Enfermedad pélvica inflamatoria por Streptococcus constellatus. Experiencia clínica y revisión de la literatura / Pelvic inflammatory disease by Streptococcus constellatus. Clinical experience and a review

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Listeria monocytogenes, a rare cause of endophthalmitis / Listeria monocytogenes, una rara causa de endoftalmitis

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Baja prevalencia de resistencias primarias frente al virus de la hepatitis B en el sur de España / Low prevalence of hepatitis B virus primary drug resistance in Southern Spain

Introducción Para decidir si es necesario investigar resistencias primarias en pacientes naïve con hepatitis B crónica es necesario conocer su prevalencia. Pacientes y métodos Hemos analizado la secuencia genética de la polimerasa en 105 pacientes naïve. Resultados En 2 pacientes (1,9%) detectamos el cambio rtV173L, mutación compensatoria para lamivudina, en un caso la mutación rtI233V y en otro la «mutación de escape» sG145R.ConclusiónNuestro estudio demuestra que, por el momento, no está justificado realizar estudio de resistencias frente al VHB en pacientes naïve (AU)

Introduction: To know the prevalence of primary resistance in chronic hepatitis B naïve patients isessential to decide on the need of routine laboratory testing. Patients and methods: The genetic sequence of the HBV polymerase from 105 naïve patients was analysed. Results: rtV173L, a lamivudine compensatory mutation, was detected in two patients (1.9%), rtI233V inone patient, and another one carried the sG145R vaccine escape mutation. Conclusion: Our study shows that studying HBV resistance in naïve patients should not be recommended in the routine laboratory setting, for the time being (AU)

[Low prevalence of hepatitis B virus primary drug resistance in Southern Spain]. / Baja prevalencia de resistencias primarias frente al virus de la hepatitis B en el sur de España.

INTRODUCTION: To know the prevalence of primary resistance in chronic hepatitis B naïve patients is essential to decide on the need of routine laboratory testing. PATIENTS AND METHODS: The genetic sequence of the HBV polymerase from 105naïve patients was analysed. RESULTS: rtV173L, a lamivudine compensatory mutation, was detected in two patients (1.9%), rtI233V in one patient, and another one carried the sG145R vaccine escape mutation. CONCLUSION: Our study shows that studying HBV resistance in naïve patients should not be recommended in the routine laboratory setting, for the time being.

Quantification of viral loads lower than 50 copies per milliliter by use of the Cobas AmpliPrep/Cobas TaqMan HIV-1 test, version 2.0, can predict the likelihood of subsequent virological rebound to >50 copies per milliliter.

After 1 year of follow-up, patients on HAART with a baseline viral load (VL) of <20 copies/ml showed significantly lower odds of virological rebound to two consecutive VLs of >50 copies/ml than those with baseline VLs of 20 to 39 and 40 to 49 (P < 0.001). The time to virological rebound was also significantly shorter (P < 0.001) for the groups with baseline VLs of 20 to 39 and 40 to 49.

Características químicas, mecanismo de acción y actividad antiviral de etravirina / Chemical characteristics, mechanism of action and antiviral activity of etravirine

Etravirina (ETR) es un derivado diarilpirimidínico. Se trata de una molécula policíclica, constituida por 3 anillos aromáticos unidos por enlaces sencillos (C20H15BrN60). Ejerce su acción mediante un mecanismo de inhibición no competitiva, al unirse a un bolsillo hidrofóbico (binding pocket), muy cercano al centro activo de la enzima, provocando un cambio alostérico hacia una conformación que distorsiona su estructura e impide la polimerización del ADN. Al tratarse de 3 anillos unidos por enlaces sencillos, la molécula está dotada de una enorme flexibilidad y capacidad de torsión. Debido a estas características, ETR puede "acomodarse" a cambios conformacionales en el binding pocket, incluidas un gran número de las conformaciones provocadas por las mutaciones de resistencia que aparecen tras el fracaso a regímenes que incluyen efavirenz o nevirapina. Esta particular estructura química explicará gran parte de sus peculiaridades y diferencias en cuanto a su potencia antiviral y su elevada barrera genética. ETR es una molécula muy activa frente a VIH-1. Presenta una elevada barrera genética y ha demostrado actividad antiviral frente a un amplio panel de virus recombinantes que incorporan mutaciones de resistencia a los no análogos de primera generación. De igual modo, ha demostrado ser eficaz frente a diversos subtipos del grupo M del virus de la inmunodeficiencia humana (VIH) 1 (A, B, C, D, F y H y formas recombinantes CRF01_AE, CRF02_AG, CRF05_ DF) y frente a aislados de VIH-1 grupo O. ETR, como el resto de no análogos, no ha demostrado actividad antiviral frente a VIH-2

Etravirine (ETR) is a diarylpyrimidine derivative with a polycyclic molecule composed of 3 aromatic rings with single bonds between the rings (C20H15BrN60). The drug acts through a mechanism of noncompetitive inhibition on binding to a hydrophobic binding pocket, very close to the active center of the enzyme, provoking an allosteric transition to a conformation that distorts its structure and impedes DNA polymerization. The 3 rings with single bonds between the rings confer the molecule with great flexibility and torsion. Because of these characteristics, etravirine can adapt to conformational changes in the binding pocket, including a large number of the conformations provoked by the resistance mutations that appear after failure to regimens that include efavirenz or nevirapine. This specific chemical structure largely explains the drug's distinguishing features in terms of its antiviral potency and high genetic barrier. ETR is a highly active molecule against HIV-1. This drug has a high genetic barrier to resistance and has demonstrated antiviral activity against a wide panel of recombinant viruses that incorporate resistance mutations to first-generation non-nucleoside analogues. Equally, ETR has demonstrated efficacy against several subtypes of the M group of HIV-1 (A, B, C, D, F and H, and recombinant forms CRF01_AE, CRF02_AG, CRF05_DF), as well as against isolates of HIV-1 group O. ETR, as the rest of non-nucleoside analogues, does not have demonstrated antiviral activity against HIV-2