Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. CONCISE COMMUNICATION Expression levels of the innate response gene RIG-I and its regulators RNF125 and TRIM25 in HIV-1 infected adult and pediatric individuals Alan Messala A. Britto a , Nı ´vea D. Amoedo b , Paula Pezzuto a , Adriana O. Afonso a,M , Ana Maria B. Martı ´nez c , Jussara Silveira c , Fernando S. Sion d , Elizabeth S. Machado e , Marcelo A. Soares a,f and Ana Lu ´ cia M. Giannini a Objective: 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). Since 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 if these levels are related to disease progression. Design: Gene expression analysis for RIG-I, RNF125 and TRIM25 were performed for HIV infected adults and children?s PBMCs. Methods: RT-qPCRs were performed in order to quantify the expression levels of RIG-I, RNF125 and TRIM 25 from control or HIV infected individuals isolated PBMCs. Results: Controls express higher levels of the three genes when compared to HIV- infected patients. These expressions are clearly distinct between healthy and progres- sors, and are reproduced in adults and children. In controls, RNF125 is the highest expressed gene while in progressors, RIG-I is either the highest expressed gene or is expressed similarly to RNF125 and TRIM25. Conclusions: 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 impor- tantly, the RNF125/RIG-I ratio is lower in patients that progress to AIDS. Our results might help to predict disease progression and unveil the role of poorly characterized host genes during HIV infection. ß 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins AIDS 2013, 27:000–000 a Departamento de Gene ´tica, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil, b Instituto de Bioquı ´mica Me ´dica, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil, c Faculdade de Medicina, Universidade Federal de Rio Grande, Rio Grande, Brazil, d Hospital Universita ´rio Gaffre ´e e Guinle, Rio de Janeiro, Brazil, e Instituto de Puericultura e Pediatria Martaga ˜o Gesteira, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil, and f Programa de Gene ´ tica, Instituto Nacional de Ca ˆncer, Rio de Janeiro, Brazil. Correspondence to Ana Lu ´ cia M. Giannini. E-mail: ana.giannini@biologia.ufrj.br  Current address: Centro de Cie ˆncias da Sau ´ de, Universidade Cato ´lica de Petro ´ polis, Petro ´ polis, Brazil. Received: 14 September 2012; revised: 26 March 2013; accepted: 3 April 2013. DOI:10.1097/QAD.0b013e328361cfbf ISSN 0269-9370 Q 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins 1