Posts filed under ‘HIV/SIDA Infeccion Aguda / Reciente’

2017-10 European AIDS Clinical Society (EACS). European guidelines for clinical management and treatment of HIV-1-infected adults in Europe 102 pag

Welcome to the EACS Guidelines!

These Guidelines were developed by the European AIDS Clinical Society (EACS), a not-for-profit organisation, whose mission is to promote excellence in standards of care, research and education in HIV infection and related co-infections, and to actively engage in the formulation of public health policy, with the aim of reducing HIV disease burden across Europe.

The EACS Guidelines were first published in 2005, and are currently available in print, online, and as a free App for both iOS and Android devices. The Guidelines are translated to a number of different languages, and are formally revised at least annually for the electronic version and biennially for the printed version. The electronic version can, however, be updated at any given moment if the panels consider it necessary.

The aim of the EACS Guidelines is to provide easily accessible and comprehensive recommendations to clinicians centrally involved in the care of HIV-positive persons.

The EACS Guidelines are covering a relatively large and diverse area geographically, with different national levels of access to care. As a natural consequence, the Guidelines aim to cover a relatively wide range of recommendations as opposed to the often more uniform national guidelines.

The Guidelines consist of five main sections, including a general overview table of all major issues in HIV infection, as well as detailed recommendations on antiretroviral treatment, diagnosis, monitoring and treatment of co-morbidities, co-infections and opportunistic diseases.

Each respective section of the Guidelines is managed by a panel of experienced European HIV experts, and additional experts, where needed. All recommendations are evidence-based whenever possible, and based on expert opinions in the rare instances where adequate evidence is unavailable. It was decided not to provide formal grades of evidence in the Guidelines. The panels make decisions by consensus or by vote when necessary. Yet, it was decided not to publish results of the votes or discrepancies if any.

A list of the main references used to produce the Guidelines is provided as a separate section. Please reference the EACS Guidelines as follows: EACS Guidelines version 9.0, October 2017. Video links to the EACS online course on Clinical Management of HIV are provided throughout the Guidelines, see Video links.

The diagnosis and management of HIV infection and related co-infections, opportunistic diseases and co-morbidities continue to require a multidisciplinary effort for which we hope the 2017 version of the EACS Guidelines will provide you with an easily accessible and updated overview.

All comments to the Guidelines are welcome and can be directed to guidelines@eacsociety.org

We wish to warmly thank all panellists, external experts, linguists, translators, the EACS Secretariat, the Sanford team and everyone else who helped to build up and to publish the EACS Guidelines for their dedicated work.

 

Enjoy!

Manuel Battegay and Lene Ryom – October 2017

PDF

http://www.eacsociety.org/files/guidelines_9.0-english.pdf

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March 19, 2019 at 4:00 pm

Guidelines for the Use of Antiretroviral Agents in Adults and Adolescents Living with HIV 332 pag – Department of Health and Human Services – OCTOBER 2018

What’s New in the Guidelines?

(Last updated October 25, 2018; last reviewed October 25, 2018)

Resistance Testing

New information has been added regarding the use of HIV-1 proviral DNA genotypic resistance tests to identify drug resistance mutations, especially in the setting of low-level viremia or when plasma HIV RNA is below the limit of detection. The section now includes a discussion on the benefits and limitations of these tests.

Co-Receptor Tropism Testing

For patients who have undetectable HIV RNA, the Panel now recommends using a proviral DNA tropism assay to assess co-receptor usage before maraviroc is initiated as part of a new regimen.

Dolutegravir and Association with Neural Tube Defects

Preliminary data from Botswana suggest that there is an increased risk of neural tube defects in infants born to women who were receiving dolutegravir (DTG) at the time of conception. In response to these preliminary data, several sections in the Adult and Adolescent Guidelines have been updated to provide guidance for clinicians who are considering the use of DTG or other integrase strand transfer inhibitors (INSTIs) in individuals who are pregnant, or in those of childbearing potential who plan to get pregnant or who are sexually active and not using effective contraception.

The sections that have been updated with this new information include:

  • What to Start
  • Virologic Failure
  • Optimizing Antiretroviral Therapy in the Setting of Viral Suppression (formerly Regimen Switching in the

Setting of   Virologic Suppression)

  • Acute and Recent (Early) HIV-1 Infection
  • Adolescents and Young Adults with HIV
  • Women with HIV

 

What to Start

The following changes have been made to the recommendations for initial antiretroviral (ARV) regimens:

  • Bictegravir/Tenofovir Alafenamide/Emtricitabine (BIC/TAF/FTC): BIC is a new INSTI that is approved by the Food and Drug Administration (FDA) as part of a single-tablet regimen (STR) that also includes TAF and FTC. This regimen is now classified as a Recommended Initial Regimen for Most People with HIV.
  • Elvitegravir/Cobicistat/Emtricitabine with Tenofovir Alafenamide or Tenofovir Disoproxil Fumarate (EVG/c/FTC/TAF or EVG/c/FTC/TDF): These regimens have been moved to the category of Recommended Initial Regimens in Certain Clinical Situations. This change was made because these combinations include cobicistat, a pharmaco-enhancer that inhibits cytochrome P450 3A4 and increases the likelihood of drug-drug interactions. EVG also has a lower barrier to resistance than DTG and BIC.
  • Doravirine (DOR): DOR, a new non-nucleoside reverse transcriptase inhibitor, was recently approved by the FDA and is available as a single-drug tablet and as part of an STR that also includes TDF and lamivudine (3TC). DOR/TDF/3TC and DOR plus TAF/FTC have been added to the category of Recommended Initial Regimens in Certain Clinical Situations.
  • Dolutegravir plus Lamivudine (DTG plus 3TC): This two-drug regimen is now one of the regimens to consider when abacavir, TAF, or TDF cannot be used or are not optimal.
  • A new table, Table 6b, has been added to provide guidance to clinicians who are considering the use of DTG or other INSTIs in those who are pregnant and in those of childbearing potential.
  • Several new tables (Tables 8a–8d) have been added to the sections for the individual drug classes. These tables compare the characteristics of the different drugs within the classes.
  • Updates have been made throughout the section with new safety and clinical trial data.

 

Virologic Failure

  • This section was updated to include newly reported data and new language on recently published clinical trial data for first- line ARV treatment failure.
  • The Panel notes that, in some persons with multidrug-resistant HIV, DTG may be the only treatment option, or one of few treatment options. Accordingly, the language on the use of DTG in those of childbearing potential has been updated. The section now emphasizes that clinicians and patients should discuss the risk of neural tube defects if pregnancy occurs while the patient is taking DTG, as well as the risk of persistent viremia in the patient and the risk of HIV transmission to the fetus if pregnancy occurs while the patient is not on effective ARV therapy. The decision of whether to initiate or continue DTG should be made after carefully considering these risks.
  • Ibalizumab (IBA), a CD4 post-attachment inhibitor, was recently approved for use in persons with multidrug-resistant HIV. A review of the results of a clinical trial on IBA use in this setting has been added to the section.

 

Optimizing Antiretroviral Therapy in the Setting of Viral Suppression

  • The title of this section has been changed from Regimen Switching in the Setting of Virologic Suppression to Optimizing Antiretroviral Therapy in the Setting of Viral Suppression to better reflect the rationale for regimen changes in this setting.

 

  • The Panel emphasizes the importance of reviewing all available resistance test results when constructing a new regimen.
  • The role of HIV-1 proviral DNA genotypic resistance testing in detecting archived drug resistance mutations in the setting of viral suppression is discussed.
  • The Panel recommends performing pregnancy testing for those of childbearing potential before a regimen switch and provides recommendations for INSTI use in these patients.
  • Clinical trial data on the use of several ARV combinations in switch studies are updated and discussed in this section.

 

Exposure-Response Relationship and Therapeutic Drug Monitoring Section

  • This section has been removed from the guidelines.
  • The subsection regarding the role of therapeutic drug monitoring in managing drug-drug interactions has been moved to the Drug-Drug Interactions section of the guidelines.

 

Additional Updates

Various tables in the guidelines have been updated with new data, as well as information related to BIC and DOR.

 

  • Hepatitis C Virus/HIV Coinfection
  • Adverse Effects of Antiretroviral Agents
  • Monthly Average Prices of Commonly Used Antiretroviral Drugs
  • Drug-Drug Interactions
  • Appendix B Tables: Characteristics of Antiretroviral Drugs and Antiretroviral Dosing Recommendations in

Patients with   Renal and Hepatic Insufficiency

 

PDF

https://aidsinfo.nih.gov/contentfiles/lvguidelines/adultandadolescentgl.pdf

 

March 19, 2019 at 3:47 pm

HIV-1 persistence following extremely early initiation of antiretroviral therapy (ART) during acute HIV-1 infection: An observational study.

PLoS Med. November 4, 2017 V.14 N.11 e1002417.     

Henrich TJ1, Hatano H2, Bacon O2,3, Hogan LE1, Rutishauser R1,2, Hill A4, Kearney MF5, Anderson EM5, Buchbinder SP2,3, Cohen SE2,3, Abdel-Mohsen M2,6, Pohlmeyer CW7, Fromentin R8, Hoh R2, Liu AY2,3, McCune JM1, Spindler J5, Metcalf-Pate K7, Hobbs KS1, Thanh C1, Gibson EA1, Kuritzkes DR9,10, Siliciano RF11,12, Price RW13, Richman DD14,15, Chomont N8, Siliciano JD10, Mellors JW16, Yukl SA17,18, Blankson JN7, Liegler T2, Deeks SG2.

Author information

1 Division of Experimental Medicine, University of California, San Francisco, California, United States of America.

2 Division of HIV, Infectious Diseases and Global Medicine, University of California, San Francisco, California, United States of America.

3 San Francisco Department of Public Health, San Francisco, California, United States of America.

4 Program for Evolutionary Dynamics, Harvard University, Cambridge, Massachusetts, United States of America.

5 HIV Dynamics and Replication Program, Center for Cancer Research, National Cancer Institute, Frederick, Maryland, United States of America.

6 The Wistar Institute, Philadelphia, Pennsylvania, United States of America.

7 Center for AIDS Research, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.

8 Centre de Recherche du CHUM and Department of Microbiology, Infectiology and Immunology, Université de Montréal, Montreal, Quebec, Canada.

9 Division of Infectious Diseases, Brigham and Women’s Hospital, Boston, Massachusetts, United States of America.

10 Harvard Medical School, Boston, Massachusetts, United States of America.

11 Division of Infectious Diseases, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.

12 Howard Hughes Medical Institute, Baltimore, Maryland, United States of America.

13 Department of Neurology, University of California, San Francisco, California, United States of America.

14 University of California San Diego, La Jolla, California, United States of America.

15 Veterans Affairs San Diego Healthcare System, San Diego, California, United States of America.

16 Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.

17 San Francisco Veterans Affairs Medical Center, San Francisco, California, United States of America.

18 University of California, San Francisco, California, Unites States of America.

Abstract

BACKGROUND:

It is unknown if extremely early initiation of antiretroviral therapy (ART) may lead to long-term ART-free HIV remission or cure. As a result, we studied 2 individuals recruited from a pre-exposure prophylaxis (PrEP) program who started prophylactic ART an estimated 10 days (Participant A; 54-year-old male) and 12 days (Participant B; 31-year-old male) after infection with peak plasma HIV RNA of 220 copies/mL and 3,343 copies/mL, respectively. Extensive testing of blood and tissue for HIV persistence was performed, and PrEP Participant A underwent analytical treatment interruption (ATI) following 32 weeks of continuous ART.

METHODS AND FINDINGS:

Colorectal and lymph node tissues, bone marrow, cerebral spinal fluid (CSF), plasma, and very large numbers of peripheral blood mononuclear cells (PBMCs) were obtained longitudinally from both participants and were studied for HIV persistence in several laboratories using molecular and culture-based detection methods, including a murine viral outgrowth assay (mVOA). Both participants initiated PrEP with tenofovir/emtricitabine during very early Fiebig stage I (detectable plasma HIV-1 RNA, antibody negative) followed by 4-drug ART intensification. Following peak viral loads, both participants experienced full suppression of HIV-1 plasma viremia. Over the following 2 years, no further HIV could be detected in blood or tissue from PrEP Participant A despite extensive sampling from ileum, rectum, lymph nodes, bone marrow, CSF, circulating CD4+ T cell subsets, and plasma. No HIV was detected from tissues obtained from PrEP Participant B, but low-level HIV RNA or DNA was intermittently detected from various CD4+ T cell subsets. Over 500 million CD4+ T cells were assayed from both participants in a humanized mouse outgrowth assay. Three of 8 mice infused with CD4+ T cells from PrEP Participant B developed viremia (50 million input cells/surviving mouse), but only 1 of 10 mice infused with CD4+ T cells from PrEP Participant A (53 million input cells/mouse) experienced very low level viremia (201 copies/mL); sequence confirmation was unsuccessful. PrEP Participant A stopped ART and remained aviremic for 7.4 months, rebounding with HIV RNA of 36 copies/mL that rose to 59,805 copies/mL 6 days later. ART was restarted promptly. Rebound plasma HIV sequences were identical to those obtained during acute infection by single-genome sequencing. Mathematical modeling predicted that the latent reservoir size was approximately 200 cells prior to ATI and that only around 1% of individuals with a similar HIV burden may achieve lifelong ART-free remission. Furthermore, we observed that lymphocytes expressing the tumor marker CD30 increased in frequency weeks to months prior to detectable HIV-1 RNA in plasma. This study was limited by the small sample size, which was a result of the rarity of individuals presenting during hyperacute infection.

CONCLUSIONS:

We report HIV relapse despite initiation of ART at one of the earliest stages of acute HIV infection possible. Near complete or complete loss of detectable HIV in blood and tissues did not lead to indefinite ART-free HIV remission. However, the small numbers of latently infected cells in individuals treated during hyperacute infection may be associated with prolonged ART-free remission.

PDF

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5675377/pdf/pmed.1002417.pdf

December 11, 2017 at 8:42 am

Fiebre de origen desconocido en pacientes HIV positivos

ANALES DE MEDICINA INTERNA (Madrid), 2001 V.18 N.4 P.181-186

BARBA, J. GÓMEZ-RODRIGO, J. MARCO, P. RONDÓN, G. EROLES,

LÓPEZ-VARAS, R. TORRES

Departamento de Medicina Interna y Enfermedades Infecciosas. Hospital Severo Ochoa.

Leganés. Madrid

RESUMEN

Objetivos

Describir la presentación clínica y la utilidad de los de tests diagnósticos habitualmente recomendados en el estudio de la fiebre de origen desconocido (FOD) en los pacientes VIH positivos.

Pacientes y métodos

Incluimos en el estudio a los 54 pacientes con infección por el VIH que ingresaron en nuestro Hospital por FOD durante un periodo de 23 meses. La FOD fue definida de acuerdo con los criterios modificados de Petersdorf´s.

Resultados

La causa de la fiebre se identificó en 48 casos (89%). La tuberculosis, la micobacteriosis atípica y la leishmaniasis pueden explicar el 68% de los casos. El aspirado de médula ósea, la punción aspiración o la biopsia de los ganglios linfáticos y los cultivos para micobacterias fueron las pruebas diagnósticas más rentables.

Conclusiones

La infección por micobacterias debe ser el primer diagnóstico de sospecha en los pacientes VIH positivos con FOD. Es posible precedir el diagnóstico de tuberculosis con una alta precisión (90,5%) con un modelo de regresión logística basado en datos clínicos y analíticos fácilmente obtenibles.

PDF

http://scielo.isciii.es/pdf/ami/v18n4/original2.pdf

November 21, 2017 at 8:41 am

FIEBRE DE ORIGEN DESCONOCIDO EN PACIENTES INFECTADOS CON EL VIRUS DE LA INMUNODEFICIENCIA HUMANA

MEDICINA (Buenos Aires) 2000 V.60 N.5 P.623-630

SEBASTIAN A. MATHURIN, SERGIO LUPO, HECTOR O. ALONSO

Primera Cátedra de Clínica Médica y Terapéutica, Facultad de Ciencias Médicas, Universidad Nacional de Rosario; Hospital Provincial del Centenario, Rosario

La fiebre de origen desconocido (FOD) es frecuente en pacientes infectados por el HIV. Existen numerosas causas que pueden originar FOD y su frecuencia relativa depende de múltiples factores. Usualmente se debe a una infección oportunista agregada.

La evaluación diagnóstica depende de la presentación clínica y del estadio de la infección por HIV. Existe una asociación entre el recuento de linfocitos CD4 y ciertas enfermedades oportunistas que pueden originar FOD.

El área geográfica y la prevalencia local de infecciones endémicas es un factor importante. Las infecciones de distribución mundial como la tuberculosis siempre deben ser consideradas y otras como la histoplasmosis diseminada son causa frecuente de FOD en áreas endémicas como la Argentina.

La mayor utilidad diagnóstica se obtiene con los cultivos de esputo y hemocultivos para micobacterias, y entre los métodos invasivos con cultivos a partir de la aspiración/biopsia de ganglio linfático, la biopsia de médula ósea y la biopsia hepática.

La eficacia del tratamiento empírico ha sido documentada en ciertas infecciones.

FULL TEXT

http://www.medicinabuenosaires.com/revistas/vol60-00/5-1/fiebredeorigen.htm

November 21, 2017 at 8:34 am

HIV-1 persistence following extremely early initiation of antiretroviral therapy (ART) during acute HIV-1 infection: An observational study.

PLoS Med November 7, 2017 V.14 P.e1002417.

Henrich TJ et al.

Abstract

Background

It is unknown if extremely early initiation of antiretroviral therapy (ART) may lead to long-term ART-free HIV remission or cure. As a result, we studied 2 individuals recruited from a pre-exposure prophylaxis (PrEP) program who started prophylactic ART an estimated 10 days (Participant A; 54-year-old male) and 12 days (Participant B; 31-year-old male) after infection with peak plasma HIV RNA of 220 copies/mL and 3,343 copies/mL, respectively. Extensive testing of blood and tissue for HIV persistence was performed, and PrEP Participant A underwent analytical treatment interruption (ATI) following 32 weeks of continuous ART.

Methods and findings

Colorectal and lymph node tissues, bone marrow, cerebral spinal fluid (CSF), plasma, and very large numbers of peripheral blood mononuclear cells (PBMCs) were obtained longitudinally from both participants and were studied for HIV persistence in several laboratories using molecular and culture-based detection methods, including a murine viral outgrowth assay (mVOA). Both participants initiated PrEP with tenofovir/emtricitabine during very early Fiebig stage I (detectable plasma HIV-1 RNA, antibody negative) followed by 4-drug ART intensification. Following peak viral loads, both participants experienced full suppression of HIV-1 plasma viremia. Over the following 2 years, no further HIV could be detected in blood or tissue from PrEP Participant A despite extensive sampling from ileum, rectum, lymph nodes, bone marrow, CSF, circulating CD4+ T cell subsets, and plasma. No HIV was detected from tissues obtained from PrEP Participant B, but low-level HIV RNA or DNA was intermittently detected from various CD4+ T cell subsets. Over 500 million CD4+ T cells were assayed from both participants in a humanized mouse outgrowth assay. Three of 8 mice infused with CD4+ T cells from PrEP Participant B developed viremia (50 million input cells/surviving mouse), but only 1 of 10 mice infused with CD4+ T cells from PrEP Participant A (53 million input cells/mouse) experienced very low level viremia (201 copies/mL); sequence confirmation was unsuccessful. PrEP Participant A stopped ART and remained aviremic for 7.4 months, rebounding with HIV RNA of 36 copies/mL that rose to 59,805 copies/mL 6 days later. ART was restarted promptly. Rebound plasma HIV sequences were identical to those obtained during acute infection by single-genome sequencing. Mathematical modeling predicted that the latent reservoir size was approximately 200 cells prior to ATI and that only around 1% of individuals with a similar HIV burden may achieve lifelong ART-free remission. Furthermore, we observed that lymphocytes expressing the tumor marker CD30 increased in frequency weeks to months prior to detectable HIV-1 RNA in plasma. This study was limited by the small sample size, which was a result of the rarity of individuals presenting during hyperacute infection.

Conclusions

We report HIV relapse despite initiation of ART at one of the earliest stages of acute HIV infection possible. Near complete or complete loss of detectable HIV in blood and tissues did not lead to indefinite ART-free HIV remission. However, the small numbers of latently infected cells in individuals treated during hyperacute infection may be associated with prolonged ART-free remission.

FULL TEXT

http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1002417

PDF

http://journals.plos.org/plosmedicine/article/file?id=10.1371/journal.pmed.1002417&type=printable

 

 

November 21, 2017 at 7:27 am

Brief Report: Enhanced Normalization of CD4/CD8 Ratio With Earlier Antiretroviral Therapy at Primary HIV Infection.

J Acquir Immune Defic Syndr. 2016 Sep 1;73(1):69-73.

Thornhill J1, Inshaw J, Kaleebu P, Cooper D, Ramjee G, Schechter M, Tambussi G, Fox J, Samuel M, Miro JM, Weber J, Porter K, Fidler S.

1 *Department of Medicine, Imperial College, London, United Kingdom; †Medical Research Council Clinical Trials Unit, University College London, London, United Kingdom; ‡Medical Research Council/Uganda Virus Research Institute Research Unit on AIDS, Entebbe, Uganda; §Kirby Institute University of New South Wales and Centre for Applied Medical Research, St Vincent’s Hospital, Sydney, Australia; ‖HIV Prevention Unit, Medical Research Council, Durban, South Africa; ¶Projeto Praça Onze, Hospital Escola Sao Francisco de Assis, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil; #Division of Infectious Diseases, Ospedale San Raffaele, Milan, Italy; **Department of HIV, Faculty of Medicine, Guys and St Thomas’ NHS Trust/Kings College London, United Kingdom; and ††Hospital Clinic – IDIBAPS, University of Barcelona, Barcelona, Spain.

Abstract

BACKGROUND:

Total CD4 T-cell counts predict HIV disease progression but do not necessarily reflect normalization of immune function. CD4/CD8 ratio is a marker of immune dysfunction, a prognostic indicator for non-AIDS mortality, and reflects viral reservoir size. Despite antiretroviral therapy (ART), recovery of CD4/CD8 ratio in chronic HIV infection is incomplete; we hypothesize enhanced CD4/CD8 ratio recovery with earlier treatment initiation in recently infected individuals.

METHODS:

CD4 count and CD4/CD8 ratio were analyzed using data from 2 cohorts: SPARTAC trial and the UK HIV Seroconverters Cohort where primary HIV infection (PHI) was defined as within 6 months from estimated date of infection. Using time-to-event methods and Cox proportional hazard models, we examined the effect of CD4/CD8 ratio at seroconversion on disease progression (CD4 <350 cells per cubic millimeter/ART initiation) and factors associated with time from ART initiation to CD4/CD8 normalization (ratio >1.0).

FINDINGS:

Of 573 seroconverters, 482 (84%) had abnormal CD4/CD8 ratios at HIV seroconversion. Individuals with higher CD4/CD8 ratio at seroconversion were significantly less likely to reach the disease progression endpoint [adjusted hazard ratio (aHR) (95% CI) = 0.52 (0.32 to 0.82), P = 0.005]. The longer the interval between seroconversion and ART initiation [HR (95% CI) = 0.98 per month increase (0.97, 0.99), P < 0.001], the less likely the CD4/CD8 ratio normalization. ART initiation within 6 months from seroconversion was significantly more likely to normalize [HR (95% CI) = 2.47 (1.67 to 3.67), P < 0.001] than those initiating later.

INTERPRETATION:

Most individuals presenting in PHI have abnormal CD4/CD8 ratios. The sooner the ART is initiated in PHI, the greater the probability of achieving normal CD4/CD8 ratio.

PDF

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4981213/pdf/qai-73-069.pdf

March 11, 2017 at 6:39 pm

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