Endocrine and metabolic disorders in HTLV-1 infected patients

Alves, Crésio de Aragão Dantas; Dourado, Luciano

doi:10.1016/s1413-8670(10)70120-3

Cited by 13 publications

(3 citation statements)

References 63 publications

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“…Hypercalcaemia is a prominent finding in 70–80% of patients with ATLL. 8 The underlying mechanisms are related to direct or indirect osteoclast activation mainly due to PTH-related peptide and pro-inflammatory cytokines and chemokines. 7 , 9 , 10 In the setting of ATLL, systemic hypercalcaemia can lead to extensive calcification.…”

Section: Discussionmentioning

confidence: 99%

Fatal cardiovascular instability secondary to hypercalcaemia and intracellular calcium deposition complicating T-cell leukaemia-lymphoma

et al. 2016

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Section: Discussionmentioning

confidence: 99%

Fatal cardiovascular instability secondary to hypercalcaemia and intracellular calcium deposition complicating T-cell leukaemia-lymphoma

et al. 2016

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“…The current knowledge of the endocrine system control of HTLV-1 viral gene expression is very limited [ 185 ]. No hormone receptors have been identified in the HTLV-1 LTR.…”

Section: Regulation Of Ltr Transcription Through Hormonal Signalinmentioning

confidence: 99%

Regulation of Expression and Latency in BLV and HTLV

Pluta

Jaworski

Douville

2020

Viruses

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Human T-lymphotrophic virus type 1 (HTLV-1) and Bovine leukemia virus (BLV) belong to the Deltaretrovirus genus. HTLV-1 is the etiologic agent of the highly aggressive and currently incurable cancer adult T-cell leukemia (ATL) and a neurological disease HTLV-1-associated myelopathy (HAM)/tropical spastic paraparesis (TSP). BLV causes neoplastic proliferation of B cells in cattle: enzootic bovine leucosis (EBL). Despite the severity of these conditions, infection by HTLV-1 and BLV appear in most cases clinically asymptomatic. These viruses can undergo latency in their hosts. The silencing of proviral gene expression and maintenance of latency are central for the establishment of persistent infection, as well as for pathogenesis in vivo. In this review, we will present the mechanisms that control proviral activation and retroviral latency in deltaretroviruses, in comparison with other exogenous retroviruses. The 5′ long terminal repeats (5′-LTRs) play a main role in controlling viral gene expression. While the regulation of transcription initiation is a major mechanism of silencing, we discuss topics that include (i) the epigenetic control of the provirus, (ii) the cis-elements present in the LTR, (iii) enhancers with cell-type specific regulatory functions, (iv) the role of virally-encoded transactivator proteins, (v) the role of repressors in transcription and silencing, (vi) the effect of hormonal signaling, (vii) implications of LTR variability on transcription and latency, and (viii) the regulatory role of non-coding RNAs. Finally, we discuss how a better understanding of these mechanisms may allow for the development of more effective treatments against Deltaretroviruses.

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“…These lesions result in motor disorders and a low quality of life [ 11 , 12 , 13 ]. HTLV-1 is also associated with infective dermatitis and Sjögren’s syndrome (immune and endocrine-metabolic disorders), as well as thyroiditis and other diseases [ 10 , 14 ].…”

Section: Introductionmentioning

confidence: 99%

Non-Structural Proteins from Human T-cell Leukemia Virus Type 1 in Cellular Membranes—Mechanisms for Viral Survivability and Proliferation

Georgieva

2018

IJMS

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Human T-cell leukemia virus type 1 (HTLV-1) is the causative agent of illnesses, such as adult T-cell leukemia/lymphoma, myelopathy/tropical spastic paraparesis (a neurodegenerative disorder), and other diseases. Therefore, HTLV-1 infection is a serious public health concern. Currently, diseases caused by HTLV-1 cannot be prevented or cured. Hence, there is a pressing need to comprehensively understand the mechanisms of HTLV-1 infection and intervention in host cell physiology. HTLV-1-encoded non-structural proteins that reside and function in the cellular membranes are of particular interest, because they alter cellular components, signaling pathways, and transcriptional mechanisms. Summarized herein is the current knowledge about the functions of the membrane-associated p8I, p12I, and p13II regulatory non-structural proteins. p12I resides in endomembranes and interacts with host proteins on the pathways of signal transduction, thus preventing immune responses to the virus. p8I is a proteolytic product of p12I residing in the plasma membrane, where it contributes to T-cell deactivation and participates in cellular conduits, enhancing virus transmission. p13II associates with the inner mitochondrial membrane, where it is proposed to function as a potassium channel. Potassium influx through p13II in the matrix causes membrane depolarization and triggers processes that lead to either T-cell activation or cell death through apoptosis.

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Endocrine and metabolic disorders in HTLV-1 infected patients

Cited by 13 publications

References 63 publications

Fatal cardiovascular instability secondary to hypercalcaemia and intracellular calcium deposition complicating T-cell leukaemia-lymphoma

Fatal cardiovascular instability secondary to hypercalcaemia and intracellular calcium deposition complicating T-cell leukaemia-lymphoma

Regulation of Expression and Latency in BLV and HTLV

Non-Structural Proteins from Human T-cell Leukemia Virus Type 1 in Cellular Membranes—Mechanisms for Viral Survivability and Proliferation

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