HIV type 1 fails to trigger innate immune factor synthesis in differentiated oral epithelium.
The oral mucosa is relatively resistant to human immunodeficiency virus type 1 (HIV-1) transmission. The mechanisms contributing to this resistance remain incompletely understood, but may include HIV-induced synthesis of innate immune factors. We used fully differentiated oral epithelium as a surrogate for the oral mucosa in vivo, exposed it to X4- and R5-tropic HIV-1 in culture, and quantified mRNA expression of six innate immune factors. Neither virus increased expression of human beta defensin 2 (hBD-2) mRNA over supernatants from uninfected lymphoblast controls. HIV-1 also failed to induce mRNA of four additional innate immunity-related genes. Similar results were obtained with oral monolayer epithelial cells. Interestingly, the X4-tropic virus inhibited mRNA expression of hBD-2, and of three of the other factors, at higher dosages in the differentiated oral epithelium but not the monolayers. The failure of HIV-1 to induce innate immune factors in the differentiated epithelium was not due to a lack of tissue penetration, as we detected fluorescence-tagged virions up to 30 mum deep from the apical surface. HIV-1 does not trigger de novo innate immune factor synthesis in oral epithelium, pointing to the role of a constitutive innate immunity for protection against HIV-1 in the oral cavity.
Epidemiology Unit, Faculty of Medicine, Prince of Songkla University, Hat Yai, Songkhla, Thailand. wipawee.ni@psu.ac.th
Wipawee
W
Nittayananta
Florian
F
Hladik
Mitchell
M
Klausner
Socorro
S
Harb
Beverly A
BA
Dale
Robert W
RW
Coombs
D002478:Cells, Cultured; D004848:Epithelium / Q000276:immunology*; D020869:Gene Expression Profiling; D015497:HIV-1 / Q000276:immunology*; D006801:Humans; D007155:Immunologic Factors / Q000096:biosynthesis*; D009061:Mouth Mucosa / Q000276:immunology*
D007155:Immunologic Factors