 5 to 10% of HTLV-1-infected individuals develop HAM/TSP. HTLV-2 was originally isolated from a patient with an atypical hairy cell leukemia and shares ca. 70% sequence homology with HTLV-1. To date, HTLV-2 infection has been rarely and controversially linked to the development of neurodegenerative diseases (2, 30).Cytokines play a critical role in physiological processes in the central nervous system (CNS), including establishing and maintaining normal homeostasis, as well as mediating inflammatory and immune responses. Cytokines have also been implicated as being the major mediators of demyelination in the CNS, resulting in a variety of inflammatory and neoplastic diseases (1). Elevated levels of tumor necrosis factor alpha (TNF-␣), interleukin-1␤ (IL-1␤), IL-1␣, and IL-6 have previously been detected in the cerebrospinal fluid of HAM/TSP patients (28,40,57), suggesting that increased expression of these proi...

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Human T‐cell lymphotropic virus type II–associated myelopathy: Clinical and immunologic profiles

Cited by 49 publications

References 52 publications

Neurologic abnormalities in HTLV-I– and HTLV-II–infected individuals without overt myelopathy

Neurologic abnormalities in HTLV-I– and HTLV-II–infected individuals without overt myelopathy

HTLV-II Risk Factors in Native Americans in Florida

Proinflammatory Cytokine Gene Induction by Human T-Cell Leukemia Virus Type 1 (HTLV-1) and HTLV-2 Tax in Primary Human Glial Cells

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