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Introduction: TLR´s play a role in host defense in HIV infection recognizing the viral DNA or RNA. Their activation induces a signaling pathway that includes the proteins MyD88, IRAK4, TRAF6 and the transcription factor NF-kBp65. Objective: To determine the expression of TLR7, TLR8 and TLR9, and activation of its signaling pathway in monocytes from patients infected with HIV. Methods. Expression of TLR7, TLR8 and TLR9 was determined in monocytes from HIV-infected patients (n= 13) and control subjects (n= 13), which were activated with specific ligands. The expression of MyD88 and NF-kBp65 were determined by flow cytometry; IRAK4 and TRAF6 were studied by immunoblotting. Results: No statistical difference was found in the expression of TLR7, 8 and 9 in monocytes from patients compared to controls, but we observed the non-significant increased expression of TLR9 in patients. The activation showed no significant difference in the expression of MyD88 and NF-kBp65 in patients when compared to controls, but were decreased in stimulated cells over non-stimulated cells. IRAK4 and TRAF6 were not detected. Conclusions: No statistical difference was observed in the expression of intracellular TLRs, MyD88 and NFkBp65 in monocytes from patients compared to controls. This was probably due to effective antiretroviral therapy being received at the time of study entry. Additional studies are needed under controlled conditions that include infected patients with and without ARVT, responders and non-responders, and work with different cell populations.

Introducción: En la infección por VIH los TLR juega un papel en la defensa del huésped al reconocer el ADN o ARN viral. Su activación induce la vía de señalización que incluye las proteínas MyD88, IRAK4, TRAF6 y el factor de transcripción NF-kBp65. Objetivo: Determinar la expresión del TLR7, TLR8 y TLR9, y activación de su vía de señalización en monocitos de pacientes infectados con VIH. Métodos: Se determinó la expresión de TLR7, TLR8 y TLR9 en monocitos de pacientes infectados con VIH (n =13) y sujetos control (n =13), se activaron con ligandos específicos y se determinó la expresión de MyD88 y NF-kBp65 por citometría de flujo. IRAK4 y TRAF6 fueron estudiadas por inmunoelectrotransferencia. Resultados: No se observó diferencia estadística en la expresión de TLR7, 8 y 9 en los monocitos de pacientes con respecto a los controles, pero observamos aumento no significante del TLR9 en los pacientes. La activación no mostró diferencia significativa en la expresión de MyD88 y NF-kBp65 en pacientes con respecto a los controles, pero se encontraron disminuidas en células estimuladas con respecto a las no estimuladas. IRAK4 y TRAF6 no se detectaron. Conclusiones: No se observó diferencia en la expresión de los TLR, ni en la expresión de MyD88 y NFkBp65, en monocitos de pacientes con respecto a los controles probablemente debido a la terapia antirretroviral recibida al momento del estudio. Se sugieren estudios con pacientes con y sin TARV, respondedores y no respondedores, y trabajar con diferentes poblaciones celulares.

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INTRODUCTION: TLR´s play a role in host defense in HIV infection recognizing the viral DNA or RNA. Their activation induces a signaling pathway that includes the proteins MyD88, IRAK4, TRAF6 and the transcription factor NF-kBp65. OBJECTIVE: To determine the expression of TLR7, TLR8 and TLR9, and activation of its signaling pathway in monocytes from patients infected with HIV. Methods. Expression of TLR7, TLR8 and TLR9 was determined in monocytes from HIV-infected patients (n= 13) and control subjects (n= 13), which were activated with specific ligands. The expression of MyD88 and NF-kBp65 were determined by flow cytometry; IRAK4 and TRAF6 were studied by immunoblotting. RESULTS: No statistical difference was found in the expression of TLR7, 8 and 9 in monocytes from patients compared to controls, but we observed the non-significant increased expression of TLR9 in patients. The activation showed no significant difference in the expression of MyD88 and NF-kBp65 in patients when compared to controls, but were decreased in stimulated cells over non-stimulated cells. IRAK4 and TRAF6 were not detected. CONCLUSIONS: No statistical difference was observed in the expression of intracellular TLRs, MyD88 and NFkBp65 in monocytes from patients compared to controls. This was probably due to effective antiretroviral therapy being received at the time of study entry. Additional studies are needed under controlled conditions that include infected patients with and without ARVT, responders and non-responders, and work with different cell populations.

INTRODUCCIÓN: En la infección por VIH los TLR juega un papel en la defensa del huésped al reconocer el ADN o ARN viral. Su activación induce la vía de señalización que incluye las proteínas MyD88, IRAK4, TRAF6 y el factor de transcripción NF-kBp65. OBJETIVO: Determinar la expresión del TLR7, TLR8 y TLR9, y activación de su vía de señalización en monocitos de pacientes infectados con VIH. MÉTODOS: Se determinó la expresión de TLR7, TLR8 y TLR9 en monocitos de pacientes infectados con VIH (n= 13) y sujetos control (n= 13), se activaron con ligandos específicos y se determinó la expresión de MyD88 y NF-kBp65 por citometría de flujo. IRAK4 y TRAF6 fueron estudiadas por inmunoelectrotransferencia. RESULTADOS: No se observó diferencia estadística en la expresión de TLR7, 8 y 9 en los monocitos de pacientes con respecto a los controles, pero observamos aumento no significante del TLR9 en los pacientes. La activación no mostró diferencia significativa en la expresión de MyD88 y NF-kBp65 en pacientes con respecto a los controles, pero se encontraron disminuidas en células estimuladas con respecto a las no estimuladas. IRAK4 y TRAF6 no se detectaron. CONCLUSIONES: No se observó diferencia en la expresión de los TLR, ni en la expresión de MyD88 y NFkBp65, en monocitos de pacientes con respecto a los controles probablemente debido a la terapia antirretroviral recibida al momento del estudio. Se sugieren estudios con pacientes con y sin TARV, respondedores y no respondedores, y trabajar con diferentes poblaciones celulares.

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OBJECTIVE: To determine the prevalence of secondary effects on lipid metabolism as a result of highly active antiretroviral therapy (HAART), as well as the impact of different types of antiretroviral regimens on lipids and glucose in a group of patients in Yucatan, Mexico. MATERIAL AND METHODS: A cross-sectional study was conducted. A questionnaire created for this study was administered to each patient and total cholesterol, triglycerides and fasting glucose values were determined. The presence of hyperlipidemia and alterations in glucose were determined as well as their relation to the epidemiological variables obtained from the questionnaire. RESULTS: A total of 211 subjects were studied [36 (17%) of which were women and 175 (83%) men]. Ninety-two patients (44%) were found to have hyperlipidemia. Of these, 43 (20%) had hypercholesterolemia (HC) and 82 (39%) hypertriglyceridaemia (HT). The presence of combined HC and HT was observed in 30 (14%) patients. Nineteen (9%) patients had alterations in glucose, six (3%) diabetes mellitus and 13 (6%) impaired glucose tolerance. The variables associated with the presence of hyperlipidemia were: levels of lymphocytes CD4 >350 cells/microl (OR = 2.79 1.08-7.27, p = 0.03), male gender (OR = 3.6 1.4-9.12, p = 0.006) and the use of nucleoside-reverse transcriptase inhibitors (NRTI) (OR = 3.1 1.2-8.1, p = 0.01). CONCLUSIONS: Patients with HIV infection who receive HAART have an increased risk of presenting hyperlipidemia. In this group of patients the presence of hyperlipidemia and impaired glucose tolerance was significant. Unlike what has been indicated in most published reports, the alterations of lipids were associated more frequently with INTR use, for which it is concluded that the pathogeny of these alterations is not unique, that it is probable that concurrent effects exist between different antiretroviral drug families and that other host factors are involved in the pathogenic mechanism of these alterations.

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OBJETIVO: Determinar la prevalencia de los efectos secundarios sobre el metabolismo de los lípidos y la glucosa provocados por la terapia antirretrovírica hiperactiva (TARHA), así como el impacto que el uso de los distintos esquemas de antirretrovíricos tiene sobre los lípidos y la glucosa en un grupo de pacientes de Yucatán, México.MATERIAL Y MÉTODOS: Se realizó un estudio transversal. A cada paciente se le aplicó un cuestionario creado para este estudio y se le determinaron los valores de colesterol total, triglicéridos y glucosa en ayuno. Se determinó la prevalencia de hiperlipidemia y alteraciones de la glucosa y su relación con las variables de la encuesta.RESULTADOS: Se estudiaron 211 pacientes, 36 (17%) mujeres y 175 (83%) hombres; 92 (44%) tuvieron hiperlipidemia. De éstos, 43 (20%) presentaron hipercolesterolemia (HC) y 82 (39%) hipertrigliceridemia (HT). La presencia de HC e HT combinadas se verificó en 30 (14%) pacientes; además, 19 (9%) pacientes exhibieron alteraciones en la glucosa, seis (3%) presentaron diabetes mellitus y 13 (6%), intolerancia a la glucosa. Las variables que se vincularon con la presencia de hiperlipidemia fueron los números de linfocitos CD4 >350 células/µl [RM= 2.79 (1.08-7.27), p= 0.03], el género masculino [RM= 3.6 (1.4-9.12), p= 0.006] y el uso de nucleósidos inhibidores de la transcriptasa inversa (NITI) [RM= 3.1 (1.2-8.1), p= 0.01].CONCLUSIONES: Los pacientes con la infección por el VIH que reciben terapia antirretroviral (TAR) tienen un riesgo aumentado de presentar dislipidemia. A diferencia de lo que informan la mayor parte las publicaciones, las alteraciones de los lípidos se asociaron con más frecuencia al uso de NITI, por lo que se concluye que la patogenia de estas alteraciones no es única y que resulta probable la existencia de un efecto sinérgico entre las distintas familias de fármacos antirretrovíricos y que otros factores del huésped participen en la génesis de estas alteraciones.

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BACKGROUND: The HTLV-II infection has been reported in patients with HIV infection as often in asymptomatic as those with acquired immunodeficiency syndrome (AIDS). The aim of this study was to determine the prevalence of HTLV-II infection in a group of patients infected by HIV in our region, as well as determining the risk factors associated with HTLV-II transmission in this group of patients and its impact on the clinical course of HIV infection. METHODS: A cross-sectional study was carried out to determine the prevalence of co-infection of HIV-1 and HTLV-II among 192 patients from Yucatán, México. Serum specimens were tested for HTLV antibodies by an enzyme-linked immunosorbent assay (ELISA) test. Positive results were confirmed and typed by Western blot. Twenty four (12.5%) patients were confirmed with antibodies for HTLV-II, but none had antibodies for HTLV-I. Specific risk factors for HTLV-II transmission were not identified. RESULTS: Candidiasis (42 vs. 12%, p = 0.0004) and more than two defining entities of AIDS (37 vs. 18%, p = 0.02) was observed with greater prevalence in the group co-infected. CONCLUSIONS: In our study, a higher frequency of candidiasis and a larger number of AIDS-defining pathologies were observed in the co-infected patients, suggesting that co-infection is associated with greater immunodeficiency.

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