title: Suppression of HIV-1 Infectivity by Human Glioma Cells.
abstract: HIV-1 infection to the central nervous system (CNS) is very common in AIDS patients. The predominant cell types infected in the brain are monocytes and macrophages, which are surrounded by several HIV-1-resistant cell types, such as astrocytes, oligodendrocytes, neurons, and microvascular cells. The effect of these HIV-1-resistant cells on HIV-1 infection is largely unknown. In this study, we examined the stability of HIV-1 cultured with several human glioblastoma cell lines, for example, NP-2, U87MG, T98G, and A172, to determine whether these HIV-1-resistant brain cells could enhance or suppress HIV-1 infection and thus modulate HIV-1 infection in the CNS. The HIV-1 titer was determined using the MAGIC-5A indicator cell line as well as naturally occurring CD4(+) T cells. We found that the stability of HIV-1 incubated with NP-2 or U87MG cells at 37°C was significantly shorter (half-life, 2.5-4 h) compared to that of HIV-1 incubated with T98G or A172 cells or in culture medium without cells (half-life, 8-18 h). The spent culture media (SCM) of NP-2 and U87MG cells had the ability to suppress both R5- and X4-HIV-1 infection by inhibiting HIV-1 attachment to target cells. This inhibitory effect was eliminated by the treatment of the SCM with chondroitinase ABC but not heparinase, suggesting that the inhibitory factor(s) secreted by NP-2 and U87MG cells was chiefly mediated by chondroitin sulfate (CS) or CS-like moiety. Thus, this study reveals that some but not all glioma cells secrete inhibitory molecules to HIV-1 infection that may contribute in lowering HIV-1 infection in the CNS in vivo.
authors.affiliation: 1 Cell and Tissue Culture Laboratory, Centre for Advanced Research in Sciences, University of Dhaka , Dhaka, Bangladesh .|2 Department of Virology and Preventive Medicine, Gunma University Graduate School of Medicine , Maebashi, Japan .
authors.forename: Sheikh Ariful
authors.initials: SA
authors.lastname: Hoque
authors.affiliation: 2 Department of Virology and Preventive Medicine, Gunma University Graduate School of Medicine , Maebashi, Japan .|3 Research Institute for Microbial Diseases, Osaka University , Osaka, Japan .
authors.forename: Atsushi
authors.initials: A
authors.lastname: Tanaka
authors.affiliation: 2 Department of Virology and Preventive Medicine, Gunma University Graduate School of Medicine , Maebashi, Japan .|4 Department of Microbiology, Jahangirnagar University , Dhaka, Bangladesh .
authors.forename: Salequl
authors.initials: S
authors.lastname: Islam
authors.affiliation: 5 Department of Public Health, School of Health & Life Sciences, North South University , Dhaka, Bangladesh .
authors.forename: Gias Uddin
authors.initials: GU
authors.lastname: Ahsan
authors.affiliation: 2 Department of Virology and Preventive Medicine, Gunma University Graduate School of Medicine , Maebashi, Japan .|6 Bioresource Center, Gunma University Graduate School of Medicine , Maebashi, Japan .
authors.forename: Atsushi
authors.initials: A
authors.lastname: Jinno-Oue
authors.affiliation: 2 Department of Virology and Preventive Medicine, Gunma University Graduate School of Medicine , Maebashi, Japan .|7 Advanced Scientific Research-Leaders Development Unit, Gunma University Graduate School of Medicine , Maebashi, Japan .
authors.forename: Hiroo
authors.initials: H
authors.lastname: Hoshino
mesh_terms: D019380:Anti-HIV Agents / Q000378:metabolism*; D015496:CD4-Positive T-Lymphocytes / Q000821:virology; D045744:Cell Line, Tumor; D002490:Central Nervous System / Q000821:virology; D019765:Chondroitin ABC Lyase / Q000494:pharmacology*; D002809:Chondroitin Sulfates / Q000378:metabolism*; D005909:Glioblastoma / Q000378:metabolism* / Q000821:virology; D015658:HIV Infections / Q000473:pathology*; D015497:HIV-1 / Q000187:drug effects*; D019763:Heparin Lyase / Q000494:pharmacology*; D006801:Humans
chemical_list: D019380:Anti-HIV Agents; D002809:Chondroitin Sulfates; D019765:Chondroitin ABC Lyase; D019763:Heparin Lyase