Journal articles: 'Retrovirus HTLV'

1

Zheng, Z. Y., and D. Zucker-Franklin. "Apparent ineffectiveness of natural killer cells vis-à-vis retrovirus-infected targets." Journal of Immunology 148, no. 11 (June 1, 1992): 3679–85. http://dx.doi.org/10.4049/jimmunol.148.11.3679.

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Abstract The role of NK cells in the defense against retroviral infections is ill defined. The discovery of the pathogenic human retroviruses and their epidemic spread have made more urgent a better understanding of how such infections may be naturally controlled. Therefore, a systematic study was undertaken to determine whether NK cells obtained from healthy individuals are able to recognize and lyse target cells that have been infected with HTLV-I, HTLV-II, or HIV. The studies demonstrated that NK cells can recognize retrovirus-infected cells as evidenced by rapid conjugation, but that neither freshly isolated, nor IL-2 stimulated cells cause lysis of such targets. As has been reported for NK-resistant tumor cells, removal of sialic acid residues rendered the retrovirus-infected target cells vulnerable to NK cell attack. Although these data do not suggest that boosting natural immunity would be a useful treatment modality for patients with AIDS or HTLV-related diseases, the observations may help to explain why the small number of cells that harbor retroviruses in patients with subclinical infection are not eliminated.

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Magin, Christine, Roswitha Löwer, and Johannes Löwer. "cORF and RcRE, the Rev/Rex and RRE/RxRE Homologues of the Human Endogenous Retrovirus Family HTDV/HERV-K." Journal of Virology 73, no. 11 (November 1, 1999): 9496–507. http://dx.doi.org/10.1128/jvi.73.11.9496-9507.1999.

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ABSTRACT cORF, a protein encoded by the human endogenous retrovirus family HTDV/HERV-K, contains amino acid motifs which resemble the nuclear import and export signals of the viral regulatory proteins Rev (human immunodeficiency virus) and Rex (human T-cell leukemia virus [HTLV]). In this study, we demonstrated that cORF indeed has a Rev-like function and mapped the cORF-responsive RNA element to a sequence in the 3′ long terminal repeat, a localization similar to RxRE, the responsive element in HTLV type 1. Accordingly, we have given the element the designation RcRE. cORF and RcRE stabilize unspliced and incompletely spliced viral transcripts and enhance their nuclear export via the CRM1 export pathway. So far, HTDV/HERV-K is the only endogenous retrovirus family with a complex regulation at the posttranscriptional level. It may be regarded as an intermediate in the evolution from simple to complex retroviruses.

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Cleveland, Susan M., and Utpal P. Dave. "Insertional Activation of GLI2 in Adult T-Cell Leukemia/Lymphoma." Blood 110, no. 11 (November 16, 2007): 4149. http://dx.doi.org/10.1182/blood.v110.11.4149.4149.

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Abstract Retroviruses induce cancer by integrating into the cellular genome and activating oncogenes or inactivating tumor suppressor genes. Human T-cell Leukemia Virus type 1 (HTLV-1), a complex retrovirus, induces Adult T-cell Leukemia/Lymphoma (ATLL) after a latency of over 30 years and in only 5% of carriers. The long latency and incomplete penetrance is similar to how slow transforming retroviruses induce cancer in mice and imply multiple oncogenic “hits” need to accumulate for clinically apparent disease. Insertional mutagenesis may be one mechanism by which ATLL develops. We used splinkerette-PCR to clone and map insertion sites from an HTLV-1 infected T-cell line, Hut-102. We identified an HTLV-1 insertion 5′ of the GLI2 gene, formerly known as Tax-Helper-Protein-1. We found GLI2 was up-regulated by promoter insertion. Interestingly, we found GLI2 protein occupied the HTLV-1 Long Terminal Repeat. The effect of GLI2 expression on viral expression was investigated by knockdown of GLI2 in Hut-102 cells. Our results show that retroviral insertional mutagenesis can be an important mechanism in HTLV-1-induced leukemias and lymphomas.

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Braoudaki, Maria, and Fotini Tzortzatou-Stathopoulou. "Tumorigenesis related to retroviral infections." Journal of Infection in Developing Countries 5, no. 11 (November 10, 2011): 751–58. http://dx.doi.org/10.3855/jidc.1773.

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Retroviral infections are considered important risk factors for cancer development in humans since approximately 15-20% of cancer worldwide is caused by an infectious agent. This report discusses the most established oncogenic retroviruses, including human immunodeficiency virus (HIV), human T-cell leukemia virus (HTLV-1 and -2), Rous sarcoma virus (RSV), Abelson murine leukemia virus (A-MuLV), Moloney murine leukemia virus (M-MuLV), murine mammary tumor virus (MMTV), bovine leukemia virus, (BLV), Jaagsiekte sheep retrovirus (JSRV), and Friend spleen focus-forming virus (SFFV). The role of retroviruses as inducers of carcinogenesis, the mechanisms underlying oncogenic transformation, and the routes of transmission of several cancer-related retroviral infections are also described. Finally, the impact of cancer-related retroviral infections in the developing world is addressed. This review is an update of carcinogenesis caused by retroviral infections.

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Hanson, Heather M., Nora A. Willkomm, Huixin Yang, and Louis M. Mansky. "Human Retrovirus Genomic RNA Packaging." Viruses 14, no. 5 (May 19, 2022): 1094. http://dx.doi.org/10.3390/v14051094.

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Two non-covalently linked copies of the retrovirus genome are specifically recruited to the site of virus particle assembly and packaged into released particles. Retroviral RNA packaging requires RNA export of the unspliced genomic RNA from the nucleus, translocation of the genome to virus assembly sites, and specific interaction with Gag, the main viral structural protein. While some aspects of the RNA packaging process are understood, many others remain poorly understood. In this review, we provide an update on recent advancements in understanding the mechanism of RNA packaging for retroviruses that cause disease in humans, i.e., HIV-1, HIV-2, and HTLV-1, as well as advances in the understanding of the details of genomic RNA nuclear export, genome translocation to virus assembly sites, and genomic RNA dimerization.

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Larkin, Julie, John T. Sinnott, Joshua Weiss, and Douglas A. Holt. "Human T-Cell Lymphotropic Virus-Type I." Infection Control & Hospital Epidemiology 11, no. 6 (June 1990): 314–18. http://dx.doi.org/10.1086/646177.

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Human T-cell lymphotropic virus type-1 (HTLV-I) is a recently recognized retrovirus identified as the cause of adult T-cell leukemia-lymphoma (ATLL) and HTLV-I-associated myelopathy (TSPI HAM). HTLV-I, a member of theRetroviridaefamily of viruses, was first described in 1980 after the isolation of the virus from a patient with a T-cell lymphoma. These pathogenic retroviruses are typically divided into theOncovirinaeandLentivirinae. The oncovirus group, including HTLV-I, HTLV-II and bovine leukemia virus (BLV), is generally associated with tumors. The lentiviruses are associated with immune deficiency and/or neurologic disease, and include agents such as the visna virus of sheep and the human immunodeficiency virus type-1 and -2 HIV-1 and HIV-2).

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Cohen, Isaac, and Jules E. Harris. "HTLV-I: The forgotten retrovirus." Medical and Pediatric Oncology 16, no. 1 (1988): 48–56. http://dx.doi.org/10.1002/mpo.2950160112.

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8

Fujita, M., K. Murata, and H. Shiku. "Selective inhibition of human T-lymphotropic virus type I-transformed human T-cell growth by a tax-targeted conditionally cytotoxic recombinant retrovirus." Blood 84, no. 8 (October 15, 1994): 2591–96. http://dx.doi.org/10.1182/blood.v84.8.2591.2591.

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Abstract Adult T-cell leukemia (ATL), a disorder associated with high mortality rates, arises from human T-lymphotropic virus type I (HTLV-I)-infected CD4+ T cells. We designed a retroviral vector-based gene therapy approach to ATL. The long terminal repeat (LTR) of HTLV-I is transactivated by the viral tax protein. We constructed a hybrid gene consisting of herpes simplex virus thymidine kinase (HSV TK) under the control of the HTLV-I LTR and inserted it into a retroviral vector. When HTLV-I-transformed and tax-expressing human T-cell lines were infected with this recombinant retrovirus (LNLTK alpha virus), they expressed high levels of HSV TK and exhibited increased sensitivity to acyclovir, a nucleoside analog that is converted to the toxic anabolite after phosphorylation by the HSV TK. On the other hand, the retroviral infection had little effect on acyclovir-induced cytotoxicity in HTLV-I- negative human hematopoietic cell lines. Our data may provide the prospect of the gene therapy for ATL by tax-targeted selective elimination of leukemic cells.

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Fujita, M., K. Murata, and H. Shiku. "Selective inhibition of human T-lymphotropic virus type I-transformed human T-cell growth by a tax-targeted conditionally cytotoxic recombinant retrovirus." Blood 84, no. 8 (October 15, 1994): 2591–96. http://dx.doi.org/10.1182/blood.v84.8.2591.bloodjournal8482591.

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Adult T-cell leukemia (ATL), a disorder associated with high mortality rates, arises from human T-lymphotropic virus type I (HTLV-I)-infected CD4+ T cells. We designed a retroviral vector-based gene therapy approach to ATL. The long terminal repeat (LTR) of HTLV-I is transactivated by the viral tax protein. We constructed a hybrid gene consisting of herpes simplex virus thymidine kinase (HSV TK) under the control of the HTLV-I LTR and inserted it into a retroviral vector. When HTLV-I-transformed and tax-expressing human T-cell lines were infected with this recombinant retrovirus (LNLTK alpha virus), they expressed high levels of HSV TK and exhibited increased sensitivity to acyclovir, a nucleoside analog that is converted to the toxic anabolite after phosphorylation by the HSV TK. On the other hand, the retroviral infection had little effect on acyclovir-induced cytotoxicity in HTLV-I- negative human hematopoietic cell lines. Our data may provide the prospect of the gene therapy for ATL by tax-targeted selective elimination of leukemic cells.

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10

Satou, Yorifumi, Paola Miyazato, Ko Ishihara, Hiroko Yaguchi, Anat Melamed, Michi Miura, Asami Fukuda, et al. "The retrovirus HTLV-1 inserts an ectopic CTCF-binding site into the human genome." Proceedings of the National Academy of Sciences 113, no. 11 (February 29, 2016): 3054–59. http://dx.doi.org/10.1073/pnas.1423199113.

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Human T-lymphotropic virus type 1 (HTLV-1) is a retrovirus that causes malignant and inflammatory diseases in ∼10% of infected people. A typical host has between 104 and 105 clones of HTLV-1–infected T lymphocytes, each clone distinguished by the genomic integration site of the single-copy HTLV-1 provirus. The HTLV-1 bZIP (HBZ) factor gene is constitutively expressed from the minus strand of the provirus, whereas plus-strand expression, required for viral propagation to uninfected cells, is suppressed or intermittent in vivo, allowing escape from host immune surveillance. It remains unknown what regulates this pattern of proviral transcription and latency. Here, we show that CTCF, a key regulator of chromatin structure and function, binds to the provirus at a sharp border in epigenetic modifications in the pX region of the HTLV-1 provirus in T cells naturally infected with HTLV-1. CTCF is a zinc-finger protein that binds to an insulator region in genomic DNA and plays a fundamental role in controlling higher order chromatin structure and gene expression in vertebrate cells. We show that CTCF bound to HTLV-1 acts as an enhancer blocker, regulates HTLV-1 mRNA splicing, and forms long-distance interactions with flanking host chromatin. CTCF-binding sites (CTCF-BSs) have been propagated throughout the genome by transposons in certain primate lineages, but CTCF binding has not previously been described in present-day exogenous retroviruses. The presence of an ectopic CTCF-BS introduced by the retrovirus in tens of thousands of genomic locations has the potential to cause widespread abnormalities in host cell chromatin structure and gene expression.

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Coffin, John M. "The discovery of HTLV-1, the first pathogenic human retrovirus." Proceedings of the National Academy of Sciences 112, no. 51 (December 22, 2015): 15525–29. http://dx.doi.org/10.1073/pnas.1521629112.

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After the discovery of retroviral reverse transcriptase in 1970, there was a flurry of activity, sparked by the “War on Cancer,” to identify human cancer retroviruses. After many false claims resulting from various artifacts, most scientists abandoned the search, but the Gallo laboratory carried on, developing both specific assays and new cell culture methods that enabled them to report, in the accompanying 1980 PNAS paper, identification and partial characterization of human T-cell leukemia virus (HTLV; now known as HTLV-1) produced by a T-cell line from a lymphoma patient. Follow-up studies, including collaboration with the group that first identified a cluster of adult T-cell leukemia (ATL) cases in Japan, provided conclusive evidence that HTLV was the cause of this disease. HTLV-1 is now known to infect at least 4–10 million people worldwide, about 5% of whom will develop ATL. Despite intensive research, knowledge of the viral etiology has not led to improvement in treatment or outcome of ATL. However, the technology for discovery of HTLV and acknowledgment of the existence of pathogenic human retroviruses laid the technical and intellectual foundation for the discovery of the cause of AIDS soon afterward. Without this advance, our ability to diagnose and treat HIV infection most likely would have been long delayed.

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12

Halbrook, Megan, Adva Gadoth, Anupama Shankar, HaoQiang Zheng, Ellsworth M. Campbell, Nicole A. Hoff, Jean-Jacques Muyembe, Emile Okitolonda Wemakoy, Anne W. Rimoin, and William M. Switzer. "Human T-cell lymphotropic virus type 1 transmission dynamics in rural villages in the Democratic Republic of the Congo with high nonhuman primate exposure." PLOS Neglected Tropical Diseases 15, no. 1 (January 28, 2021): e0008923. http://dx.doi.org/10.1371/journal.pntd.0008923.

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The Democratic Republic of the Congo (DRC) has a history of nonhuman primate (NHP) consumption and exposure to simian retroviruses yet little is known about the extent of zoonotic simian retroviral infections in DRC. We examined the prevalence of human T-lymphotropic viruses (HTLV), a retrovirus group of simian origin, in a large population of persons with frequent NHP exposures and a history of simian foamy virus infection. We screened plasma from 3,051 persons living in rural villages in central DRC using HTLV EIA and western blot (WB). PCR amplification of HTLV tax and LTR sequences from buffy coat DNA was used to confirm infection and to measure proviral loads (pVLs). We used phylogenetic analyses of LTR sequences to infer evolutionary histories and potential transmission clusters. Questionnaire data was analyzed in conjunction with serological and molecular data. A relatively high proportion of the study population (5.4%, n = 165) were WB seropositive: 128 HTLV-1-like, 3 HTLV-2-like, and 34 HTLV-positive but untypeable profiles. 85 persons had HTLV indeterminate WB profiles. HTLV seroreactivity was higher in females, wives, heads of households, and increased with age. HTLV-1 LTR sequences from 109 persons clustered strongly with HTLV-1 and STLV-1 subtype B from humans and simians from DRC, with most sequences more closely related to STLV-1 from Allenopithecus nigroviridis (Allen’s swamp monkey). While 18 potential transmission clusters were identified, most were in different households, villages, and health zones. Three HTLV-1-infected persons were co-infected with simian foamy virus. The mean and median percentage of HTLV-1 pVLs were 5.72% and 1.53%, respectively, but were not associated with age, NHP exposure, village, or gender. We document high HTLV prevalence in DRC likely originating from STLV-1. We demonstrate regional spread of HTLV-1 in DRC with pVLs reported to be associated with HTLV disease, supporting local and national public health measures to prevent spread and morbidity.

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Carcone, Auriane, Chloé Journo, and Hélène Dutartre. "Is the HTLV-1 Retrovirus Targeted by Host Restriction Factors?" Viruses 14, no. 8 (July 23, 2022): 1611. http://dx.doi.org/10.3390/v14081611.

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Human T cell leukemia virus type 1 (HTLV-1), the etiological agent of adult T cell leukemia/lymphoma (ATLL) and of HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), was identified a few years before Human Immunodeficiency Virus (HIV). However, forty years later, our comprehension of HTLV-1 immune detection and the host immune responses to HTLV-1 is far more limited than for HIV. In addition to innate and adaptive immune responses that rely on specialized cells of the immune system, host cells may also express a range of antiviral factors that inhibit viral replication at different stages of the cycle, in a cell-autonomous manner. Multiple antiviral factors allowing such an intrinsic immunity have been primarily and extensively described in the context HIV infection. Here, we provide an overview of whether known HIV restriction factors might act on HTLV-1 replication. Interestingly, many of them do not exert any antiviral activity against HTLV-1, and we discuss viral replication cycle specificities that could account for these differences. Finally, we highlight future research directions that could help to identify antiviral factors specific to HTLV-1.

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Toro Rueda, C., B. Rodés Soldevila, E. Poveda López, and V. Soriano Vázquez. "Infecciones por retrovirus. HTLV-I/II." Medicine - Programa de Formación Médica Continuada Acreditado 8, no. 73 (January 2002): 3915–22. http://dx.doi.org/10.1016/s0304-5412(02)70726-9.

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Krichbaum-Stenger, K., BJ Poiesz, P. Keller, G. Ehrlich, J. Gavalchin, BH Davis, and JL Moore. "Specific adsorption of HTLV-I to various target human and animal cells." Blood 70, no. 5 (November 1, 1987): 1303–11. http://dx.doi.org/10.1182/blood.v70.5.1303.1303.

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Abstract In this report, we describe a flow cytometric analysis of HTLV-I specific binding to fresh and cultured cells on a single cell basis. This assay uses rhodamine hydrocarbon tagged, purified HTLV-I virions according to the procedure originally described for avian retroviruses. Successful HTLV-I transmission was detected by analysis of integrated HTLV-I DNA, virion-associated reverse transcriptase, and/or intracellular HTLV-I core antigen p19 expression. Only a specific virus- cell interaction was detected because nonrhodamine-tagged homologous virus or related HTLV-II interfered with tagged HTLV-I binding. In contrast, an unrelated, nonlabeled animal retrovirus was unable to block tagged HTLV binding. Of the cell lines tested, 2 nonlymphoid mammalian and 3 human lymphoid bound significantly high to moderate levels of HTLV-I-tagged virions. The other three human lymphocyte cell lines were insensitive to HTLV-I adsorption. A direct correlation was observed between HTLV-I binding sites and infectivity of human lymphoid cells alone and not other nonlymphoid animal cells. Fresh normal human mononuclear cells bound low levels of HTLV-I virions. As expected, T lymphocytes demonstrated more binding than did the non-T cell population. Enhancement of HTLV-I cell binding in a subpopulation of mononuclear target cells was achieved with phytohemagglutinin (PHA) activation and interleukin 2 (IL2) stimulation, which correlates well with previously published infectivity studies.

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Krichbaum-Stenger, K., BJ Poiesz, P. Keller, G. Ehrlich, J. Gavalchin, BH Davis, and JL Moore. "Specific adsorption of HTLV-I to various target human and animal cells." Blood 70, no. 5 (November 1, 1987): 1303–11. http://dx.doi.org/10.1182/blood.v70.5.1303.bloodjournal7051303.

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In this report, we describe a flow cytometric analysis of HTLV-I specific binding to fresh and cultured cells on a single cell basis. This assay uses rhodamine hydrocarbon tagged, purified HTLV-I virions according to the procedure originally described for avian retroviruses. Successful HTLV-I transmission was detected by analysis of integrated HTLV-I DNA, virion-associated reverse transcriptase, and/or intracellular HTLV-I core antigen p19 expression. Only a specific virus- cell interaction was detected because nonrhodamine-tagged homologous virus or related HTLV-II interfered with tagged HTLV-I binding. In contrast, an unrelated, nonlabeled animal retrovirus was unable to block tagged HTLV binding. Of the cell lines tested, 2 nonlymphoid mammalian and 3 human lymphoid bound significantly high to moderate levels of HTLV-I-tagged virions. The other three human lymphocyte cell lines were insensitive to HTLV-I adsorption. A direct correlation was observed between HTLV-I binding sites and infectivity of human lymphoid cells alone and not other nonlymphoid animal cells. Fresh normal human mononuclear cells bound low levels of HTLV-I virions. As expected, T lymphocytes demonstrated more binding than did the non-T cell population. Enhancement of HTLV-I cell binding in a subpopulation of mononuclear target cells was achieved with phytohemagglutinin (PHA) activation and interleukin 2 (IL2) stimulation, which correlates well with previously published infectivity studies.

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Frias, Diego, Joana P. Monteiro-Cunha, Aline C. Mota-Miranda, Vagner S. Fonseca, Tulio De Oliveira, Bernardo Galvao-Castro, and Luiz C. J. Alcantara. "Human Retrovirus Codon Usage from tRNA Point of View: Therapeutic Insights." Bioinformatics and Biology Insights 7 (January 2013): BBI.S12093. http://dx.doi.org/10.4137/bbi.s12093.

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The purpose of this study was to investigate the balance between transfer ribonucleic acid (tRNA) supply and demand in retrovirus-infected cells, seeking the best targets for antiretroviral therapy based on the hypothetical tRNA Inhibition Therapy (TRIT). Codon usage and tRNA gene data were retrieved from public databases. Based on logistic principles, a therapeutic score (T-score) was calculated for all sense codons, in each retrovirus-host system. Codons that are critical for viral protein translation, but not as critical for the host, have the highest T-score values. Theoretically, inactivating the cognate tRNA species should imply a severe reduction of the elongation rate during viral mRNA translation. We developed a method to predict tRNA species critical for retroviral protein synthesis. Four of the best TRIT targets in HIV-1 and HIV-2 encode Large Hydrophobic Residues (LHR), which have a central role in protein folding. One of them, codon CUA, is also a TRIT target in both HTLV-1 and HTLV-2. Therefore, a drug designed for inactivating or reducing the cytoplasmatic concentration of tRNA species with anticodon TAG could attenuate significantly both HIV and HTLV protein synthesis rates. Inversely, replacing codons ending in UA by synonymous codons should increase the expression, which is relevant for DNA vaccine design.

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Shah, N. P., W. Wachsman, A. J. Cann, L. Souza, D. J. Slamon, and I. S. Chen. "Comparison of the trans-activation capabilities of the human T-cell leukemia virus type I and II chi proteins." Molecular and Cellular Biology 6, no. 11 (November 1986): 3626–31. http://dx.doi.org/10.1128/mcb.6.11.3626-3631.1986.

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The mechanism of cellular transformation by the human T-cell leukemia viruses (HTLVs) is thought to involve a novel retrovirus gene known as chi. The chi gene is essential for HTLV replication and acts by enhancing transcription from the viral long terminal repeat. By using the HTLV type I and II chi gene-coding regions inserted into a highly efficient expression vector, we directly compared the efficiencies of the two chi proteins to trans activate the HTLV type I and II long terminal repeats. We demonstrate that the two chi proteins have different patterns of trans activation. The patterns were highly reproducible in all mammalian cells tested. A different pattern of activation was observed in avian cells. These results suggest that the mechanism of trans activation involves specific cellular factors that are highly conserved throughout mammalian species but different in avian cells. Understanding the mechanism of trans activation by the chi gene product may provide insights into mechanisms of cellular transformation by HTLV.

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Shah, N. P., W. Wachsman, A. J. Cann, L. Souza, D. J. Slamon, and I. S. Chen. "Comparison of the trans-activation capabilities of the human T-cell leukemia virus type I and II chi proteins." Molecular and Cellular Biology 6, no. 11 (November 1986): 3626–31. http://dx.doi.org/10.1128/mcb.6.11.3626.

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The mechanism of cellular transformation by the human T-cell leukemia viruses (HTLVs) is thought to involve a novel retrovirus gene known as chi. The chi gene is essential for HTLV replication and acts by enhancing transcription from the viral long terminal repeat. By using the HTLV type I and II chi gene-coding regions inserted into a highly efficient expression vector, we directly compared the efficiencies of the two chi proteins to trans activate the HTLV type I and II long terminal repeats. We demonstrate that the two chi proteins have different patterns of trans activation. The patterns were highly reproducible in all mammalian cells tested. A different pattern of activation was observed in avian cells. These results suggest that the mechanism of trans activation involves specific cellular factors that are highly conserved throughout mammalian species but different in avian cells. Understanding the mechanism of trans activation by the chi gene product may provide insights into mechanisms of cellular transformation by HTLV.

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Macchi, B., S. Grelli, C. Favalli, M. De Carli, Garaci, and A. Mastino. "Characteristics of Interleukin 2 and Interleukin 4 Dependent T Cell Lines Infected with HTLV-1 in Vitro." International Journal of Immunopathology and Pharmacology 10, no. 3 (September 1997): 189–94. http://dx.doi.org/10.1177/039463209701000304.

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Human T-cell leukemia/lymphoma virus type 1 (HTLV-1) is a lymphotropic retrovirus. Cells infected with HTLV-1 in vitro, when maintained in interleukin-2 (IL-2) can be immortalized, remaining for a long time strictly dependent on IL-2 addition. In this study we have compared the effect of interleukin-4 (IL-4) and interleukin-2 on HTLV-1 infection of cord blood or normal adult mononuclear cells. The results showed that either cultures of cord blood or normal adult T cells are susceptible to HTLV-1 infection in presence of IL-4 as well as IL-2. Moreover HTLV-1 infected cells in the presence of IL-4 survived only for a limited length of time in culture, while those grown in IL-2 showed the characteristics of immortalized cell lines. Moreover the profile of cytokine production showed a different pattern in HTLV-1 infected cell lines maintained in IL-4 or IL-2. This suggests that the lymphokines differently modulate retrovirus infection in vitro.

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GASTALDELLO, René, Sandra GALLEGO, María Beatriz ISA, Eduardo MATURANO, Santos SILEONI, Silvia NATES, and Silvia MEDEOT. "Immunofluorescence assay reactivity patterns of serum samples presenting indeterminate Western blot results for antibodies to HIV-1 and HTLV-I/II in Cordoba, Argentina." Revista do Instituto de Medicina Tropical de São Paulo 43, no. 5 (October 2001): 277–82. http://dx.doi.org/10.1590/s0036-46652001000500008.

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Serum samples (n: 110) from blood donors and high risk individuals from Cordoba, Argentina with indeterminate HIV-1 and HTLV-I/II Wb profiles were studied for specific antibodies to HTLV-I/II and HIV-1 by indirect immunofluorescence assay (IFA) and for the presence or absence of HIV-1 and HTLV-I/II specific bands by Wb. This study was carried out in order to characterize their putative reactions with HIV-1 and HTLV-I/II proteins and to resolve the retrovirus infection status of these individuals. Results indicated that blood donors sera displaying indeterminate HIV-1 or HTLV-I/II Wb patterns were not immunoreactive to HTLV-I/II and HIV-1 on IFA. However, a high rate of indeterminate HIV-1 and HTLV-I/II Wb samples from high risk individuals had positive HTLV-I/II and HIV-1 IFA results respectively. Our study supports the growing evidence that HTLV-HIV indeterminate seroreactivity in low risk population is due to a cross reaction against nonviral antigens, and in high risk populations the indeterminate samples show serological cross-recognition between HIV-1 proteins and HTLV-I/II proteins on Wb. These results point out the necessity to investigate the HTLV-I/II reactivity in indeterminate HIV-1 samples and viceversa in order to confirm the diagnosis. Finally, this study shows the potential usefulness of IFA in elucidating the status of HIV-1 and HTLV-I/II infection of individuals with indeterminate Wb profiles, thus enabling resolution of retrovirus infection status.

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Hogan, Victoria, and Welkin E. Johnson. "Unique Structure and Distinctive Properties of the Ancient and Ubiquitous Gamma-Type Envelope Glycoprotein." Viruses 15, no. 2 (January 18, 2023): 274. http://dx.doi.org/10.3390/v15020274.

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After the onset of the AIDS pandemic, HIV-1 (genus Lentivirus) became the predominant model for studying retrovirus Env glycoproteins and their role in entry. However, HIV Env is an inadequate model for understanding entry of viruses in the Alpharetrovirus, Gammaretrovirus and Deltaretrovirus genera. For example, oncogenic model system viruses such as Rous sarcoma virus (RSV, Alpharetrovirus), murine leukemia virus (MLV, Gammaretrovirus) and human T-cell leukemia viruses (HTLV-I and HTLV-II, Deltaretrovirus) encode Envs that are structurally and functionally distinct from HIV Env. We refer to these as Gamma-type Envs. Gamma-type Envs are probably the most widespread retroviral Envs in nature. They are found in exogenous and endogenous retroviruses representing a broad spectrum of vertebrate hosts including amphibians, birds, reptiles, mammals and fish. In endogenous form, gamma-type Envs have been evolutionarily coopted numerous times, most notably as placental syncytins (e.g., human SYNC1 and SYNC2). Remarkably, gamma-type Envs are also found outside of the Retroviridae. Gp2 proteins of filoviruses (e.g., Ebolavirus) and snake arenaviruses in the genus Reptarenavirus are gamma-type Env homologs, products of ancient recombination events involving viruses of different Baltimore classes. Distinctive hallmarks of gamma-type Envs include a labile disulfide bond linking the surface and transmembrane subunits, a multi-stage attachment and fusion mechanism, a highly conserved (but poorly understood) “immunosuppressive domain”, and activation by the viral protease during virion maturation. Here, we synthesize work from diverse retrovirus model systems to illustrate these distinctive properties and to highlight avenues for further exploration of gamma-type Env structure and function.

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Islam, Shariful, Claudia M. Espitia, Daniel O. Persky, Jennifer S. Carew, and Steffan T. Nawrocki. "Targeting JAK/STAT Signaling Antagonizes Resistance to Oncolytic Reovirus Therapy Driven by Prior Infection with HTLV-1 in Models of T-Cell Lymphoma." Viruses 13, no. 7 (July 20, 2021): 1406. http://dx.doi.org/10.3390/v13071406.

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Human T-cell leukemia virus type 1 (HTLV-1) is a retrovirus that infects at least 10 million people worldwide and is associated with the development of T-cell lymphoma (TCL). The treatment of TCL remains challenging and new treatment options are urgently needed. With the goal of developing a novel therapeutic approach for TCL, we investigated the activity of the clinical formulation of oncolytic reovirus (Reolysin, Pelareorep) in TCL models. Our studies revealed that HTLV-1-negative TCL cells were highly sensitive to Reolysin-induced cell death, but HTLV-1-positive TCL cells were resistant. Consistent with these data, reovirus displayed significant viral accumulation in HTLV-1-negative cells, but failed to efficiently replicate in HTLV-1-positive cells. Transcriptome analyses of HTLV-1-positive vs. negative cells revealed a significant increase in genes associated with retroviral infection including interleukin-13 and signal transducer and activator of transcription 5 (STAT5). To investigate the relationship between HTLV-1 status and sensitivity to Reolysin, we infected HTLV-1-negative cells with HTLV-1. The presence of HTLV-1 resulted in significantly decreased sensitivity to Reolysin. Treatment with the JAK inhibitor ruxolitinib suppressed STAT5 phosphorylation and expression of the key anti-viral response protein MX1 and enhanced the anti-TCL activity of Reolysin in both HTLV-1-positive and negative cells. Our data demonstrate that the inhibition of the JAK/STAT pathway can be used as a novel approach to antagonize the resistance of HTLV-1-positive cells to oncolytic virus therapy.

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Corradin, Alberto, Barbara Di Camillo, Vincenzo Ciminale, Gianna Toffolo, and Claudio Cobelli. "Sensitivity Analysis of Retrovirus HTLV-1 Transactivation." Journal of Computational Biology 18, no. 2 (February 2011): 183–93. http://dx.doi.org/10.1089/cmb.2010.0219.

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Valenti, William M. "Infection Control and Employee Health: AIDS Update Part 2." Infection Control 6, no. 10 (October 1985): 421–24. http://dx.doi.org/10.1017/s0195941700063529.

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The Acquired Immune Deficiency Syndrome (AIDS) continues to perplex health care providers. As our knowledge has increased, so has the number of questions, especially those related to infection control and employee health. Since the last time AIDS was reviewed in this column, additional information has become available which elaborates on some of the infection control aspects of this disease.The human T-cell lymphotropic retrovirus (HTLV-III) appears to be the cause of AIDS. Other names used for HTLV-III are lymphadenopathy-associated virus (LAV) and AIDS-associated retrovirus. So called co-factors may be necessary to initiate disease after an individual acquires HTLV-III infection. Agents such as cytomegalovirus, the Epstein-Barr virus and multiple exposures to HTLV-III have been suggested as possible cofactors. Only a relatively small percentage of individuals who acquire HTLV-III antibody eventually develop overt disease or “full-blown AIDS.” Studies to date have shown that after 1 to 5 years of follow-up, 4% to 19% of seropositives developed AIDS.In addition, the spectrum of disease caused by HTLV-III appears to be broader than originally thought. An additional 25% of those with antibody may have developed AIDS-related diseases including neurological symptoms, fever, weight loss, diarrhea, oral candidiasis and lymphadenopathy during the follow-up period.

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Kanner, S. B., C. Cheng-Mayer, R. B. Geffin, W. P. Parks, G. A. Beltz, L. O. Arthur, K. P. Samuel, and T. S. Papas. "Human retroviral env and gag polypeptides: serologic assays to measure infection." Journal of Immunology 137, no. 2 (July 15, 1986): 674–78. http://dx.doi.org/10.4049/jimmunol.137.2.674.

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Abstract Humoral antiviral responses to human retrovirus infections identify persistently infected individuals and can be used to characterize virus-host interactions. Antibodies to native viral polypeptides have been reliably measured, although quantitation of env antibodies is difficult due to a lack of purified antigens. To quantitate antibodies to env antigens, bacterially expressed cloned env polypeptides from the transmembrane regions of human T lymphotropic virus types I and III were applied to nitrocellulose filters in an immunodot assay. A combination of the sensitivity of the Western blot procedure and the specificity of peptides from defined viral sequences was used to detect 49/49 HTLV-III/LAV-infected individuals previously defined as seropositive by radioimmunoprecipitation sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Of these HTLV-III/LAV envelope seropositive people, 22% lacked antibody to p24 in a radioimmunoassay. In contrast, the sensitivity of antibody detection to HTLV-I env antigens and p24 were comparable. Antibodies to HTLV-I and HTLV-III/LAV env transmembrane peptides were not cross-reactive. Levels of antibody to env antigens of both HTLV-I and HTLV-III/LAV persisted without change for at least 26 mo, suggesting that most infections represent stable virus-host interactions. The use of bacterially expressed env peptides offers a rapid serologic approach for distinguishing human retroviral infections and can be used to define immune responses to specific regions of the viral genome.

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Nishimura, M., A. Adachi, M. Maeda, I. Akiguchi, A. Ishimoto, and J. Kimura. "Human T lymphotrophic virus type I may not be associated with multiple sclerosis in Japan." Journal of Immunology 144, no. 5 (March 1, 1990): 1684–88. http://dx.doi.org/10.4049/jimmunol.144.5.1684.

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Abstract To study the possible involvement of human T lymphotrophic virus type I (HTLV-I) or a related retrovirus in Japanese cases of multiple sclerosis (MS), we first performed a Western blot analysis with purified Ag of HTLV-I. Ten out of 31 MS patients (32.2%), 19 of 66 patients (28.8%) with other neurologic diseases, and 2 of 64 healthy blood donors (3.1%) had antibodies reactive with Ag corresponding to the group-specific Ag (gag) proteins (p15, p19, p24) on their sera. There were no significant differences between MS and other neurologic diseases concerning the patterns and the frequency. Second, we tried to establish T cell lines from PBMC of 22 MS patients with crude IL-2 without accessory cells, because HTLV-I-infected T cells can be immortalized in a high ratio under those conditions. Only one T cell line (MS-14C), however, could be maintained in long term culture. MS-14C and cultured T cells for 3 to 5 wk derived from MS patients were examined by Southern blot analysis under both stringent and low stringent conditions with HTLV-I as a probe. No HTLV-I related bands could be detected. By polymerase chain reaction examination, we also could not detect HTLV-I provirus genome in the fresh PBMC from 20 MS patients, although some of them had gag-reactive antibodies. Our data do not favor the hypothesis of HTLV-I or an HTLV-I-related human retrovirus in the etiology of MS.

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Rabaaoui, Samira, Fatima Zouhiri, Agnès Lançon, Hervé Leh, Jean d'Angelo, and Eric Wattel. "Inhibitors of Strand Transfer That Prevent Integration and Inhibit Human T-Cell Leukemia Virus Type 1 Early Replication." Antimicrobial Agents and Chemotherapy 52, no. 10 (March 3, 2008): 3532–41. http://dx.doi.org/10.1128/aac.01361-07.

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ABSTRACT The replication of the retrovirus human T-cell leukemia virus type 1 (HTLV-1) is linked to the development of lymphoid malignancies and inflammatory diseases. Data from in vitro, ex vivo, and in vivo studies have revealed that no specific treatment can prevent or block HTLV-1 replication and therefore that there is no therapy for the prevention and/or treatment of HTLV-1-associated diseases in infected individuals. HTLV-1 and human immunodeficiency virus type 1 (HIV-1) integrases, the enzymes that specifically catalyze the integration of these retroviruses in host cell DNA, share important structural properties, suggesting that compounds that inhibit HIV-1 integration could also inhibit HTLV-1 integration. We developed quantitative assays to test, in vitro and ex vivo, the efficiencies of styrylquinolines and diketo acids, the two main classes of HIV-1 integrase inhibitors. The compounds were tested in vitro in an HTLV-1 strand-transfer reaction and ex vivo by infection of fresh peripheral blood lymphocytes with lethally irradiated HTLV-1-positive cells. In vitro, four styrylquinoline compounds and two diketo acid compounds significantly inhibited HTLV-1 integration in a dose-dependent manner. All compounds active in vitro decreased cell proliferation ex vivo, although at low concentrations; they also dramatically decreased both normalized proviral loads and the number of integration events during experimental ex vivo primary infection. Accordingly, diketo acids and styrylquinolines are the first drugs that produce a specific negative effect on HTLV-1 replication in vitro and ex vivo, suggesting their potential efficiency for the prevention and treatment of HTLV-1-associated diseases.

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Le Blanc, Isabelle, Vincent Blot, Isabelle Bouchaert, Jean Salamero, Bruno Goud, Arielle R. Rosenberg, and Marie-Christine Dokhélar. "Intracellular Distribution of Human T-Cell Leukemia Virus Type 1 Gag Proteins Is Independent of Interaction with Intracellular Membranes." Journal of Virology 76, no. 2 (January 15, 2002): 905–11. http://dx.doi.org/10.1128/jvi.76.2.905-911.2002.

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ABSTRACT Retrovirus Gag proteins are synthesized on free ribosomes, and are sufficient to govern the assembly and release of virus particles. Like type C retroviruses, human T-cell leukemia virus type 1 (HTLV-1) assembles and buds at the plasma membrane. After immunofluorescence staining, HTLV-1 Gag proteins appear as punctuated intracellular clusters, which suggests that they are associated either with intracellular membranes or with the plasma membrane. However, colocalization experiments using a panel of markers demonstrated that Gag proteins were not associated with the membranes involved in the secretory or endocytosis pathway. Small amounts of Gag proteins were detected at the plasma membrane and colocalized with the envelope glycoproteins. Moreover, Gag proteins were excluded from streptolysin-O permeabilized cells and in this respect behaved like cytoplasmic proteins. This suggests that the trafficking of HTLV-1 Gag proteins through the cytoplasm of the host cell is independent of any cell membrane system.

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Tagaya, Yutaka, Masao Matsuoka, and Robert Gallo. "40 years of the human T-cell leukemia virus: past, present, and future." F1000Research 8 (February 28, 2019): 228. http://dx.doi.org/10.12688/f1000research.17479.1.

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It has been nearly 40 years since human T-cell leukemia virus-1 (HTLV-1), the first oncogenic retrovirus in humans and the first demonstrable cause of cancer by an infectious agent, was discovered. Studies indicate that HTLV-1 is arguably one of the most carcinogenic agents to humans. In addition, HTLV-1 causes a diverse array of diseases, including myelopathy and immunodeficiency, which cause morbidity and mortality to many people in the world, including the indigenous population in Australia, a fact that was emphasized only recently. HTLV-1 can be transmitted by infected lymphocytes, from mother to child via breast feeding, by sex, by blood transfusion, and by organ transplant. Therefore, the prevention of HTLV-1 infection is possible but such action has been taken in only a limited part of the world. However, until now it has not been listed by the World Health Organization as a sexually transmitted organism nor, oddly, recognized as an oncogenic virus by the recent list of the National Cancer Institute/National Institutes of Health. Such underestimation of HTLV-1 by health agencies has led to a remarkable lack of funding supporting research and development of treatments and vaccines, causing HTLV-1 to remain a global threat. Nonetheless, there are emerging novel therapeutic and prevention strategies which will help people who have diseases caused by HTLV-1. In this review, we present a brief historic overview of the key events in HTLV-1 research, including its pivotal role in generating ideas of a retrovirus cause of AIDS and in several essential technologies applicable to the discovery of HIV and the unraveling of its genes and their function. This is followed by the status of HTLV-1 research and the preventive and therapeutic developments of today. We also discuss pending issues and remaining challenges to enable the eradication of HTLV-1 in the future.

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Taylor, J. M., M. Brown, M. Nejmeddine, K. J. Kim, L. Ratner, M. Lairmore, and C. Nicot. "Novel Role for Interleukin-2 Receptor-Jak Signaling in Retrovirus Transmission." Journal of Virology 83, no. 22 (September 2, 2009): 11467–76. http://dx.doi.org/10.1128/jvi.00952-09.

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ABSTRACT Human T-lymphotropic virus type 1 (HTLV-1) is the etiological agent of adult T-cell leukemia/lymphoma, and it encodes a number of nonstructural proteins that are involved in virus replication and immune evasion. The viral protein p12 previously has been characterized to interfere with major histocompatibility complex class, ICAM-1, and ICAM-2 expression, and it activates STAT5. Using a previously established T-cell line immortalized with an HTLV-1 molecular clone deleted for p12, we assessed the role of p12 in regulating cellular growth and virus transmission. These cells were complemented for p12 expression by the transduction of a lentivirus vector expressing p12. We report that p12 conferred a selective growth advantage in vitro and increased the colony formation of human T cells in soft-agar assays. Consistently with previous studies, p12− and p12+ cell lines produced similar amounts of virus particles released into the supernatant of cultured cells, although we found that p12 expression greatly enhanced virus transmission. Moreover, we found that interleukin-2 (IL-2) stimulation also increased HTLV-1 transmission whether p12 was expressed or not, and inversely, that the inhibition of Jak signaling significantly reduced HTLV-1 transmission. Intriguingly, IL-2/Jak signaling was not associated with changes in viral gene expression, viral RNA encapsidation, the maturation of the virus particle, cell-cell adherence, or Gag polarization and virological synapse formation. We do demonstrate, however, that IL-2 stimulation and p12 expression significantly increased the rate of syncytium formation, revealing a novel role for IL-2 signaling and Jak activation in HTLV-1 virus transmission.

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Busch, MP, M. Laycock, SH Kleinman, JW Jr Wages, M. Calabro, JE Kaplan, RF Khabbaz, and CG Hollingsworth. "Accuracy of supplementary serologic testing for human T-lymphotropic virus types I and II in US blood donors. Retrovirus Epidemiology Donor Study." Blood 83, no. 4 (February 15, 1994): 1143–48. http://dx.doi.org/10.1182/blood.v83.4.1143.1143.

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Abstract Blood donations in the United States have been screened for antibody to human T-lymphotropic virus type I (HTLV-I) by HTLV-I enzyme immunoassay (EIA) since November 1988. Specimens repeatedly found to be reactive by EIA undergo confirmation by supplementary serologic tests. We assessed the accuracy of blood center testing of 994 HTLV-I EIA repeat-reactive specimens in five US blood centers between November 1988 and December 1991. Of 410 confirmed HTLV-I/II donations, 407 (99.3%) were infected with HTLV-I/II, as determined by polymerase chain reaction (PCR) (403 cases) and by repeat serologic testing (4 cases). The three false- positive results occurred in the first year of testing. Of 425 HTLV-indeterminate specimens, 6 (1.4%) were found to be infected by PCR (5 with HTLV-II and 1 with HTLV-I). None of 159 confirmatory test-negative donations was PCR positive. Of HTLV-I/II-seropositive specimens, 80.2% to 95.4% could be typed as HTLV-I or HTLV-II by type-specific serologic assays. These results support recommendations that HTLV-I/II- seropositive donors should be advised that they are infected with HTLV- I, HTLV-II, or HTLV-I/II (depending on results of type-specific assays). HTLV-indeterminate donors should be advised that their results only rarely indicate HTLV infection. HTLV confirmatory test-negative donors should be reassured that they are not infected with HTLV-I or HTLV-II.

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Busch, MP, M. Laycock, SH Kleinman, JW Jr Wages, M. Calabro, JE Kaplan, RF Khabbaz, and CG Hollingsworth. "Accuracy of supplementary serologic testing for human T-lymphotropic virus types I and II in US blood donors. Retrovirus Epidemiology Donor Study." Blood 83, no. 4 (February 15, 1994): 1143–48. http://dx.doi.org/10.1182/blood.v83.4.1143.bloodjournal8341143.

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Blood donations in the United States have been screened for antibody to human T-lymphotropic virus type I (HTLV-I) by HTLV-I enzyme immunoassay (EIA) since November 1988. Specimens repeatedly found to be reactive by EIA undergo confirmation by supplementary serologic tests. We assessed the accuracy of blood center testing of 994 HTLV-I EIA repeat-reactive specimens in five US blood centers between November 1988 and December 1991. Of 410 confirmed HTLV-I/II donations, 407 (99.3%) were infected with HTLV-I/II, as determined by polymerase chain reaction (PCR) (403 cases) and by repeat serologic testing (4 cases). The three false- positive results occurred in the first year of testing. Of 425 HTLV-indeterminate specimens, 6 (1.4%) were found to be infected by PCR (5 with HTLV-II and 1 with HTLV-I). None of 159 confirmatory test-negative donations was PCR positive. Of HTLV-I/II-seropositive specimens, 80.2% to 95.4% could be typed as HTLV-I or HTLV-II by type-specific serologic assays. These results support recommendations that HTLV-I/II- seropositive donors should be advised that they are infected with HTLV- I, HTLV-II, or HTLV-I/II (depending on results of type-specific assays). HTLV-indeterminate donors should be advised that their results only rarely indicate HTLV infection. HTLV confirmatory test-negative donors should be reassured that they are not infected with HTLV-I or HTLV-II.

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Ghosh, SK, JT Abrams, H. Terunuma, EC Vonderheid, and E. DeFreitas. "Human T-cell leukemia virus type I tax/rex DNA and RNA in cutaneous T- cell lymphoma." Blood 84, no. 8 (October 15, 1994): 2663–71. http://dx.doi.org/10.1182/blood.v84.8.2663.2663.

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Abstract Peripheral blood mononuclear cells (PBMCs) and T-cell lines from patients with Sezary syndrome (SS) and skin lesions from patients with mycosis fungoides (MF) were examined by polymerase chain reaction (PCR) for DNA sequences homologous to the human retroviruses human T- lymphotropic virus (HTLV)-I and -II. Results obtained using primers and probes from the tax/rex region of HTLV-I indicate that 72% (18/25) of SS patients PBMCs, 80% (20/25) of T-cell lines established from SS- PBMC, and 30% (3/10) of skin lesions from MF patients were positive for HTLV-I tax/rex region DNA. Sequence analysis of the 127-bp fragment amplified by the tax/rex primers from 4 of these individuals was found to be identical to that in prototypic HTLV-I. Negative results were obtained using primers and probes from the HTLV-I gag region and the HTLV-II gag and tax regions. No PCR products were obtained using all primers and probes using DNA from 9 healthy blood donors and 10 cord bloods. Expression of HTLV-I tax/rex mRNA was found in 4 of 8 Sezary patients, as determined by RNA-PCR, indicating that this viral region is being transcribed in vivo. Exposure to Tax/Rex protein in SS- patients is supported by the fact that serum antibodies against p27rex and p40tax was observed in 43% and 29% of these SS patients, respectively. Although the causal relationship between the HTLV-I tax/rex region and cutaneous T-cell lymphoma (CTCL) remains unclear, these findings support the presence of a truncated HTLV-I retrovirus in CTCL patients.

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Ghosh, SK, JT Abrams, H. Terunuma, EC Vonderheid, and E. DeFreitas. "Human T-cell leukemia virus type I tax/rex DNA and RNA in cutaneous T- cell lymphoma." Blood 84, no. 8 (October 15, 1994): 2663–71. http://dx.doi.org/10.1182/blood.v84.8.2663.bloodjournal8482663.

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Peripheral blood mononuclear cells (PBMCs) and T-cell lines from patients with Sezary syndrome (SS) and skin lesions from patients with mycosis fungoides (MF) were examined by polymerase chain reaction (PCR) for DNA sequences homologous to the human retroviruses human T- lymphotropic virus (HTLV)-I and -II. Results obtained using primers and probes from the tax/rex region of HTLV-I indicate that 72% (18/25) of SS patients PBMCs, 80% (20/25) of T-cell lines established from SS- PBMC, and 30% (3/10) of skin lesions from MF patients were positive for HTLV-I tax/rex region DNA. Sequence analysis of the 127-bp fragment amplified by the tax/rex primers from 4 of these individuals was found to be identical to that in prototypic HTLV-I. Negative results were obtained using primers and probes from the HTLV-I gag region and the HTLV-II gag and tax regions. No PCR products were obtained using all primers and probes using DNA from 9 healthy blood donors and 10 cord bloods. Expression of HTLV-I tax/rex mRNA was found in 4 of 8 Sezary patients, as determined by RNA-PCR, indicating that this viral region is being transcribed in vivo. Exposure to Tax/Rex protein in SS- patients is supported by the fact that serum antibodies against p27rex and p40tax was observed in 43% and 29% of these SS patients, respectively. Although the causal relationship between the HTLV-I tax/rex region and cutaneous T-cell lymphoma (CTCL) remains unclear, these findings support the presence of a truncated HTLV-I retrovirus in CTCL patients.

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Lindholm, Paul F., Fatah Kashanchi, and John N. Brady. "Transcriptional regulation in the human retrovirus HTLV-1." Seminars in Virology 4, no. 1 (February 1993): 53–60. http://dx.doi.org/10.1016/1044-5773(93)80008-c.

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Silveira, Júlia Meireles da Silva, Sheila de Oliveira Medeiros, Renata Fernandes Ferreira de Moraes, Erica Cristina Rocha Roier, Bruna de Azevedo Baêta, Letícia Patrão de Macedo Gomes, Gustavo Mendes Gomes, and Ana Paula Abreu. "Cytomorphological similarities between feline viral leukemia, bovine enzootic leukosis and adult T-cell leukemia/lymphoma: A review." Research, Society and Development 10, no. 9 (July 22, 2021): e13010917900. http://dx.doi.org/10.33448/rsd-v10i9.17900.

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Leukemias are malignant neoplasms of hematological origin and originating from bone marrow cells. Innumerable species can be affected by this disease, which can be originated by several causes, including infection by viruses belonging to the Retroviridae family. In felines, humans and cattle, the leukemia-inducing retroviruses are Feline Leukemia Virus (FeLV), human T-cell lymphotropic virus type 1 (HTLV-1) and Bovine Leukosis Virus (BLV), respectively. In Brazil, the number of domestic cats infected with FeLV grows progressively, when compared to the incidence of infected animals in developed countries, such as the United States. In cattle, viral leukemia or enzootic bovine leukosis (EBL), caused by BLV, although asymptomatic, leads to decreased production and economic losses. In humans, HTLV-1 was the first human retrovirus described in the 1980s. In this work, the similarities between cytomorphological changes in felines, cattle and humans affected by FeLV, BLV and HTLV-1, respectively, were analyzed. The bibliographic findings showed that the affected species addressed share the presence of atypical and/or reactive lymphocytes, smudge cells, immature cells and nuclear cell atypias in peripheral blood.

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Mosquera, Carmen, Elvia Aspiazu, Jacobus H. De Waard, and Miguel Angel Garcia-Bereguiain. "Infección por virus HTLV-1/2 confirmada por serología y detección de provirus en pacientes ecuatorianos de paraparesis espástica tropical." Infectio 24, no. 2 (February 8, 2020): 57. http://dx.doi.org/10.22354/in.v24i2.832.

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Introduccion: La infección con el virus linfotrópico de células T humano (HTLV) de tipo 1 y 2 es endémica en América del Sur. Existen muy pocos reportes clínicos de este retrovirus en pacientes de Ecuador y nunca confirmaron la presencia del virus con el aislamiento o la detección de su ADN. Esta infección se encuentra desatendida por las autoridades de salud pública, sin que existan estudios epidemiológicos de prevalencia a nivel del país. Objetivos: Este estudio tiene como objetivo la detección de infección por HTLV -1/2 en individuos sintomáticos de paraparesis espástica tropical (TSP) utilizando por primera vez en Ecuador diagnóstico serológico y la detección del provirus por biología molecular.Diseño del estudio. Se tomaron muestras de nueve pacientes con un diagnóstico de mielopatía y sospechoso de TSP, que fueron analizadas para la detección del virus HTLV-1/2 usando tres metodologías: ELISA comercial, ensayo de inmunofluorescencia indirecta (IF) y PCR anidada. Resultados: Cinco de los 9 (55.5%) pacientes fueron positivos tanto para la prueba de ELISA como para IF y PCR anidada. Conclusión: La alta prevalencia de infección por HTLV-1/2 entre individuos sintomáticos de mielopatía muestra la endemicidad de este retrovirus en Ecuador, la asociación de HTLV-1/2 con TSP y la necesidad de implementar estrategias de control y prevención para evitar la diseminación de esta enfermedad infecciosa desatendida.

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Ouattara, S. A., J. Chotard, M. Meite, A. M. Selly-Essis, and G. De-The. "Retrovirus infections (LAV/HTLV III AND HTLV-I) in ivory coast, West Africa." Annales de l'Institut Pasteur / Virologie 137 (January 1986): 303–10. http://dx.doi.org/10.1016/s0769-2617(86)80221-0.

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Machado, Caio Bezerra, Leidivan Sousa da Cunha, Jersey Heitor da Silva Maués, Flávia Melo Cunha de Pinho Pessoa, Marcelo Braga de Oliveira, Rodrigo Monteiro Ribeiro, Germison Silva Lopes, et al. "Role of miRNAs in Human T Cell Leukemia Virus Type 1 Induced T Cell Leukemia: A Literature Review and Bioinformatics Approach." International Journal of Molecular Sciences 23, no. 10 (May 14, 2022): 5486. http://dx.doi.org/10.3390/ijms23105486.

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Human T cell leukemia virus type 1 (HTLV-1) was identified as the first pathogenic human retrovirus and is estimated to infect 5 to 10 million individuals worldwide. Unlike other retroviruses, there is no effective therapy to prevent the onset of the most alarming diseases caused by HTLV-1, and the more severe cases manifest as the malignant phenotype of adult T cell leukemia (ATL). MicroRNA (miRNA) dysfunction is a common feature of leukemogenesis, and it is no different in ATL cases. Therefore, we sought to analyze studies that reported deregulated miRNA expression in HTLV-1 infected cells and patients’ samples to understand how this deregulation could induce malignancy. Through in silico analysis, we identified 12 miRNAs that stood out in the prediction of targets, and we performed functional annotation of the genes linked to these 12 miRNAs that appeared to have a major biological interaction. A total of 90 genes were enriched in 14 KEGG pathways with significant values, including TP53, WNT, MAPK, TGF-β, and Ras signaling pathways. These miRNAs and gene interactions are discussed in further detail for elucidation of how they may act as probable drivers for ATL onset, and while our data provide solid starting points for comprehension of miRNAs’ roles in HTLV-1 infection, continuous effort in oncologic research is still needed to improve our understanding of HTLV-1 induced leukemia.

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Hatayama, Yasuyoshi, Yutaro Yamaoka, Takeshi Morita, Sundararaj Stanleyraj Jeremiah, Kei Miyakawa, Mayuko Nishi, Yayoi Kimura, et al. "Development of a Monoclonal Antibody Targeting HTLV-1 Envelope gp46 Glycoprotein and Its Application to Near-Infrared Photoimmuno-Antimicrobial Strategy." Viruses 14, no. 10 (September 29, 2022): 2153. http://dx.doi.org/10.3390/v14102153.

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Human T-cell leukemia virus type 1 (HTLV-1), a retrovirus, causes adult T-cell leukemia-lymphoma, HTLV-1 associated myelopathy/tropical spastic paraparesis, and HTLV-1 uveitis. Currently, no antiretroviral therapies or vaccines are available for HTLV-1 infection. This study aimed to develop an antibody against the HTLV-1 envelope protein (Env) and apply it to a near-infrared photoimmuno-antimicrobial strategy (NIR-PIAS) to eliminate HTLV-1 infected cells. We established mouse monoclonal antibodies (mAbs) against HTLV-1 Env by immunization with a complex of liposome and the recombinant protein. Detailed epitope mapping revealed that one of the mAbs bound to the proline-rich region of gp46 and exhibited no obvious neutralizing activity to inhibit viral infection. Instead, the mAb was rarely internalized intracellularly and remained on the cell surface of HTLV-1-infected cells. The antibody conjugated to the photosensitive dye IRDye700Dx recognized HTLV-1 infected cells and killed them following NIR irradiation. These results suggest that the novel mAb and NIR-PIAS could be developed as a new targeted therapeutic tool against HTLV-1 infected cells.

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Nishimura, M., S. Jacobson, T. Uchiyama, M. Ohta, and T. Saida. "Human T Lymphotropic Virus Type I (Htlv-I)-Specific T Helper Cell Responses from Htlv-I Seronegative Patients with Chronic Myelopathy and Ms in Japan." Multiple Sclerosis Journal 1, no. 4 (February 1996): 200–203. http://dx.doi.org/10.1177/135245859600100402.

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Human T lymphotropic virus type I (HTLV-I) is a human retrovirus etiologically linked to Adult T cell leukemia (ATL) and HTLV-I associated myelopathyltropical spastic paraparesis (HAM/TSP). Although most HAM/TSP patients have high anti-HTLV-I antibody titers in their sera, HTLV-I infected but seronegative patients with neurological diseases have been reported. To clarify whether seronegative, HTLV-I related neurological disease may exist, we have developed a method that measures the production of interleukin-2 (IL-2) from HTLV-I synthetic peptide-stimulated peripheral blood lymphocytes (PBL) of HTLV-I infected persons. This method is sensitive enough to detect exposure to HTLV-I before seroconversion or even before detection by PCR. We examined 12 patients with chronic progressive myelopathy and eight patients with multiple sclerosis (MS) in central Japan, where the prevalence rate of HTLV-I is between one and four percent among asymptomatic blood donors, using the IL-2 production assay. None of them were positive by the assay, suggesting seronegative HTLV-I myelopathy is very rare among patients with chronic progressive myelopathy and MS in Japan.

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Casoli, Claudio, Maria Carla Re, Paola Monari, Giuliano Furlini, Giovanna Tosi, Chiara Gradozzi, Pier Paolo Dall'Aglio, Umberto Bertazzoni, and Roberto S. Accolla. "Human T-Cell Leukemia Virus Type II Directly Acts on CD34+ Hematopoietic Precursors by Increasing Their Survival Potential. Envelope-Associated HLA Class II Molecules Reverse This Effect." Blood 91, no. 7 (April 1, 1998): 2296–304. http://dx.doi.org/10.1182/blood.v91.7.2296.

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Abstract The role of human T-cell leukemia virus type II (HTLV-II) in human lymphoproliferative and hematopoietic abnormalities in which the retrovirus can be isolated is still elusive. Here we show that the C344 T-cell–derived lymphotropic HTLV-II type IIa Mo strain acts directly on CD34+ hematopoietic precursors by rescuing them from apoptosis induced by interleukin-3 (IL-3) deprivation. This effect is viral strain-specific, as it is not observed with the B-lymphotropic HTLV-II type IIb Gu strain, it does not require infection of the hematopoietic precursors, and, interestingly, it is strongly dependent on the infected cellular host from which the virus was derived. Indeed, growth adaptation of the Mo strain to the permissive B-cell line, BJAB, renders the virus no longer capable of mediating the antiapoptotic effect. However, pretreatment of the BJAB-adapted Mo strain with antibodies specific for HLA class II, but not class I, histocompatibility antigens restores the antiapoptotic potential of the virus. These results constitute the first evidence that HTLV-II retrovirus can directly influence the homeostasis of human progenitors, without infecting them, and that this crucial activity is strongly inhibited by the presence of host-derived envelope-associated HLA class II antigens.

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44

Casoli, Claudio, Maria Carla Re, Paola Monari, Giuliano Furlini, Giovanna Tosi, Chiara Gradozzi, Pier Paolo Dall'Aglio, Umberto Bertazzoni, and Roberto S. Accolla. "Human T-Cell Leukemia Virus Type II Directly Acts on CD34+ Hematopoietic Precursors by Increasing Their Survival Potential. Envelope-Associated HLA Class II Molecules Reverse This Effect." Blood 91, no. 7 (April 1, 1998): 2296–304. http://dx.doi.org/10.1182/blood.v91.7.2296.2296_2296_2304.

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The role of human T-cell leukemia virus type II (HTLV-II) in human lymphoproliferative and hematopoietic abnormalities in which the retrovirus can be isolated is still elusive. Here we show that the C344 T-cell–derived lymphotropic HTLV-II type IIa Mo strain acts directly on CD34+ hematopoietic precursors by rescuing them from apoptosis induced by interleukin-3 (IL-3) deprivation. This effect is viral strain-specific, as it is not observed with the B-lymphotropic HTLV-II type IIb Gu strain, it does not require infection of the hematopoietic precursors, and, interestingly, it is strongly dependent on the infected cellular host from which the virus was derived. Indeed, growth adaptation of the Mo strain to the permissive B-cell line, BJAB, renders the virus no longer capable of mediating the antiapoptotic effect. However, pretreatment of the BJAB-adapted Mo strain with antibodies specific for HLA class II, but not class I, histocompatibility antigens restores the antiapoptotic potential of the virus. These results constitute the first evidence that HTLV-II retrovirus can directly influence the homeostasis of human progenitors, without infecting them, and that this crucial activity is strongly inhibited by the presence of host-derived envelope-associated HLA class II antigens.

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Araújo, Abelardo Q. C., Ana Claudia C. Leite, Marco Antonio S. D. Lima, and Marcus Tulius T. Silva. "HTLV-1 and neurological conditions: when to suspect and when to order a diagnostic test for HTLV-1 infection?" Arquivos de Neuro-Psiquiatria 67, no. 1 (March 2009): 132–38. http://dx.doi.org/10.1590/s0004-282x2009000100036.

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HTLV-1 is a retrovirus associated with a myriad of clinical conditions, especially hematological and neurological ones. Regarding nervous system diseases, it is of utmost importance to select those cases in which HTLV-1 infection could really be associated. This is particularly true for patients from endemic areas and for HIV-infected patients and drug users, since that these groups are at a higher risk for HTLV infection. This caution in selecting neurological patients for HTLV diagnostic tests is justified by the fact that in some circumstances the seropositivity may merely represent an epiphenomenon. In this paper we enroll some neurological conditions that have been associated with HTLV-1/2 infection in the literature and discuss the real need for HTLV-1/2 diagnostic tests in each one. Because HIV/HTLV-co-infected patients seem to be at an increased risk for neurological diseases development, a special consideration about this matter is also made.

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46

Salim, Mohammad, Mohammad Shahid Masroor, and Shagufta Parween. "Human T-Cell Lymphotropic Virus-1 Causing Diseases and Cancer in Human." Clinical Medicine And Health Research Journal 2, no. 3 (May 10, 2022): 132–35. http://dx.doi.org/10.18535/cmhrj.v2i3.49.

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Human T-cell leukaemia virus-1(HTLV-1) is a kind of retrovirus which after entering in the human body reversely transcribed into several proviruses integrating the host genome develops a lethal blood cancer known as adult T-cell leukaemia (ATL). HTLV-1 also develops some other life threatening diseases like HTLV-1 associated myelopathy or tropical spastic myelopathy (HAM/TSP) in human. The present paper is an attempt to discuss discovery, epidemiology, diagnosis and transmission of the virus with their diseases and cancer causing abilities in the light of recent researches done so far in the field of microbial origin of cancer.

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Coskun, Ayse Kubra, and Richard E. Sutton. "Expression of Glucose Transporter 1 Confers Susceptibility to Human T-Cell Leukemia Virus Envelope-Mediated Fusion." Journal of Virology 79, no. 7 (April 1, 2005): 4150–58. http://dx.doi.org/10.1128/jvi.79.7.4150-4158.2005.

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ABSTRACT Human T-cell leukemia virus type 1 (HTLV-1) was the first human retrovirus identified and causes both adult T-cell leukemia/lymphoma and tropical spastic paraparesis/HTLV-1-associated myelopathy, among other disorders. In vitro, HTLV-1 has an extremely broad host cell tropism in that it is capable of infecting most mammalian cell types, although at the same time viral titers remain relatively low. Despite years of study, only recently has a bona fide candidate cellular receptor, glucose transporter 1 (glut-1), been identified. Although glut-1 was shown to bind specifically to the ectodomain of HTLV-1 and HTLV-2 envelope glycoproteins, which was reversible with small interfering RNA directed against glut-1, cellular susceptibility to HTLV upon expression of glut-1 was not established. Here we show that expression of glut-1 in relatively resistant MDBK cells conferred increased susceptibility to both HTLV-1- and HTLV-2-pseudotyped particles. glut-1 also markedly increased syncytium formation in MDBK cells after exposure to HTLV-1. Another assay also demonstrated HTLV-1 envelope-cell fusion in the presence of glut-1. Taken together, these results provide additional evidence that glut-1 is a receptor for HTLV.

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Lemasson, Isabelle, Nicholas J. Polakowski, Paul J. Laybourn, and Jennifer K. Nyborg. "Transcription Regulatory Complexes Bind the Human T-Cell Leukemia Virus 5′ and 3′ Long Terminal Repeats To Control Gene Expression." Molecular and Cellular Biology 24, no. 14 (July 15, 2004): 6117–26. http://dx.doi.org/10.1128/mcb.24.14.6117-6126.2004.

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ABSTRACT The human T-cell leukemia virus type 1 (HTLV-1) is a retrovirus that integrates randomly into the T-cell genome. Two long terminal repeats (LTRs) flank the integrated provirus. The upstream and downstream LTRs carry identical promoter sequences. Studies with other retroviruses suggest that the downstream promoter is silent and that RNA polymerases initiating at the upstream promoter proceed through the 3′ LTR. In this study, we used the chromatin immunoprecipitation assay to compare the binding of transcription regulatory proteins at both the upstream and downstream promoters in HTLV-1-infected cell lines and adult T-cell leukemia-lymphoma cells. Unexpectedly, we detected a nearly equal distribution of activator (Tax, CREB, ATF-1, ATF-2, c-Fos, and c-Jun) and regulatory protein (CBP, p300, TAFII250, and polymerase II) binding at both the upstream and downstream promoters. Consistent with this observation, we found that the downstream promoter was transcriptionally active, suggesting that the two promoters are functionally equivalent. We also detected asymmetrical binding of histone deacetylases (HDAC-1, -2, and -3) at both promoters. All three HDACs strongly repressed Tax transactivation, and this repression correlated with displacement of Tax from the HTLV-1 promoter. These effects were reciprocal, as Tax expression reversed HDAC repression and displaced HDACs from the HTLV-1 promoter. These data suggest that HTLV-1 transcriptional regulation at both the 5′ and 3′ LTRs is mediated, in part, through the mutually exclusive binding of Tax and HDACs at the proviral promoters.

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Maksimova, Victoria, and Amanda R. Panfil. "Human T-Cell Leukemia Virus Type 1 Envelope Protein: Post-Entry Roles in Viral Pathogenesis." Viruses 14, no. 1 (January 13, 2022): 138. http://dx.doi.org/10.3390/v14010138.

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Human T-cell leukemia virus type 1 (HTLV-1) is an oncogenic retrovirus that is the causative infectious agent of adult T-cell leukemia/lymphoma (ATL), an aggressive and fatal CD4+ T-cell malignancy, and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), a chronic neurological disease. Disease progression in infected individuals is the result of HTLV-1-driven clonal expansion of CD4+ T-cells and is generally associated with the activities of the viral oncoproteins Tax and Hbz. A closely related virus, HTLV-2, exhibits similar genomic features and the capacity to transform T-cells, but is non-pathogenic. In vitro, HTLV-1 primarily immortalizes or transforms CD4+ T-cells, while HTLV-2 displays a transformation tropism for CD8+ T-cells. This distinct tropism is recapitulated in infected people. Through comparative studies, the genetic determinant for this divergent tropism of HTLV-1/2 has been mapped to the viral envelope (Env). In this review, we explore the emerging roles for Env beyond initial viral entry and examine current perspectives on its contributions to HTLV-1-mediated disease development.

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de Mendoza, Carmen, José M. Bautista, Susana Pérez-Benavente, Roger Kwawu, Julius Fobil, Vicente Soriano, and Amalia Díez. "Screening for retroviruses and hepatitis viruses using dried blood spots reveals a high prevalence of occult hepatitis B in Ghana." Therapeutic Advances in Infectious Disease 6 (January 2019): 204993611985146. http://dx.doi.org/10.1177/2049936119851464.

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Background: Recent advances in antiviral therapy show potential for a cure and/or control of most human infections caused by hepatitis viruses and retroviruses. However, medical success is largely dependent on the identification of the large number of people unaware of these infections, especially in developing countries. Dried blood spots (DBS) have been demonstrated to be a good tool for collecting, storing and transporting clinical specimens from rural areas and limited-resource settings to laboratory facilities, where viral infections can be more reliably diagnosed. Methods: The seroprevalence and virological characterization of hepatitis B virus (HBV) and hepatitis C virus (HCV), as well as human retroviruses (HIV-1, HIV-2, human T-cell leukaemia virus type 1 [HTLV-1] and human T-cell leukaemia virus type 2 [HTLV-2]), were investigated in clinical specimens collected from DBS in Ghana. Results: A total of 305 consecutive DBS were collected. A high prevalence of chronic HBV (8.5%) and occult hepatitis B (14.2%) was found, whereas rates were lower for HIV-1, HTLV-1 and HCV (3.2%, 1.3% and 0.6%, respectively). HIV-2 and HTLV-2 were absent. CRF02_AG was the predominant HIV-1 subtype, whereas genotype E was the most frequent HBV variant. Conclusions: DBS are helpful in the diagnosis and virological characterization of hepatitis and retrovirus infections in resource-limited settings. The high rate of hepatitis B in Ghana, either overt or occult, is noteworthy and confirms recent findings from other sub-Saharan countries. This should encourage close clinical follow up and antiviral treatment assessment in this population, as well as universal HBV vaccine campaigns.

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Journal articles on the topic 'Retrovirus HTLV'

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