Conference highlights of the 15th international conference on human retrovirology: HTLV and related retroviruses, 4-8 june 2011, Leuven, Gembloux, Belgium

Martin, Fabiola; Bangham, Charles R. M.; Ciminale, Vincenzo; Lairmore, Michael Dale; Murphy, Edward L.; Switzer, William M.; Mahieux, Renaud

doi:10.1186/1742-4690-8-86

Cited by 16 publications

(19 citation statements)

References 151 publications

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“…Thus, data indicate that immune-mediated mechanisms contribute to the pathogenesis of HAM/TSP. 12,13,20,22,24,[69][70][71][72][73] For example, HAM/TSP patients make immune responses to a number of viral targets including HTLV-1 tax, env, and gag that separates them from control populations. [74][75][76][77] Immunologically, HAM/TSP patients develop CD8 + , human leukocyte antigen (HLA)-2-restricted cytotoxic T lymphocytes (CTLs) specific for tax and CD4 + responses to both tax and env that are thought to contribute to disease.…”

Section: Contribution Of Neurodegeneration To the Pathogenesis Of Immmentioning

confidence: 99%

“…27,28 MS and HAM/TSP patients also exhibit some of these symptoms. [21][22][23][24] Pathologically, progressive MS, HAM/TSP, and HSP are characterized by damage to and neurodegeneration of the long tracts of the CNS, including the corticospinal tracts and posterior column/medial lemniscal sensory system (Table 1). 7,11,[27][28][29][30][31][32][33] …”

mentioning

confidence: 99%

“…[11][12][13][14][15] HAM/TSP is caused by HTLV-1, which allows for the direct comparison of the infecting agent with host antigens. [16][17][18][19][20][21][22][23][24] Importantly, HAM/TSP patients are similar clinically, pathologically, and immunologically to people with progressive MS. In fact, many HAM/TSP patients were initially diagnosed with PPMS.…”

mentioning

confidence: 99%

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Pathogenic mechanisms of neurodegeneration based on the phenotypic expression of progressive forms of immune-mediated neurologic disease

Levin¹,

Lee²,

Gardner³

et al. 2012

DNND

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Considering there are no treatments for progressive forms of multiple sclerosis (MS), a comprehensive understanding of the role of neurodegeneration in the pathogenesis of MS should lead to novel therapeutic strategies to treat it. Many studies have implicated viral triggers as a cause of MS, yet no single virus has been exclusively shown to cause MS. Given this, human and animal viral models of MS are used to study its pathogenesis. One example is human T-lymphotropic virus type 1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Importantly, HAM/TSP is similar clinically, pathologically, and immunologically to progressive MS. Interestingly, both MS and HAM/TSP patients were found to make antibodies to heterogeneous nuclear ribonucleoprotein (hnRNP) A1, an RNA-binding protein overexpressed in neurons. Anti-hnRNP A1 antibodies reduced neuronal firing and caused neurodegeneration in neuronal cell lines, suggesting the autoantibodies are pathogenic. Further, microarray analyses of neurons exposed to anti-hnRNP A1 antibodies revealed novel pathways of neurodegeneration related to alterations of RNA levels of the spinal paraplegia genes (SPGs). Mutations in SPGs cause hereditary spastic paraparesis, genetic disorders clinically indistinguishable from progressive MS and HAM/TSP. Thus, there is a strong association between involvement of SPGs in neurodegeneration and the clinical phenotype of progressive MS and HAM/TSP patients, who commonly develop spastic paraparesis. Taken together, these data begin to clarify mechanisms of neurodegeneration related to the clinical presentation of patients with chronic immune-mediated neurological disease of the central nervous system, which will give insights into the design of novel therapies to treat these neurological diseases.

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Section: Contribution Of Neurodegeneration To the Pathogenesis Of Immmentioning

confidence: 99%

mentioning

confidence: 99%

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Pathogenic mechanisms of neurodegeneration based on the phenotypic expression of progressive forms of immune-mediated neurologic disease

Levin¹,

Lee²,

Gardner³

et al. 2012

DNND

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show abstract

“…Although first identified in hairy T-cell leukemia, HTLV-2 is currently not believed to be associated with any neoplasia. By contrast, the association between HTLV-1 and Adult T-cell Leukemia has been well established for more than 30 years [2]. HTLV-1 is also the etiological agent of inflammatory diseases such as HTLV-1 associated Myelopathy (HAM)/Tropical Spastic Paraparesis (TSP) [3], uveitis, infective dermatitis and myositis.…”

Section: Introductionmentioning

confidence: 99%

The importance of ubiquitination and sumoylation on the transforming activity of HTLV Tax-1 and Tax-2

Zane

Jeang

2012

Retrovirology

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Human T-cell Leukemia Virus type 1 (HTLV-1) and 2 (HTLV-2) are two closely related human retroviruses. HTLV-1 is associated with an aggressive Adult T-cell Leukemia (ATL) while there is no evidence for an association of HTLV-2 with any human malignancies. The two viruses encode transactivator proteins, Tax-1 and Tax-2 respectively. In ATL, Tax-1 is thought to play a central role in the transformation of a normal T-cell into a leukemic cell; however, it has not been entirely clear how post-translational modifications of Tax-1 influence its transforming activity. Here, we discuss three recent papers that report on the ubiquitination and sumoylation of Tax-1 and Tax-2. We comment on their divergent findings implicating the importance (or lack of importance) of these modifications and other events on Tax activation of NF-κB as related to cellular transformation.

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“…HTLV-1 infects an estimated 15 to 20 million individuals worldwide (3,4). HTLV-1 predominantly infects CD4 ϩ lymphocytes and is primarily transmitted through cell-to-cell contact; free virions do not efficiently infect cells (5,6).…”

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confidence: 99%

The Cellular Autophagy Pathway Modulates Human T-Cell Leukemia Virus Type 1 Replication

Tang

Chen

Klase

et al. 2013

J Virol

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Autophagy, a general homeostatic process for degradation of cytosolic proteins or organelles, has been reported to modulate the replication of many viruses. The role of autophagy in human T-cell leukemia virus type 1 (HTLV-1) replication has, however, been uncharacterized. Here, we report that HTLV-1 infection increases the accumulation of autophagosomes and that this accumulation increases HTLV-1 production. We found that the HTLV-1 Tax protein increases cellular autophagosome accumulation by acting to block the fusion of autophagosomes to lysosomes, preventing the degradation of the former by the latter. Interestingly, the inhibition of cellular autophagosome-lysosome fusion using bafilomycin A increased the stability of the Tax protein, suggesting that cellular degradation of Tax occurs in part through autophagy. Our current findings indicate that by interrupting the cell's autophagic process, Tax exerts a positive feedback on its own stability.

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Conference highlights of the 15th international conference on human retrovirology: HTLV and related retroviruses, 4-8 june 2011, Leuven, Gembloux, Belgium

Cited by 16 publications

References 151 publications

Pathogenic mechanisms of neurodegeneration based on the phenotypic expression of progressive forms of immune-mediated neurologic disease

Pathogenic mechanisms of neurodegeneration based on the phenotypic expression of progressive forms of immune-mediated neurologic disease

The importance of ubiquitination and sumoylation on the transforming activity of HTLV Tax-1 and Tax-2

The Cellular Autophagy Pathway Modulates Human T-Cell Leukemia Virus Type 1 Replication

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