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B. Liu, Z. Li, S. Mahesh, S. Kurup, C.–Z. Giam, R. Nussenblatt; HTLV–1 Infection of Human Retinal Pigment Epithelial Cells and Inhibition of Viral Infection by an Antibody to ICAM–1 . Invest. Ophthalmol. Vis. Sci. 2006;47(13):3073.
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© ARVO (1962-2015); The Authors (2016-present)
To examine whether Human T–cell leukemia virus type 1 (HTLV–1) can infect a human retinal pigment epithelial (RPE) cell line, ARPE–19 in vitro and investigate its regulation.
A co–culture system with ARPE–19 and irradiated cells of an HTLV–1–producing T cell line, MT2 was used to determine the permissivity of RPE to HTLV–1 infection in vitro. The susceptibility to HTLV–1 was assessed by detection of viral DNA using the polymerase chain reaction (PCR), viral mRNA transcripts with reverse transcription PCR (RT–PCR) and viral antigen by immunofluorescence staining. An HTLV–1 Tax–activated HTLV–LTR–luciferase reporter assay was developed to quantitatively measure viral infection. The ICAM–1 expression on co–cultured ARPE–19 cells was detected by flow cytometry and an ICAM–1 neutralizing antibody was used to test ICAM–1’s role in the infection of HTLV–1 to ARPE–19. The regulation of HTLV–1 infection was investigated by culturing ARPE–19 cells with pro–inflammatory cytokines.
HTLV–1 infected ARPE–19 cells in vitro. The infection correlated with elevated expression of intercellular adhesion molecule 1 (ICAM–1) on the surface of ARPE–19 cells. ICAM–1 neutralizing antibody dramatically inhibited viral infection. Furthermore, pro–inflammatory cytokines dramatically suppressed HTLV–1 viral infection.
The tropism of HTLV–1 to retinal pigment epithelium could provide an explanation for the pathogenesis of HTLV–1 related ophthalmic diseases. A better understanding of specific roles of pro–inflammatory cytokines in the development of ophthalmic diseases may be beneficial for the treatment.
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