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Spinal Cord Disease
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
HTLV is transmitted via breast milk (vertical transmission), sexual contact, and contaminated blood products. The virus directly promotes an inflammatory response in the CNS. There is possible molecular mimicry leading to secondary autoimmune-mediated tissue damage. Clinical features include: Indolent spastic weakness.Transverse myelopathy syndrome with lower extremity sensory loss (both dorsal columns and spinothalamic tracts), prominent bowel/bladder dysfunction.Progression over years: Thoracic spine is most commonly affected.First few years of clinical symptoms can be more rapidly progressive with a plateau or gradual progression in subsequent years.
Human Monoclonal Antibodies and Immune Modulation in Viral Hepatitis, Schistosomiasis, and HTLV Infection
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Thomas F. Kresina, Garry A. Neil, Steven K. H. Foung
The utility of human monoclonal antibodies for diagnostic purposes is illustrated by our investigation to identify and characterize immunogenic domains of human T-lymphotropic type I and type II viruses (HTLV-1 and HTLV-11). These viruses are human retroviruses that are increasingly recognized as important pathogens. Human T-lymphotropic virus-I is the causative agent of adult T-cell leukemia/lymphoma and a chronic neurological disorder termed HTLV-I-associated myelopathy or tropical spastic paraparesis (HAM/TSP) [37,38]. It has been also linked to uveitis and possibly to polymyositis. Although HTLV-II is structurally similar to HTLV-I, diseases associated with HTLV-II have been more difficult to identify and are just beginning to emerge. We and other investigators have recently [39–42] reported on patients with HAM/TSP-like illnesses who are seropositive for HTLV-II and whose peripheral blood lymphocytes were demonstrated to contain HTLV-II by polymerase chain reaction (PCR) analysis.
Neuropathogenesis of viral infections
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Avindra Nath, Joseph R. Berger
Most often once the virus has replicated to critical levels at the site of entry, it then spreads to the brain hematogenously. It may infect cells that form the immune system thus evading their onslaught. These cells as they traffic the nervous system result in spread of the virus to brain cells. For example, JCV infects B cells. HIV infects CD4 lymphocytes and macrophages. HTLV-I infects T-lymphocytes. Viruses may enter the brain by crossing the blood capillaries either as free virus or by residing in the leukocytes that traffic the brain parenchyma. The latter has been termed the “Trojan Horse” phenomenon. Virus or virus infected cells may also enter the brain via the choroids plexus and get disseminated via CSF pathways. This mode of spread most often results in viral meningitis.
HTLV-I associated bronchioloalveolar disorder (HABA): disease concept and differential diagnosis of an unsolved disease entity
Published in Expert Review of Anti-infective Therapy, 2023
Akihiro Ohmoto, Shigeo Fuji, Satoshi Kohmo, Kaoruko Katsura
HTLV-1-associated myelopathy (HAM) or tropical spastic paraparesis (TSP) is most well-known non-neoplastic disease related to HTLV-1 infection, and is characterized by chronic inflammation of the spinal cord causing weakness or paralysis of the legs, lower back pain, and urinary symptoms [6]. Another complication of HTLV-1 is HTLV-1 uveitis, also known as HTLV-1-associated ocular disease, which is characterized by infiltration of inflammatory cells into the vitreous [7]. However, HAM/TSP and HTLV-1 uveitis are rare and non-lethal complications that do not sufficiently explain the significant impact of HTLV-1 infection on overall mortality. HTLV-1-associated bronchioloalveolar disorder (HABA) is an immune-mediated state induced by HTVL-1. Currently, we do not have adequate information regarding the incidence and clinical features of HABA. The disease concept is not solid, and there are no clinical guidelines. Furthermore, reports on HABA are limited and have been chiefly published by researchers from endemic areas including Japan. Therefore, international recognition and interest in HABA is expected to be deficient.
Successfully treated acute adult T-cell leukemia with haploidentical stem cell transplantation
Published in Baylor University Medical Center Proceedings, 2022
Aswani Thurlapati, Christopher Graham, Kyle Boudreaux, Tamna Wangjam
ATL consists of four variants, including indolent chronic and smoldering forms and aggressive acute and lymphomatous types (Table 1).7 Our patient falls under the acute type due to a positive anti–HTLV-1 antibody, elevated T lymphocyte count, lactate dehydrogenase, and hypercalcemia, and infiltration of additional tissues. Acute ATL has the highest burden of peripherally circulating leukemic cells.8 The gold standard diagnostic study is flow cytometry, which reveals abnormally high lymphocytes that express CD4, CD5, CD25, and lack CD7 and terminal deoxynucleotidyl transferase. These findings, along with a positive HTLV-1 antibody test, are substantial to make the diagnosis. The peripheral blood smear may show pathognomic clover-leaf cells, as seen in our patient, which represent atypical lymphocytes with basophilic cytoplasm and hyperdense convoluted nuclei.
Biomedical and genetic characteristics of the Ryukyuans: demographic history, diseases and physical and physiological traits
Published in Annals of Human Biology, 2019
Kae Koganebuchi, Ryosuke Kimura
Generally, the regional difference in the prevalence of HTLV-1-related diseases is attributed to the difference in the frequency of the carriers. However, the difference in clinical features may be partly caused by the HTLV-1 genotype. The viral gene expression and the onset and development of ATL depend on a transcriptional regulator encoded by pX (Tax). It has been reported that the distribution of the HTLV-1 Tax genotypes in Ryukyuan ALT patients (taxA, 44%; taxB, 56%) differed from that in patients from Kagoshima Prefecture in southern Kyushu (taxA, 10%; taxB, 90%) and that the estimated hazard ratio of taxA compared with taxB was 2.68 (Sakihama et al. 2017). These findings suggest that the tax genotype could explain the clinical features of aggressive ATL in Okinawa Prefecture. In addition, it has been shown that, compared with those in other regions of Japan, aggressive ALT in Okinawa Prefecture is associated with a higher proportion of patients over 90 years old, a poorer outcome and a higher prevalence of strongyloidiasis (Nishi et al. 2016).