Regulation of Expression and Latency in BLV and HTLV

<i>Human T-lymphotrophic virus type 1</i> (HTLV-1) and <i>Bovine leukemia virus</i> (BLV) belong to the <i>Deltaretrovirus</i> genus. HTLV-1 is the etiologic agent of the highly aggressive and currently incurable cancer adult T-cell leukemia (ATL) and a neurologic...

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Main Authors: Aneta Pluta, Juan P. Jaworski, Renée N. Douville
Format: Article
Language:English
Published: MDPI AG 2020-09-01
Series:Viruses
Subjects:
Online Access:https://www.mdpi.com/1999-4915/12/10/1079
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author Aneta Pluta
Juan P. Jaworski
Renée N. Douville
author_facet Aneta Pluta
Juan P. Jaworski
Renée N. Douville
author_sort Aneta Pluta
collection DOAJ
description <i>Human T-lymphotrophic virus type 1</i> (HTLV-1) and <i>Bovine leukemia virus</i> (BLV) belong to the <i>Deltaretrovirus</i> 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 <i>cis</i>-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 <i>Deltaretroviruses</i>.
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spelling doaj.art-c2f3028849f2470f819b98f16229956f2023-11-20T15:07:48ZengMDPI AGViruses1999-49152020-09-011210107910.3390/v12101079Regulation of Expression and Latency in BLV and HTLVAneta Pluta0Juan P. Jaworski1Renée N. Douville2Department of Biochemistry, National Veterinary Research Institute, 24-100 Puławy, PolandConsejo Nacional de Investigaciones Científicas y Tecnológicas (CONICET), Instituto Nacional de Tecnología Agropecuaria (INTA), Instituto de Virología, Nicolás Repetto y De los Reseros (s/n), CP1686 Hurlingham, Buenos Aires, ArgentinaDepartment of Biology, The University of Winnipeg, Winnipeg, MB R3B 2E9, Canada<i>Human T-lymphotrophic virus type 1</i> (HTLV-1) and <i>Bovine leukemia virus</i> (BLV) belong to the <i>Deltaretrovirus</i> 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 <i>cis</i>-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 <i>Deltaretroviruses</i>.https://www.mdpi.com/1999-4915/12/10/1079<i>Retrovirus</i><i>Deltaretrovirus</i><i>Human T-lymphotrophic virus type 1</i> (HTLV-1)<i>Bovine leukemia virus</i> (BLV)<i>Human immunodeficiency virus type 1</i> (HIV-1)long terminal repeat (LTR)
spellingShingle Aneta Pluta
Juan P. Jaworski
Renée N. Douville
Regulation of Expression and Latency in BLV and HTLV
Viruses
<i>Retrovirus</i>
<i>Deltaretrovirus</i>
<i>Human T-lymphotrophic virus type 1</i> (HTLV-1)
<i>Bovine leukemia virus</i> (BLV)
<i>Human immunodeficiency virus type 1</i> (HIV-1)
long terminal repeat (LTR)
title Regulation of Expression and Latency in BLV and HTLV
title_full Regulation of Expression and Latency in BLV and HTLV
title_fullStr Regulation of Expression and Latency in BLV and HTLV
title_full_unstemmed Regulation of Expression and Latency in BLV and HTLV
title_short Regulation of Expression and Latency in BLV and HTLV
title_sort regulation of expression and latency in blv and htlv
topic <i>Retrovirus</i>
<i>Deltaretrovirus</i>
<i>Human T-lymphotrophic virus type 1</i> (HTLV-1)
<i>Bovine leukemia virus</i> (BLV)
<i>Human immunodeficiency virus type 1</i> (HIV-1)
long terminal repeat (LTR)
url https://www.mdpi.com/1999-4915/12/10/1079
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