
HIV protease inhibitors alter innate immune response signaling to double-stranded RNA in oral epithelial cells: implications for immune reconstitution inflammatory syndrome?
Author(s) -
Robert J. Danaher,
Charlotte S. Kaetzel,
Richard N. Greenberg,
Chunmei Wang,
Maria E. C. Bruno,
Craig S. Miller
Publication year - 2010
Publication title -
aids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.195
H-Index - 216
eISSN - 1473-5571
pISSN - 0269-9370
DOI - 10.1097/qad.0b013e32833f4022
Subject(s) - innate immune system , immune system , lopinavir , biology , immunology , monocyte , tumor necrosis factor alpha , protease , inflammation , virus , viral load , enzyme , biochemistry , antiretroviral therapy
In this investigation, several HIV protease inhibitors altered the virally associated, double-stranded RNA (dsRNA)-stimulated, innate immune response. Lopinavir, the most potent inducer of interleukin (IL)-8 expression, also inhibited dsRNA-induced monocyte chemotactic protein 1 expression. Further analyses demonstrated that nuclear factor-κB is required for lopinavir's induction of IL-8. These findings demonstrate that protease inhibitors, such as lopinavir, differentially dysregulate innate immune signaling in a manner that could affect immune (reconstitution) inflammatory responses in oral epithelium.