Highly divergent molecular variants of human T-lymphotropic virus type I from isolated populations in Papua New Guinea and the Solomon Islands.

Gessian, A; Yanagihara, Richard; Franchini, Genoveffa; Garruto, Ralph M.; Jenkins, Carol; Ajdukiewicz, A.B.; Gallo, Robert C.; Gajdusek, D. Carleton

doi:10.1073/pnas.88.17.7694

Cited by 132 publications

(64 citation statements)

References 30 publications

(28 reference statements)

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“…In spite of the fact that in the present study we Saksena et al, 1992;Gessain et at., 1991Bastian et al, 1993). The presence of distant molecular variants of HTLV-I probably resulted from a genetic drift over several millennia in remote populations which originated 10000 to 40000 years ago from the Indomalay region (Yanagihara et at., 1991;Gessain et al, 1991Gessain et al, , 1993Sherman et al, 1992;Saksena et al, 1992).…”

Section: Short Communicationcontrasting

confidence: 45%

“…The presence of distant molecular variants of HTLV-I probably resulted from a genetic drift over several millennia in remote populations which originated 10000 to 40000 years ago from the Indomalay region (Yanagihara et at., 1991;Gessain et al, 1991Gessain et al, , 1993Sherman et al, 1992;Saksena et al, 1992). Despite centuries or millennia of in vivo evolution, the very low level of mutation occurring in the transcriptional enhancers of the 5' LTR of 12 new proviral DNAs demonstrates the existence of a high genetic constraint maintaining the critical role of these regulatory elements for viral expression.…”

Section: Short Communicationmentioning

confidence: 99%

“…In these regions, between 0-5 and 20 % of the general population, depending on age and sex, have HTLV-I antibodies and are considered to be healthy HTLV-I carriers. The question whether the same HTLV-I strain could induce several diseases through different pathways, as in the EBV system (De Th6, 1993), or whether there are specific gene mutations that direct tissue tropism and pathogenesis, as in the case of murine leukaemia retroviruses (Desgroseillers et al, 1985;Rassart et al, 1986;Li et al, 1987;Szurek et al, 1988), led to the comparative molecular analysis of different HTLV-I viral strains (Daenke et al, 1990;De et al, 1991;Komurian et al, 1991;Gessain et al, 1991Gessain et al, , 1992aKinoshita et al,Kinoshita et al, 1991 ;Ratner et al, 1991 ;Gessain et al, 1992a). Furthermore, the puzzling epidemiological distribution of HTLV-I with the existence of geographical molecular clusters, and the recent discovery of distant molecular variants of HTLV-I in Central Africa (Ratner et al, 1985;Gessain et al, 1992a, b;Boeri et al, 1993) and Melanesia (Gessain et al, 1991Saksena et al, 1992;Bastian et al, 1993) raised new questions concerning the origin and evolution of this human oncoretrovirus.…”

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confidence: 99%

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Phylogenetic classification of human T cell leukaemia/lymphoma virus type I genotypes in five major molecular and geographical subtypes

Vidal

Gessain²,

Yoshida³

et al. 1994

Journal of General Virology

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Proviral DNA was obtained from ex vivo peripheral blood mononuclear cells of 75 human T cell leukaemia/ lymphoma virus type I (HTLV-I)-infected individuals who were either asymptomatic or had adult T cell leukaemia or tropical spastic paraparesis/HTLV-I-associated myelopathy. Amplified long terminal repeats (LTRs) were analysed for restriction fragment length polymorphisms (RFLPs). The results, together with previously published LTR data (a total of 180 specimens analysed), showed the presence of 12 different RFLP profiles with four major molecular subtypes. Furthermore, a fragment of 413 bp (nucleotides 22 to 434) of the U3/R region was sequenced for 12 new HTLV-I specimens originating from Central and West Africa (8 cases), Iran (1 case), Caribbean (2 cases) and Reunion Island (1 case). Phylogenetic analysis using three different techniques (maximum parsimony, neighbourjoining and UPGMA) comparing these 12 strains (including four new African HTLV-I variants) with the 30 published partial HTLV-I LTR sequences (nt 120 to 434) showed the existence of clusters of molecular variants in discrete geographical areas. The topology of the phylogenetic trees is thought to reflect HTLV-I evolution and the migrations of virally infected populations in the recent or distant past. Furthermore, there was a nearly perfect concordance between the clustering based on the LTR sequence homologies and the LTR RFLP subtypes suggesting that this rapid and simple technique is well suited to the investigation of HTLV-I molecular epidemiology. These results allow a new phylogenetic classification of HTLV-I genotypes into five major molecular subtypes:Cosmopolitan (C) subtype widespread all over the world, Japanese (J) subtype, West African (WA) subtype, Central African (CA) subtype and Melanesian (M) subtype.

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Section: Short Communicationcontrasting

confidence: 45%

Section: Short Communicationmentioning

confidence: 99%

mentioning

confidence: 99%

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Phylogenetic classification of human T cell leukaemia/lymphoma virus type I genotypes in five major molecular and geographical subtypes

Vidal

Gessain²,

Yoshida³

et al. 1994

Journal of General Virology

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“…The resultant LTR-directed expression occurred primarily within the CNS (Gonzalez-Dunia et al, 1992). Furthermore, several HTLV-I proviruses isolated from ATL or HAM/TSP patients as well as HTLV-I-infected asymptomatic carriers have been isolated and sequenced (Yoshida et al, 1982;Josephs et al, 1984;Jacobson et al, 1988;Gessian et al, 1991;Komurian et al, 1991;Nerurkar et al, 1993). Although there was 95% homology between the sequenced clones, a number of the differences in nucleotide sequence between the clones lie in and around the U3 region of the LTR, which contains the viral promoter (Paine et al, 1991;Ratner et al, 1991).…”

Section: Viral Transmission and Productive T Cell Infectionmentioning

confidence: 99%

Human T cell leukemia virus type I and neurologic disease: Events in bone marrow, peripheral blood, and central nervous system during normal immune surveillance and neuroinflammation

Grant

Barmak

Alefantis

et al. 2002

Journal Cellular Physiology

101

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Human T cell lymphotropic/leukemia virus type I (HTLV‐I) has been identified as the causative agent of both adult T cell leukemia (ATL) and HTLV‐I‐associated myelopathy/tropical spastic paraparesis (HAM/TSP). Although the exact sequence of events that occur during the early stages of infection are not known in detail, the initial route of infection may predetermine, along with host, environmental, and viral factors, the subset of target cells and/or the primary immune response encountered by HTLV‐I, and whether an HTLV‐I‐infected individual will remain asymptomatic, develop ATL, or progress to the neuroinflammatory disease, HAM/TSP. Although a large number of studies have indicated that CD4+ T cells represent an important target for HTLV‐I infection in the peripheral blood (PB), additional evidence has accumulated over the past several years demonstrating that HTLV‐I can infect several additional cellular compartments in vivo, including CD8+ T lymphocytes, PB monocytes, dendritic cells, B lymphocytes, and resident central nervous system (CNS) astrocytes. More importantly, extensive latent viral infection of the bone marrow, including cells likely to be hematopoietic progenitor cells, has been observed in individuals with HAM/TSP as well as some asymptomatic carriers, but to a much lesser extent in individuals with ATL. Furthermore, HTLV‐I+ CD34+ hematopoietic progenitor cells can maintain the intact proviral genome and initiate viral gene expression during the differentiation process. Introduction of HTLV‐I‐infected bone marrow progenitor cells into the PB, followed by genomic activation and low level viral gene expression may lead to an increase in proviral DNA load in the PB, resulting in a progressive state of immune dysregulation including the generation of a detrimental cytotoxic Tax‐specific CD8+ T cell population, anti‐HTLV‐I antibodies, and neurotoxic cytokines involved in disruption of myelin‐producing cells and neuronal degradation characteristic of HAM/TSP. J. Cell. Physiol. 190: 133–159, 2002. © 2002 Wiley‐Liss, Inc.

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“…Three main types are described: endemic BL, sporadic BL and BL associated with HIV infection [31]. In all three forms, the lymphoma that has become the leading cause of death in men and the fourth among women in Africa [36].…”

Section: Epstein-barr Virus (Ebv) and Burkitt's Lymphomamentioning

confidence: 99%

Virus-Induced Cancers in Africa: Epidemiology and Carcinogenesis Mechanisms

Moukassa¹,

Boumba²,

Ngatali³

et al. 2018

OJPathology

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The resurgence of infectious diseases on the African continent plays a major role in the increase in cancer occurrence. Whereas in developed countries the causes of occurrence of cancers are related mainly to non-infectious factors; cancers of infectious origin become a dramatic particularity in Africa. The proportion of virus-induced cancers may reach up to 75% of cancer cases in certain countries. Oncogenic viruses such as human papilloma virus (HPV), hepatitis viruses B and C, human herpes virus 8 and Epstein Barr virus in association with human immunodeficiency virus are the main viral etiologies of cancers in Africa, representing around 30% of cancers causes. Optimistically, 30% of cancers could be prevented in Africa. However, health burden prevails on the continent due to the weakness of health policy especially regarding preventive medicine, but also the limited technical facilities, poor manpower and insufficient political commitment. We felt urgent to review the state of the art of the question, and necessary to analyze and publicize the current epidemiological advances in oncogenic viruses and virus-induced cancers in Africa. Prevention implies understanding, which is compulsory to reverse the current trends and to potentially instate a control of virus-induced cancers.

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Highly divergent molecular variants of human T-lymphotropic virus type I from isolated populations in Papua New Guinea and the Solomon Islands.

Cited by 132 publications

References 30 publications

Phylogenetic classification of human T cell leukaemia/lymphoma virus type I genotypes in five major molecular and geographical subtypes

Phylogenetic classification of human T cell leukaemia/lymphoma virus type I genotypes in five major molecular and geographical subtypes

Human T cell leukemia virus type I and neurologic disease: Events in bone marrow, peripheral blood, and central nervous system during normal immune surveillance and neuroinflammation

Virus-Induced Cancers in Africa: Epidemiology and Carcinogenesis Mechanisms

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