Human T-cell lymphotropic virus type 1 can infect primary rat retinal glial cells and induce gene expression of inflammatory cytokines

Sato, Yasuhiro; Ito, Kinji; Moritoyo, Takashi; Fujino, Yujiro; Masuda, Kohji; Yamaguchi, Kazunari; Mochizuki, Manabu; Izumo, Shuji; Osame, Mitsuhiro; Watanabe, Toshiki

doi:10.1076/ceyr.16.8.782.8982

Cited by 10 publications

(9 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…11) It was also reported that the supernatant of irradiated MT-2 cells contained about 250 pg/ml of HTLV-1 p19 antigen. 36) The virus preparation from c77 cells used in this study contained about 100 times more p19 antigen than the reported MT-2 cell culture supernatant. Mouse cell lines used previously are mostly fibroblasts, LMTK− and LMTK− derived mouse/human hybrid cells.…”

Section: Discussionmentioning

confidence: 71%

Cell‐free Entry of Human T‐Cell Leukemia Virus Type 1 to Mouse Cells

Feng

Kabayama

Uchida

et al. 2001

Japanese Journal of Cancer Research

View full text Add to dashboard Cite

Human T-cell leukemia virus type 1 (HTLV-1) is the etiologic agent for adult T-cell leukemia and HTLV-1-associated myelopathy/tropical spastic paraparesis. Recently we infected newborn mice by inoculating HTLV-1-producing human cells, and found that T-cells, B-cells and granulocytes were infected in vivo. To understand the mechanism of viral-cell interaction and the pathogenesis of HTLV-1 using the mouse model, it is important to clarify the cellular tropism using a cell-free HTLV-1 transmission system. We employed a highly transmissible cell-free HTLV-1 produced by a feline kidney cell line, c77, and studied the susceptibility of 9 kinds of mouse cell lines, EL4, RLm1, CTLL-2, J774.1, DA-1, Ba/F3, WEHI-3, NIH3T3 and B1, and two kinds of human cell lines, Molt-4 and Hut78. HTLV-1 proviral sequence was found by PCR in all 9 mouse cell lines as well as in 2 human cell lines and viral entry was blocked with sera from an HTLV-1 carrier and an adult T-cell leukemia patient. Unexpectedly, mouse cell lines EL4 and RLm1 and human cell lines Molt-4 and Hut78 showed similar efficiency for viral entry. These results suggest a wide distribution of HTLV-1 receptor in mouse cells.

show abstract

Section: Discussionmentioning

confidence: 71%

Cell‐free Entry of Human T‐Cell Leukemia Virus Type 1 to Mouse Cells

Feng

Kabayama

Uchida

et al. 2001

Japanese Journal of Cancer Research

View full text Add to dashboard Cite

show abstract

“…The proviral copy numbers showed a gradual decrease after infection. This transient infection was noted in retinal glial cells [ 19 ]. The possibility that HTLV-I-infected lung epithelial cells do not produce a large amount of virus and show a slower growth rate was raised by a report of Sato et al [ 19 ].…”

Section: Discussionmentioning

confidence: 99%

“…However, little is known about the tropism of HTLV-I for lung epithelial cells. Because HTLV-I exhibits tropism for synoviocytes, thyrocytes and retinal glial cells [ 17 - 19 ], we sought to determine whether lung epithelial cells can be infected with HTLV-I and whether such infection modulates the expression of cellular genes.…”

Section: Introductionmentioning

confidence: 99%

Human T-cell leukemia virus type I infects human lung epithelial cells and induces gene expression of cytokines, chemokines and cell adhesion molecules

et al. 2008

View full text Add to dashboard Cite

Background: Human T-cell leukemia virus type I (HTLV-I) is associated with pulmonary diseases, characterized by bronchoalveolar lymphocytosis, which correlates with HTLV-I proviral DNA in carriers. HTLV-I Tax seems to be involved in the development of such pulmonary diseases through the local production of inflammatory cytokines and chemokines in T cells. However, little is known about induction of these genes by HTLV-I infection in lung epithelial cells.

show abstract

“…Indeed, several studies have shown that astrocytes can be infected by HTLV-1 both in vivo and in vitro (23,24,28). An increased secretion of cytokines, such as granulocyte-macrophage colony-stimulating factor and TNF-␣, by HTLV-1-infected glial cells appears to be responsible for an increased expression of matrix metalloproteinases (MMPs) 3 and 9 and of tissue inhibitor of metalloproteinase 3 by these cells (6,28,37). In addition, a recent study detected MMP-9 in the cerebrospinal fluid of HTLV-1-infected patients with TSP/HAM (7).…”

Section: Discussionmentioning

confidence: 99%

Interactions between Brain Endothelial Cells and Human T-Cell Leukemia Virus Type 1-Infected Lymphocytes: Mechanisms of Viral Entry into the Central Nervous System

Romero

Prévost

Perret

et al. 2000

J Virol

View full text Add to dashboard Cite

Human T-cell leukemia virus type 1 (HTLV-1) is associated with a variety of clinical manifestations, including tropical spastic paraparesis or HTLV-1-associated myelopathy (TSP/HAM). Viral detection in the central nervous system (CNS) of TSP/HAM patients demonstrates the ability of HTLV-1 to cross the bloodbrain barrier (BBB). To investigate viral entry into the CNS, rat brain capillary endothelial cells were exposed to human lymphocytes chronically infected by HTLV-1 (MT2), to lymphocytes isolated from a seropositive patient, or to a control lymphoblastoid cell line (CEM). An enhanced adhesion to and migration through brain endothelial cells in vitro was observed with HTLV-1-infected lymphocytes. HTLV-1-infected lymphocytes also induced a twofold increase in the paracellular permeability of the endothelial monolayer. These effects were associated with an increased production of tumor necrosis factor alpha by HTLV-1-infected lymphocytes in the presence of brain endothelial cells. Ultrastructural analysis showed that contact between endothelial cells and HTLV-1-infected lymphocytes resulted in a massive and rapid budding of virions from lymphocytes, followed by their internalization into vesicles by brain endothelial cells and apparent release onto the basolateral side, suggesting that viral particles may cross the BBB using the transcytotic pathway. Our study also demonstrates that cell-cell fusion occurs between HTLV-1-infected lymphocytes and brain endothelial cells, with the latter being susceptible to transient HTLV-1 infection. These aspects may help us to understand the pathogenic mechanisms associated with neurological diseases induced by HTLV-1 infection.

show abstract

Human T-cell lymphotropic virus type 1 can infect primary rat retinal glial cells and induce gene expression of inflammatory cytokines

Cited by 10 publications

References 45 publications

Cell‐free Entry of Human T‐Cell Leukemia Virus Type 1 to Mouse Cells

Cell‐free Entry of Human T‐Cell Leukemia Virus Type 1 to Mouse Cells

Human T-cell leukemia virus type I infects human lung epithelial cells and induces gene expression of cytokines, chemokines and cell adhesion molecules

Interactions between Brain Endothelial Cells and Human T-Cell Leukemia Virus Type 1-Infected Lymphocytes: Mechanisms of Viral Entry into the Central Nervous System

Contact Info

Product

Resources

About