TLRs (Toll-like receptors) and RLRs (RIG-I-like receptors) mediate innate immune responses by detecting microorganism invasion. RIG-I activation results in the production of interferon (IFN) type 1 and IFN responsive genes (ISGs). As the ubiquitin ligases RNF125 and TRIM25 are involved in regulating RIG-I function, our aim was to assess whether the levels of these three genes vary between healthy and HIV-infected individuals and whether these levels are related to disease progression.
Gene expression analyses for RIG-I, RNF125, and TRIM25 were performed for HIV-infected adults and the children's peripheral blood mononuclear cells (PBMCs).
Reverse transcription-quantitative PCRs (RT-qPCRs) were performed in order to quantify the expression levels of RIG-I, RNF125 and TRIM25 from PBMCs purified from control or HIV-infected individuals.
Controls express higher levels of the three genes when compared to HIV-infected patients. These expressions are clearly distinct between healthy and progressors, and are reproduced in adults and children. In controls, RNF125 is the highest expressed gene, whereas in progressors, RIG-I is either the highest expressed gene or is expressed similarly to RNF125 and TRIM25.
A pattern of expression of RIG-I, RNF125, and TRIM25 genes in HIV patients is evident. The high expression of RNF125 in healthy individuals reflects the importance of keeping RIG-I function off, inhibiting unnecessary IFN production. Consistent with this assumption, RNF125 levels are lower in HIV patients and importantly, the RNF125/RIG-I ratio is lower in patients who progress to AIDS. Our results might help to predict disease progression and unveil the role of poorly characterized host genes during HIV infection.
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aDepartamento de Genética, Instituto de Biologia
bInstituto de Bioquímica Médica, UFRJ, Rio de Janeiro
cFaculdade de Medicina, UFRG, Rio Grande
dHospital Universitário Gaffrée e Guinle, UNIRIO
eInstituto de Puericultura e Pediatria Martagão Gesteira, UFRJ
fPrograma de Genética, INCA, Rio de Janeiro, Brazil.
Correspondence to Ana Lúcia M. Giannini, CCS-Departamento de Genética, Instituto de Biologia, UFRJ, Rua Rodolpho P. Rocco, s/n, Bl. A, room A2-066, Ilha do Fundão, CEP 21941-617, Rio de Janeiro, RJ, Brazil. E-mail: email@example.com
Received 14 September, 2012
Revised 26 March, 2013
Accepted 3 April, 2013
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