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Human T lymphotropic virus type 1 (HTLV-1)
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
HTLV-1 is a retrovirus in the genus Deltaretrovirus, subfamily Orthoretrovirinae. Risk of transmission increases with number of exposures and depends on the route of transmission, infectivity of the donor, and susceptibility of the recipient. Routes of exposure and their risk of transmission include: Non-leukocyte depleted blood transfusion (8.6%–64%), sharing needles and syringes (presumed high), breastfeeding (22%), transplacental exposure (3%–5%) and unprotected sexual intercourse (1% per year) [7]. Cell-free blood product transmission risk is negligible, and therefore direct cell-to-cell contact is a presumed requirement for virus transmission. The virologic synapse that enables cell to cell transmission between HTLV-1 infected and uninfected cells is likely mediated by the glucose transporter 1 (GLUT-1), heparin sulfate proteoglycans (HSPG), and neuropilin 1 (NRP-1). Investigations continue in fully characterizing viral transmission [10,11].
Viruses
Published in Loretta A. Cormier, Pauline E. Jolly, The Primate Zoonoses, 2017
Loretta A. Cormier, Pauline E. Jolly
Deltaretrovirus includes the Primate T-lymphotropic virus (PTLV), which consists of four human types, HTLV (I–IV) and four corresponding wild primate counterparts STLV (I–IV) (Ahuka-Mundeke et al. 2011; Richard et al. 2015). HTLV-I was first isolated in 1979 from a patient with T-cell lymphoma, and the case represented the first identification of a retrovirus in humans (Poiesz et al. 1980). In 1982, HTLV-II was described in a patient with hairy cell leukemia (Kalyanaraman et al. 1982). HTLV-I has a number of subtypes: A has spread worldwide, B is found in central Africa, C in Melanesia/Australia, and D also in central Africa (Ayouba and Peeters 2015; Vandamme et al. 1998). It is estimated that 10–20 million people have been infected (Johnson et al. 2001). The prevalence of HTLV-II is not well known, but has been identified in several Amerindian populations and in drug abusers in the U.S., Europe, and Asia (Rosadas et al. 2014). Only a few cases of HTLV-III have been identified in African individuals living in the vicinity of infected primates, and only one case of HTLV-IV has been identified to date in a hunter from Cameroon (Richard et al. 2015).
Order Ortervirales
Published in Paul Pumpens, Peter Pushko, Philippe Le Mercier, Virus-Like Particles, 2022
Paul Pumpens, Peter Pushko, Philippe Le Mercier
For a long time, bovine leukemia virus (BLV), a member of the genus Deltaretrovirus, served only as a pioneering source of epitopes for insertion into such carrier vectors as HBc (see Chapter 38), until its Gag was chosen as a potent VLP carrier candidate (Kakker et al. 1999). The baculovirus-driven expression of the BLV Pr44gag gene encoding the Gag precursor protein in insect cells resulted in the self-assembly and release of VLPs. The recombinant baculoviruses expressing matrix (MA) or capsid-nucleocapsid (CA-NC) proteins of BLV were generated, but neither of these domains was capable, however, of assembling into particulate structures. Moreover, chimeras exchanging MA and CA-NC proteins of BLV and other leukemia viruses (e.g., human T-cell leukemia virus type I) or such an evolutionarily divergent retrovirus group as lentiviruses (e.g., simian immunodeficiency virus) assembled efficiently and budded as VLPs (Kakker et al. 1999). In parallel, the formation of VLPs in insect cells was achieved for human lymphotropic T-cell virus type II (HTLV-II) (Takahashi et al. 1999). However, it is noteworthy that Hertig et al. (1994) were the first who showed that the expression of the BLV gag-pro or gag-pro-pol genes by recombinant vaccinia virus led to production of the BLV Gag VLPs. Therefore, the assembly of the Gag VLPs occurred in the absence of env products and other BLV-specific proteins, and the budding and particle maturation did not require copackaging of genomic viral RNA. The BLV VLPs exhibited morphology similar to that of BLV, and their diameters ranged from 80 to 115 nm in diameter (Hertig et al. 1994)
Antiviral therapy for the sexually transmitted viruses: recent updates on vaccine development
Published in Expert Review of Clinical Pharmacology, 2020
Kimia Kardani, Parya Basimi, Mehrshad Fekri, Azam Bolhassani
HTLV-1 was described by Robert Gallo’s team in 1980 at the National Cancer Institute/National Institutes of Health (NCI/NIH) as the first human retrovirus, before the discovery of HIV-1. Moreover, it is one of the first human viruses which showed oncogenic effects in humans [54,55,75]. HTLV-1 was classified as a complex type C retrovirus belonging to the genus Deltaretrovirus, the family Retroviridae, and the subfamily Orthoretrovirinae [76]. Shortly after the discovery of HTLV-1, another human retrovirus was discovered named as human T-cell leukemia virus type 2 (HTLV-2) which was closely similar to HTLV-1 in genome structure and nucleotide sequence. Unlike HTLV-1, HTLV-2 was not associated with human pathology [77,78]. The virus genome includes a positive single-stranded RNA which often infects T lymphocytes (CD4+ T-cells) leading to adult T cell leukemia/lymphoma (ATL/L) [67]. HTLV-1 manifests many diseases including ATL, HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), inflammatory disorders especially uveitis, arthritis, dermatitis, and an immune-deficient state resulting in bronchiectasis [79,80]. HTLV-1 Env is synthesized as a precursor glycoprotein 61 (gp6l) which is proteolytically cleaved into the gp46 and gp21, and plays a crucial role during the virus entry process [81]. The genetic structure and regulation of HTLV-1 were more complex than those of other leukemia viruses with animal hosts. In addition to the structural genes (i.e. gag, pro, pol, and env) encoding the virion proteins, the HTLV-1 genome also carries genes encoding the nonstructural proteins, Tax and HBZ, which are needed for regulating viral gene expression [67]. HTLV-1 can be transmitted from mother to baby mainly through breastfeeding, the horizontal transmission by sex, blood transfusion with infected lymphocytes and organ transplant. HTLV-1 infection requires cell-to-cell contact. The cell-free virions generally do not cause infection [79]. HTLV-1 primarily infects CD4+ T-cells but it has the potential to infect a wide variety of cells such as CD8+ T-cells, endothelial cells, myeloid cells, B-lymphocytes, fibroblasts, and also other mammalian cells. This wide range of target cells was due to the ability of the surface subunit of the HTLV-1 Env to interact with three widely distributed cellular surface receptors including glucose transporter (GLUT1), heparin sulfate proteoglycan (HSPG), and VEGF-165 receptor neuropilin-1 (NRP-1) [77,82,83,84]. HTLV-1 infection led to the changes in the systemic immune response even in asymptomatic patients [76].