HTLV-1 in Ophthalmology

Kamoi, Koju

doi:10.3389/fmicb.2020.00388

Cited by 29 publications

(26 citation statements)

References 97 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Human T-lymphotropic virus type 1 (HTLV-1) was the first retrovirus found to be infectious and pathogenic in humans ( Miyoshi et al, 1981 ; Kamoi et al, 2018 ). HTLV-1 has been reported in many regions of the world, and it is highly endemic in the Caribbean islands, parts of central Africa, and Japan ( Martin et al, 2018 ; Kamoi, 2020 ). HTLV-1 causes adult T-cell lymphoma, HTLV-1-associated myelopathy, and HTLV-1 uveitis (HU; Tagaya et al, 2019 ; Yamauchi et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

Mechanism of Secondary Glaucoma Development in HTLV-1 Uveitis

et al. 2022

Self Cite

View full text Add to dashboard Cite

Human T-cell lymphotropic virus type 1 (HTLV-1) was the first retrovirus identified as the causative agent of human diseases, such as adult T-cell leukemia, HTLV-1-associated myelopathy, and HTLV-1 uveitis (HU). HU is one of the most frequent ocular inflammatory diseases in endemic areas, which has raised considerable public health concerns. Approximately 30% of HU patients develop secondary glaucoma, which is higher than the general uveitis incidence. We therefore investigated the mechanism underlying the high incidence of glaucoma secondary to HU in vitro. After contact with HTLV-1-producing T cells (MT-2), human trabecular meshwork cells (HTMCs) were infected. The infected cells increased in number, and nuclear factor (NF)-κB expression was activated. Contact between MT-2 cells and HTMCs resulted in significantly upregulated production of inflammatory cytokines, such as IL-6, and chemokines, such as CXCL10, CCL2, and CXCL-8. These findings indicate that the mechanism underlying secondary glaucoma in HU may involve proliferation of trabecular meshwork tissue after contact with HTLV-1-infected cells, resulting in decreased aqueous humor outflow. Upregulated production of inflammatory cytokines and chemokines simultaneously disrupts the normal trabecular meshwork function. This mechanism presumably leads to increased intraocular pressure, eventually resulting in secondary glaucoma.

show abstract

Section: Introductionmentioning

confidence: 99%

Mechanism of Secondary Glaucoma Development in HTLV-1 Uveitis

et al. 2022

Self Cite

View full text Add to dashboard Cite

show abstract

“…and also HTLV-1-associated ocular diseases. These diseases are known as HTLV-1 uveitis (HU) and ATL-related ocular [3]. Certainly, the reported numbers are not terrible, but there is no standard treatment for all types of diseases [4].…”

Section: Introductionmentioning

confidence: 99%

Comparative study of the unbinding process of some HTLV-1 protease inhibitors using Unbiased Molecular Dynamics simulation

Tiyoula

Aryapour

Moghadam

2022

Preprint

View full text Add to dashboard Cite

The HTLV-1 protease is one of the major antiviral targets to overwhelm this virus. Several research groups have been developing protease inhibitors over the years, but none has been successful. In this regard, the development of new HTLV-1 protease inhibitors based on fixing the defects of previous inhibitors will overcome the absence of curative treatment for this oncovirus. Thus, we decided to study the unbinding pathways of the most potent (compound 10, Ki = 15 nM) and one of the weakest (compound 9, Ki = 7900 nM) protease inhibitors, which are very structurally similar, with the PDB IDs: 4YDG, 4YDF, using the Supervised Molecular Dynamics (SuMD) method. In this project, we had various short and long-time-scale simulations, that in total, we could have 12 successful unbindings (a total of 14.8 μs) for the two compounds in both mp forms. This comparative study measured all the essential factors simultaneously in two different inhibitors, which improved our results. This study revealed that Asp32 or Asp32′ in the two forms of mp state similarly exert super power effects on maintaining both potent and weak inhibitors in the binding pocket of HTLV-1 protease. In parallel with the important impact of these two residues, in the potent inhibitor’s unbinding process, His66′ was a great supporter, that was absent in the weak inhibitor’s unbinding pathway. In contrast, in the weak inhibitor’s unbinding process, Trp98/Trp98′ by pi-pi stacking interactions were unfavorable for the stability of the inhibitor in the binding site. In our opinion, these results will assist in designing more potent and effective inhibitors for the HTLV-1 protease.

show abstract

“…The pathogenesis of HAM/TSP and other HTLV-1-associated diseases, such as infective dermatitis and myositis, are derived from inflammation due to HTLV-1 infection [4,5]. HTLV-1 uveitis, which has long been recognized in the field of ophthalmology, is also associated with inflammation caused by HTLV-1 [6]. Infective dermatitis associated with HTLV-1 (IDH) is a recurrent eczema that affects vertically infected children [7,8].…”

Section: Introductionmentioning

confidence: 99%

Mother-to-Child Transmission of Human T-Cell Leukemia Virus Type 1: Mechanisms and Nutritional Strategies for Prevention

Itabashi

Miyazawa

2021

Cancers

View full text Add to dashboard Cite

Approximately 95% of mother-to-child transmission (MTCT) of human T-cell leukemia virus type-1 (HTLV-1) is derived from prolonged breastfeeding, which is a major cause of adult T-cell leukemia (ATL). Exclusive formula feeding (ExFF) is therefore generally used to prevent MTCT. A recent cohort study revealed that 55% of pregnant carriers chose short-term breastfeeding for ≤ 3 months in Japan. Our meta-analysis showed that there was no significant increase in the risk of MTCT when breastfeeding was carried out for ≤ 3 months compared with ExFF (pooled relative risk (RR), 0.72; 95% confidence interval (CI), 0.30–1.77), but there was an almost threefold increase in risk when breastfeeding was carried out for up to 6 months (pooled RR, 2.91; 95% CI, 1.69–5.03). Thus, short-term breastfeeding for ≤ 3 months may be useful in preventing MTCT. Breastmilk is the best nutritional source for infants, and any approach to minimizing MTCT by avoiding or limiting breastfeeding must be balanced against the impact on the child’s health and mother–child bonding. To minimize the need for nutritional interventions, it is necessary to identify factors that predispose children born to carrier mothers to MTCT and thereby predict MTCT development with a high degree of accuracy.

show abstract

HTLV-1 in Ophthalmology

Cited by 29 publications

References 97 publications

Mechanism of Secondary Glaucoma Development in HTLV-1 Uveitis

Mechanism of Secondary Glaucoma Development in HTLV-1 Uveitis

Comparative study of the unbinding process of some HTLV-1 protease inhibitors using Unbiased Molecular Dynamics simulation

Mother-to-Child Transmission of Human T-Cell Leukemia Virus Type 1: Mechanisms and Nutritional Strategies for Prevention

Contact Info

Product

Resources

About