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Journal articles on the topic 'Co-infection ar le VIH'

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Published: 4 June 2021

Last updated: 5 February 2022

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1

Fall, N., N. F. Ngom-Gueye, N. M. Diop, N. Touré-Badiane, Y. Dia Kane, A. Diatta, and A. Niang. "Co-infection tuberculose/VIH." Revue des Maladies Respiratoires 31 (January 2014): A157. http://dx.doi.org/10.1016/j.rmr.2013.10.549.

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2

Harmouche, H., and W. Ammouri. "La co-infection VIH – Tuberculose." La Revue de Médecine Interne 30 (December 2009): S273—S276. http://dx.doi.org/10.1016/j.revmed.2009.09.009.

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3

Borand, Laurence, Phearavin Pheng, Manil Saman, Chanthy Leng, Phalla Chea, Sao Sarady Ay, Sophea Suom, Nimul Roat Men, Eric Nerrienet, and Olivier Marcy. "Co-infection tuberculose et VIH." médecine/sciences 29, no. 10 (October 2013): 908–11. http://dx.doi.org/10.1051/medsci/20132910020.

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4

Turcu, A., M. Vincent-Martin, NO Olsson, L. Piroth, P. Bielefeld, and JF Besancenot. "Co-infection VIH-VHC et anticardiolipines." La Revue de Médecine Interne 19 (January 1998): 431. http://dx.doi.org/10.1016/s0248-8663(98)90126-6.

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5

Busato, F., D. Grasset, S. Métivier, C. Bordères, N. Puech, and C. Seigneuric. "Co-infection VIH-VHC : attention aux mitochondries!" La Revue de Médecine Interne 22 (December 2001): 563s—564s. http://dx.doi.org/10.1016/s0248-8663(01)80296-4.

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6

Lesprit, Ph, and J. M. Molina. "La co-infection VIH-tuberculose : causes et conséquences." Médecine et Maladies Infectieuses 26, no. 11 (November 1996): 918–21. http://dx.doi.org/10.1016/s0399-077x(96)80197-1.

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7

Piroth, L. "La co-infection VHC-VIH : état des lieux." Gastroentérologie Clinique et Biologique 33 (March 2009): S94—S96. http://dx.doi.org/10.1016/s0399-8320(09)72446-7.

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8

Berkchi, M., M. Daoudi, M. Soualhi, R. Zahraoui, K. Marc, J. Benamor, and J. E. Bourkadi. "Profil de la co-infection VIH et tuberculose." Revue des Maladies Respiratoires Actualités 12, no. 1 (January 2020): 162. http://dx.doi.org/10.1016/j.rmra.2019.11.358.

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9

Williams, C., and D. Klínzman. "La co-infection VIH et virus GBC est favorable." Revue Française des Laboratoires 2004, no. 365 (September 2004): 14. http://dx.doi.org/10.1016/s0338-9898(04)80186-0.

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10

Salmon-Céron, D., P. Gouëzel, E. Delarocque-Astagneau, L. Piroth, P. Dellamonica, P. Marcellin, and G. Pialoux. "Co-infection VIH-VHC à l'hôpital. Enquête nationale juin 2001." Médecine et Maladies Infectieuses 33, no. 2 (February 2003): 78–83. http://dx.doi.org/10.1016/s0399-077x(03)00022-2.

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11

Manga, N. M., A. Poda, N. Bazolo, O. Sané, G. Batista, N. F. Guèye, P. S. Sow, and C. I. Badiane. "Syndrome de reconstitution immunitaire et co-infection lèpre et VIH." Médecine et Maladies Infectieuses 41, no. 7 (July 2011): 390–91. http://dx.doi.org/10.1016/j.medmal.2011.02.012.

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12

Boumlil, W., H. Baha, F. Hali, and S. Chiheb. "CO 17 : Gale hyperkératosique révélant une infection VIH chez un enfant." Annales de Dermatologie et de Vénéréologie 143, no. 4 (April 2016): S26. http://dx.doi.org/10.1016/s0151-9638(16)30144-2.

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13

Perronne, C., and F. Bani-Sadr. "Co-infection par le VIH et le virus de l'hépatite C." Médecine et Maladies Infectieuses 30, no. 6 (June 2000): 344–46. http://dx.doi.org/10.1016/s0399-077x(00)89103-9.

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14

Soumaré, D., K. Ouattara, Y. Toloba, B. F. Sissoko, F. Sidibé, S. Daou, and S. Diallo. "Co-infection TB/VIH : tuberculose à l’ère du VIH en Afrique : expérience du CHU du point-G." Revue des Maladies Respiratoires 29 (January 2012): A197. http://dx.doi.org/10.1016/j.rmr.2011.10.894.

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15

Okwuraiwe, A. P., R. A. Audu, F. A. Ige, O. B. Salu, C. K. Onwuamah, and A. Z. Musa. "Long term outcomes of highly active antiretroviral therapy in HIV infected Nigerians and those co-infected with hepatitis B and C viruses." African Journal of Clinical and Experimental Microbiology 22, no. 1 (January 26, 2021): 67–73. http://dx.doi.org/10.4314/ajcem.v22i1.9.

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Background: HIV co-infection with hepatitis B (HBV) and/or hepatitis C virus (HCV) is common, largely due to shared routes of transmission, but paucity of data exists for long term treatment outcomes of HIV infected patients, and those co-infected with HBV and HCV despite the high burden in Nigeria. The aim of study was to describe the longterm treatment outcomes in HIV infected Nigerians and to assess the effect of HBV and HCV co-infections on longterm response to antiretroviral therapy (ART).Methodology: This was a retrospective study of HIV infected adults (> 18 years old) consecutively initiating ART between July 2004 and December 2007, who were followed up for 7 years (2011 and 2014). HBV and HCV infections were diagnosed by detection of serum hepatitis B surface antigen (HBsAg) and HCV antibody (HCVAb) respectively. HIV viral load and CD4 count were monitored 3-monthly after initiating ART, and treatment outcomes based on these were compared between patients with HIV mono-infection, HIV/HBV, HIV/HCV and HIV/HBV/HCV co-infections. Clinical and laboratory data of the patients were abstracted from the medical databases, FileMaker Pro, v 10, entered into Microsoft Excel, and analyzed using SPSS version 20.0.Results: A total of 2,800 adults were evaluated (median age of 35.5 years; 64.2% female), of whom 197 (7.0%) were co-infected with HBV, 53 (1.9%) with HCV, and 15 (0.5%) with HBV and HCV. During the 7-year period, 369 (13.2%) patients were lost to follow up. Immune reconstitution, measured by CD4 recovery, was lower in both HBV and HCV co-infections compared to HIV mono-infection, but this was not statistically significant (p>0.05). Median baseline HIV viral load was 4.63 log copies/ml for all groups, which decreased to undetectable level at a median time of 6 months and remained so for the study duration.Conclusion: This study revealed a higher virologic failure among HIV/HCV co-infected group compared to other groups. No immunological difference in ART treatment outcomes between HIV mono-infected and those co-infected with HBV and HCV after 7-year follow-up. Gradual rise in CD4 was found to be an immunological evidence of the body’s recovery from HIV, buttressed by the drop in viral load over the 7-year period. Keywords: ART, HIV, HBV, HCV co-infection, long term outcomes English title: Résultats à long terme du traitement antirétroviral hautement actif chez les Nigérians infectés par le VIH et ceux co-infectés par les virus des hépatites B et C Contexte: La co-infection par le VIH avec l'hépatite B (VHB) et/ou le virus de l'hépatite C (VHC) est courante, engrande partie en raison des voies de transmission partagées, mais il existe peu de données sur les résultats dutraitement à long terme des patients infectés par le VIH, et ceux co -infectés par le VHB et le VHC malgré le fardeau élevé au Nigéria. Le but de l'étude était de décrire les résultats du traitement à long terme chez les Nigérians infectés par le VIH et d'évaluer l'effet des co-infections par le VHB et le VHC sur la réponse à long terme au traitement antirétroviral (TAR).Méthodologie: Il s'agissait d'une étude rétrospective sur des adultes infectés par le VIH (>18 ans) ayant commencé un traitement antirétroviral consécutivement entre juillet 2004 et décembre 2007, suivis pendant 7 ans (2011 et 2014). Les infections par le VHB et le VHC ont été diagnostiquées par détection de l'antigène de surface sérique de l'hépatite B (AgHBs) et des anticorps anti-VHC (HCVAb) respectivement. La charge virale du VIH et la numération des CD4 ont été surveillées tous les trois mois après le début du TAR, et les résultats du traitement basés sur ceuxci ont été comparés entre les patients atteints de mono-infection VIH, VIH/VHB, VIH/VHC et VIH/VHB/VHC. Les données cliniques et de laboratoire des patients ont été extraites des bases de données médicales, FileMaker Pro, v 10, saisies dans Microsoft Excel et analysées à l'aide de SPSS version 20.0.Résultats: Un total de 2800 adultes ont été évalués (âge médian de 35,5 ans; 64,2% de femmes), dont 197 (7,0%) étaient co-infectés par le VHB, 53 (1,9%) par le VHC et 15 (0,5%) par le VHB et VHC. Au cours de la période de 7 ans, 369 (13,2%) patients ont été perdus de vue. La reconstitution immunitaire, mesurée par la récupération des CD4, était plus faible dans les co-infections par le VHB et le VHC que dans la mono-infection par le VIH, mais cela n'était pas statistiquement significatif (p>0,05). La charge virale VIH de base médiane était de 4,63 log copies / ml pour tous les groupes, ce qui a diminué à un niveau indétectable à une période médiane de 6 mois et le reste pendant toute la durée de l'étude.Conclusion: Cette étude a révélé un échec virologique plus élevé parmi le groupe co-infecté par le VIH / VHC par rapport aux autres groupes. Aucune différence immunologique dans les résultats du traitement TAR entre le VIH mono-infecté et ceux co-infectés par le VHB et le VHC après un suivi de 7 ans. L’augmentation progressive des CD4 s’est avérée être une preuve immunologique de la guérison du corps du VIH, étayée par la baisse de la charge virale au cours de la période de 7 ans. Mots clés: TAR, VIH, VHB, co-infection par le VHC, résultats à long terme

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16

Catorze, G., J. Alberto, A. Afonso, R. Vieira, S. Cortes, and L. Campino. "Co-infection Leishmania infantum/VIH : lésions cutanées après traitement d’une leishmaniose viscérale." Annales de Dermatologie et de Vénéréologie 133, no. 1 (January 2006): 39–42. http://dx.doi.org/10.1016/s0151-9638(06)70841-9.

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17

Dalma, J. B., R. Arcani, M. Koubi, P. Rossi, G. Kaplanski, E. Bernit, V. Veit, et al. "Pneumocystose en médecine interne en dehors d’une co-infection par le VIH." La Revue de Médecine Interne 38 (December 2017): A146. http://dx.doi.org/10.1016/j.revmed.2017.10.082.

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18

Peigne, V., F. Dromer, O. Lidove, and O. Lortholary. "Co-infection histoplasmose-VIH en France métropolitaine à l’ère des thérapies antirétrovirales efficaces." La Revue de Médecine Interne 29 (December 2008): S295. http://dx.doi.org/10.1016/j.revmed.2008.10.026.

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19

Randrianasolo, D., C. Michaux, M. A. Vandenhende, M. Bonarek, D. Lacoste, N. Bernard, P. Morlat, and F. Bonnet. "Purpura thrombotique thrombocytopénique induit par interféron au cours d’une co-infection VIH VHC." La Revue de Médecine Interne 30 (June 2009): S112. http://dx.doi.org/10.1016/j.revmed.2009.03.233.

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20

Ba, P. S., A. Niang, A. K. Fall, A. Ndao Fall, and K. M. Ba Fall. "B-01: La co-infection VIH/VHB/VHC à l’hôpital principal de Dakar." Médecine et Maladies Infectieuses 44, no. 6 (June 2014): 29. http://dx.doi.org/10.1016/s0399-077x(14)70122-2.

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21

Soumare, D. D. N., K. Ouattara, T. Kanoute, J. P. Dembele, Y. Toloba, and S. Diallo. "La co-infection TB/VIH en Afrique : aspects épidémiocliniques au CHU Point-G." Revue des Maladies Respiratoires 35 (January 2018): A174—A175. http://dx.doi.org/10.1016/j.rmr.2017.10.397.

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22

Filoche, P., M. Adoun, C. Godet, F. Caron, R. Robert, E. Donal, and J. C. Meurice. "Co-infection a Mycobacterium Tuberculosis et Pneumocystis Carinii chez une patiente non VIH." Revue des Maladies Respiratoires 21, no. 4 (September 2004): 869. http://dx.doi.org/10.1016/s0761-8425(04)71447-3.

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23

Joomaye, Z., P. Perney, J. Ramos, C. Chapoutot, P. Beaufort, B. Hanslik, and F. Blanc. "Hépatite à cellules géantes de l’adulte associée à une co-infection VIH–VHC." La Revue de Médecine Interne 21, no. 11 (November 2000): 1005–6. http://dx.doi.org/10.1016/s0248-8663(00)00261-7.

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24

Attia, K. A. "Co-infection VIH-VHB au sud du Sahara : données épidémiologiques, cliniques et thérapeutiques." Journal Africain d’Hépato-Gastroentérologie 1, no. 1 (April 2007): 51–53. http://dx.doi.org/10.1007/s12157-007-0011-z.

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25

Dagnra, A. Y., K. Adjoh, S. Tchaptchet Heunda, A. A. Patassi, D. Sadzo Hetsu, F. Awokou, and O. Tidjani. "Prévalence de la co-infection VIH-tuberculose et impact de l’infection VIH sur l’évolution de la tuberculose pulmonaire au Togo." Bulletin de la Société de pathologie exotique 104, no. 5 (September 4, 2010): 342–46. http://dx.doi.org/10.1007/s13149-010-0079-3.

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26

Rakotomizao, J., S. J. B. Rakotondravelo, J. Rajaoarifetra, J. J. Rakotoson, V. Razoelinirina, and A. C. F. Andrianarisoa. "Prévalence de la co-infection VIH/Tuberculose dans l’unité de pneumologie du CHU d’Antananarivo." Revue des Maladies Respiratoires 23 (January 2006): 45. http://dx.doi.org/10.1016/s0761-8425(06)72196-9.

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27

Chanet, V., O. Baud, C. Henquel, D. Bailly, J. Beytout, and H. Laurichesse. "Spasmes artériels récidivants chez un patient ayant une co-infection VIH-VHC, sous trithérapie." Médecine et Maladies Infectieuses 31, no. 6 (January 2001): 447–48. http://dx.doi.org/10.1016/s0399-077x(01)00219-0.

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28

Ilboudo, D., A. Sawadogo, and J. Simpore. "Co-infection hépatite C et VIH chez les femmes enceintes à Ouagadougou (Burkina Faso)." Médecine et Maladies Infectieuses 33, no. 5 (May 2003): 278–79. http://dx.doi.org/10.1016/s0399-077x(02)00004-5.

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29

Joomaye, Z., P. Perney, J. Ramos, C. Chapoutot, P. Beaufort, B. Hanslik, and F. Blanc. "Hépatite à cellules géantes de l'adulte : responsabilité de la co-infection VIH et VHC." La Revue de Médecine Interne 19 (January 1998): 448. http://dx.doi.org/10.1016/s0248-8663(98)90161-8.

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30

Agodokpessi, G., G. Ade, S. Ade, P. Wachinou, D. Affolabi, S. Anagonou, and M. Gninafon. "Aspects épidémio-cliniques et évolutifs de la co-infection tuberculose et VIH à Cotonou." Revue des Maladies Respiratoires 29 (January 2012): A48—A49. http://dx.doi.org/10.1016/j.rmr.2011.10.100.

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31

Bennani, M. A., K. Machou, F. Z. Drissi, S. Kebbati, M. Metahri, A. Snouber, and M. Guermaz. "Prévalence de la co-infection tuberculose VIH dans trois villes du nord-ouest Algérien." Revue des Maladies Respiratoires 31 (January 2014): A160. http://dx.doi.org/10.1016/j.rmr.2013.10.559.

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32

Hull, Mark, Pierre Giguère, Marina Klein, Stephen Shafran, Alice Tseng, Pierre Côté, Marc Poliquin, and Curtis Cooper. "Le Domaine des Co-infections et des Maladies Concomitantes du Réseau Canadien pour les Essais VIH des IRSC : Lignes Directrices Canadiennes pour la Prise en Charge et le Traitement de la Co-Infection par le VIH et l’Hépatite C chez les Adultes." Canadian Journal of Infectious Diseases and Medical Microbiology 25, no. 1 (2014): 39–62. http://dx.doi.org/10.1155/2014/921314.

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HISTORIQUE: De 20 % à 30 % des Canadiens qui vivent avec le VIH sont co-infectés par le virus de l’hépatite C (VHC), lequel est responsable d’une morbidité et d’une mortalité importantes. La prise en charge du VIH et du VHC est plus complexe en raison de l’évolution accélérée de la maladie hépatique, du choix et des critères d’initiation de la thérapie antirétrovirale et du traitement anti-VHC, de la prise en charge de la santé mentale et des toxicomanies, des obstacles socioéconomiques et des interactions entre les nouvelles thérapies antivirales à action directe du VHC et les antirétrovirauxOBJECTIF: Élaborer des normes nationales de prise en charge des adultes co-infectés par le VHC et le VIH dans le contexte canadien.MÉTHODOLOGIE: Le Réseau canadien pour les essais VIH des Instituts de recherche en santé du Canada a réuni un groupe d’experts possédant des compétences cliniques en co-infection par le VIH et le VHC pour réviser les publications à jour ainsi que les lignes directrices et les protocoles en place. Après une vaste sollicitation afin d’obtenir des points de vue, le groupe de travail a approuvé des recommandations consensuelles, qu’il a caractérisées au moyen d’une échelle de qualité des preuves fondée sur la classe (bienfaits par rapport aux préjudices) et sur la catégorie (degré de certitude).RÉSULTATS: Toutes les personnes co-infectées par le VIH et le VHC devraient subir une évaluation en vue de recevoir un traitement du VHC. Les personnes qui ne sont pas en mesure d’entreprendre un traitement du VHC devraient être soignées pour le VIH afin de ralentir l’évolution de la maladie hépatique. La norme de traitement du VHC de génotype 1 est un régime comprenant de l’interféron pégylé et de la ribavirine dosée en fonction du poids, associés à un inhibiteur de la protéase du VHC. Pour les génotypes 2 ou 3, une bithérapie classique est recommandée pendant 24 semaines s’il y a clairance virologique à la semaine 4 ou, pour les génotypes 2 à 6, à 48 semaines. On peut envisager de reporter le traitement chez les personnes ayant une maladie hépatique légère. Le VIH ne devrait pas être considéré comme un obstacle à la transplantation hépatique chez les patients co-infectés.EXPOSÉ: Les recommandations ne se substituent pas au jugement clinique personnel.

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33

Dulioust, A., J. P. Brosseau, A. A. Mazet, A. Hidar, Y. Taoufik, and J. Gasnault. "H-08 Leucoencéphalite multifocale progressive : évolution clinique défavorable en cas de co-infection VIH-VHC." Médecine et Maladies Infectieuses 39 (June 2009): S39. http://dx.doi.org/10.1016/s0399-077x(09)74381-1.

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34

Toloba, Y., B. F. Sissoko, A. Keita, B. Sangaré, K. Ouattara, D. Soumaré, S. Dao, and S. Diallo. "Co-infection TB/VIH : apport de la culture dans le diagnostic des cas de TPM." Revue des Maladies Respiratoires 29 (January 2012): A111—A112. http://dx.doi.org/10.1016/j.rmr.2011.10.368.

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35

Pialoux, G. "Efficacité de l’interféron pégylé associé à la ribavirine en cas de co-infection VIH-VHC." La Presse Médicale 34, no. 20 (November 2005): 1589–91. http://dx.doi.org/10.1016/s0755-4982(05)84230-7.

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36

Filoche, P., M. Adoun, F. Caron, C. Godet, R. Robert, and J. C. Meurice. "Co-infection à Mycobacterium tuberculosis et Pneumocystis jiroveci chez une patiente non infectée par le VIH." Revue des Maladies Respiratoires 23, no. 1 (February 2006): 83–87. http://dx.doi.org/10.1016/s0761-8425(06)71467-x.

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37

Pol, S. "ANRS HC 02 RIBAVIC: Impact de la stéatose au cours de la co-infection VHC-VIH." Gastroentérologie Clinique et Biologique 33 (March 2009): S110—S112. http://dx.doi.org/10.1016/s0399-8320(09)72450-9.

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38

Abdelmalek, R., S. Anane, N. Chabchoub, R. Essid, K. Aoun, T. Ben Chaabéne, and A. Bouratbine. "Co-infection par des microsporidies et des cryptosporidies chez un nouveau-né infecté par le VIH." Archives de Pédiatrie 18, no. 5 (May 2011): 562–64. http://dx.doi.org/10.1016/j.arcped.2011.02.016.

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39

Cipriano, Patrícia, Ana Cláudia Miranda, Isabel Antunes, and Kamal Mansinho. "Leishmaniose Visceral em Doentes com Infeção VIH: O Desafio da Recaída e Falência Terapêutica." Acta Médica Portuguesa 30, no. 6 (June 30, 2017): 443. http://dx.doi.org/10.20344/amp.8291.

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Introduction: Visceral leishmaniasis is an endemic disseminated infection, considered to be the third most frequent opportunistic parasitic infection in Europe. It is especially prevalent in patients co-infected with human immunodeficiency virus, in whom it poses a great therapeutic challenge due to increased risk of relapse. The goal of this study is to characterize a population of co-infected patients, as well as the efficiency of the adopted treatment strategies.Material and Methods: Retrospective study with a sample composed of all patients with visceral leishmaniasis and human immunodeficiency virus admitted in an Infectious Diseases ward over a period of 10 years.Results: Of the 23 enrolled patients, two were female (8.7%). The mean TCD4+ cell count was 104.4 cells/uL (± 120.3cells/uL), only two patients had undetectable viral load (< 20 copies/mL) and 16 (69.6%) were not under antiretroviral therapy at the time of diagnosis. Treatment-wise, liposomal amphotericin B was used in 18 patients, meglumine antimoniate in four and miltefosine in one. Fourteen (60.9%) were adherent to secondary prophylaxis protocol. A relapse rate of 26.1% was observed (six patients).Discussion: Co-infection is responsible for higher treatment failure rates and more relapses. TCD4+ cell count is the main predictive factor of relapse, and strict adherence to chemoprophylaxis protocols unequivocally results in a reduction of relapse rate. Combined treatment strategies using liposomal amphotericin B and miltefosine yield fewer therapeutic failures than the classic approach.Conclusion: We therefore conclude that alternative, combined therapeutic protocols seem to be a viable solution for these patients.

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40

Wa Ilunga, E. N., R. K. Muya, A. A. Kaponda, C. M. A. Kaput, S. M. Kalonji, V. B. Chiribagula, B. N. Nshikala, A. N. N'sasi, and J. B. L. Simbi. "Prévalence de la co-infection VIH-tuberculose et impact du VIH sur les tuberculeux dans la zone de santé de Lubumbashi de 2014 à 2015." Revue de Pneumologie Clinique 74, no. 1 (February 2018): 9–15. http://dx.doi.org/10.1016/j.pneumo.2017.12.002.

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41

Wilson, CR, and RAC Jones. "Resistance to potato leafroll virus infection and accumulation in potato cultivars, and the effects of previous infection with other viruses on expression of resistance." Australian Journal of Agricultural Research 44, no. 8 (1993): 1891. http://dx.doi.org/10.1071/ar9931891.

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A selection of potato cultivars and breeding lines was evaluated for presence of resistance to infection with potato leafroll virus (PLRV) via viruliferous aphid vectors ( IR) and/or resistance to accumulation of PLRV antigen ( AR) in infected leaf tissue. Cultivars Aracy, Delcora, Omega and Spunta, and breeding lines BR63.15 and B71.240.2 carried both IR and AR , Bismark, Serrana INTA and L/T1 had alone and Delaware had AR alone. The other cultivars tested had neither. Within both the resistant and susceptible classes for AR, the level of PLRV antigen accumulation achieved varied with cultivar. Previous infection with potato virus X (PVX) or potato virus S (PVS) either alone or together did not diminish the expression of IR or AR. However, the presence of PVX sometimes significantly increased the accumulation of PLRV in susceptible cv. Desiree and this effect was most pronounced in mature leaves of older plants. In contrast, presence of PVX in susceptible cv. Desiree did not increase the numbers of plants becoming infected with PLRV. Identifying potato genotypes with and IR AR will help the Australian potato industry to select cultivars which become infected with PLRV more slowly under conditions of high infection pressure and/or are suitable for use as parental lines in breeding virus-resistant cultivars.

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Powell, S. M., G. N. Brooke, H. C. Whitaker, V. Reebye, S. C. Gamble, D. Chotai, D. A. Dart, B. Belandia, and C. L. Bevan. "Mechanisms of androgen receptor repression in prostate cancer." Biochemical Society Transactions 34, no. 6 (October 25, 2006): 1124–27. http://dx.doi.org/10.1042/bst0341124.

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Anti-androgens used in prostate cancer therapy inhibit AR (androgen receptor) activity via largely unknown mechanisms. Although initially successful in most cases, they eventually fail and the disease progresses. We need to elucidate how anti-androgens work to understand why they fail, and prolong their effects or design further therapies. Using a cellular model, we found different anti-androgens have diverse effects on subcellular localization of AR, revealing that they work via different mechanisms and suggesting that an informed sequential treatment regime may benefit patients. In the presence of the anti-androgens bicalutamide and hydroxyflutamide, a significant proportion of the AR is translocated to the nucleus but remains inactive. Receptor inhibition under these conditions is likely to involve recruitment of co-repressor proteins, which interact with antagonist-occupied receptor but inhibit receptor-dependent transcription. Which co-repressors are required in vivo for AR repression by anti-androgens is not clear, but one candidate is the Notch effector Hey1. This inhibits ligand-dependent activity of the AR but not other steroid receptors. Further, it is excluded from the nucleus in most human prostate cancers, suggesting that abnormal subcellular distribution of co-repressors may contribute to the aberrant hormonal responses observed in prostate cancer. A decrease in co-repressor function is one possible explanation for the development of anti-androgen-resistant prostate cancer, and this suggests that it may not occur at the gross level of protein expression.

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Rosenthal, E., P. Marty, F. Faraut-Gambarelli, F. Pratlong, J. P. Dedet, J. P. Cassuto, and Y. Le Fichoux. "Épidémiologie de la co-infection Leishmania/VIH dans le sud de la France entre 1986 et 1997." La Revue de Médecine Interne 20 (June 1999): s73. http://dx.doi.org/10.1016/s0248-8663(99)80211-2.

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Durand, JM, R. Jean, I. Genty, P. Roche, C. Figarella, G. Kaplanski, and J. Soubeyrand. "Vascularite cérébrale et syndrome des doigts rouges révélateurs d’une co-infection par le VIH et le VHC." La Revue de Médecine Interne 18 (January 1997): 549s. http://dx.doi.org/10.1016/s0248-8663(97)80096-3.

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Bottero, J. "Évaluation des marqueurs non invasifs de fibrose hépatique dans le contexte de la co-infection VIH-VHB." Revue d'Épidémiologie et de Santé Publique 56, no. 3 (June 2008): 221. http://dx.doi.org/10.1016/j.respe.2008.05.014.

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Chuang, Kuang-Hsiang, Saleh Altuwaijri, Gonghui Li, Jiann-Jyh Lai, Chin-Yi Chu, Kuo-Pao Lai, Hung-Yun Lin, et al. "Neutropenia with impaired host defense against microbial infection in mice lacking androgen receptor." Journal of Experimental Medicine 206, no. 5 (May 4, 2009): 1181–99. http://dx.doi.org/10.1084/jem.20082521.

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Neutrophils, the major phagocytes that form the first line of cell-mediated defense against microbial infection, are produced in the bone marrow and released into the circulation in response to granulocyte-colony stimulating factor (G-CSF). Here, we report that androgen receptor knockout (ARKO) mice are neutropenic and susceptible to acute bacterial infection, whereas castration only results in moderate neutrophil reduction in mice and humans. Androgen supplement can restore neutrophil counts via stabilizing AR in castrated mice, but not in ARKO and testicular feminization mutant (Tfm) mice. Our results show that deletion of the AR gene does not influence myeloid lineage commitment, but significantly reduces the proliferative activity of neutrophil precursors and retards neutrophil maturation. CXCR2-dependent migration is also decreased in ARKO neutrophils as compared with wild-type controls. G-CSF is unable to delay apoptosis in ARKO neutrophils, and ARKO mice show a poor granulopoietic response to exogenous G-CSF injection. In addition, AR can restore G-CSF–dependent granulocytic differentiation upon transduction into ARKO progenitors. We further found that AR augments G-CSF signaling by activating extracellular signal-regulated kinase 1/2 and also by sustaining Stat3 activity via diminishing the inhibitory binding of PIAS3 to Stat3. Collectively, our findings demonstrate an essential role for AR in granulopoiesis and host defense against microbial infection.

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Meda, N., Z. Ganame, H. Hien, D. Zingue, A’ Kabore, and I. Moyenga. "Situation de la co-infection tuberculose/infection par le VIH dans la région sanitaire des Hauts-Bassins à l’Ouest du Burkina Faso." Revue d'Épidémiologie et de Santé Publique 62 (September 2014): S232—S233. http://dx.doi.org/10.1016/j.respe.2014.06.198.

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Lu, Tianjing, Wen-Jye Lin, Kouji Izumi, Xiaohai Wang, Defeng Xu, Lei-Ya Fang, Lei Li, Qi Jiang, Jie Jin, and Chawnshang Chang. "Targeting Androgen Receptor to Suppress Macrophage-induced EMT and Benign Prostatic Hyperplasia (BPH) Development." Molecular Endocrinology 26, no. 10 (October 1, 2012): 1707–15. http://dx.doi.org/10.1210/me.2012-1079.

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Abstract Early studies suggested macrophages might play roles in inflammation-associated benign prostatic hyperplasia (BPH) development, yet the underlying mechanisms remain unclear. Here we first showed that CD68+ macrophages were identified in both epithelium and the stromal area of human BPH tissues. We then established an in vitro co-culture model with prostate epithelial and macrophage cell lines to study the potential impacts of infiltrating macrophages in the BPH development and found that co-culturing prostate epithelial cells with macrophages promoted migration of macrophages. In a three-dimensional culture system, the sphere diameter of BPH-1 prostate cells was significantly increased during coculture with THP-1 macrophage cells. Mechanism dissection suggested that expression levels of epithelial-mesenchymal transition (EMT) markers, such as N-cadherin, Snail, and TGF-β2, were increased, and administration of anti-TGF-β2 neutralizing antibody during co-culture suppressed the EMT and THP-1-mediated growth of BPH-1 cells, suggesting THP-1 might go through EMT to influence the BPH development and progression. Importantly, we found that modulation of androgen receptor (AR) in BPH-1 and mPrE cells significantly increased THP-1 and RAW264.7 cell migration, respectively, and enhanced expression levels of EMT markers, suggesting that AR in prostate epithelial cells might play a role in promoting macrophage-mediated EMT in prostate epithelial cells. Silencing AR function via an AR degradation enhancer, ASC-J9, decreased the macrophage migration to BPH-1 cells and suppressed EMT marker expression. Together, these results provide the first evidence to demonstrate that prostate epithelial AR function is important for macrophage-mediated EMT and proliferation of prostate epithelial cells, which represents a previously unrecognized role of AR in the cross-talk between macrophages and prostate epithelial cells. These results may provide new insights for a new therapeutic approach to battle BPH via targeting AR and AR-mediated inflammatory signaling pathways.

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Garcia, Erin P., and Erin Epson. "Developing a Public Health Model for Regional Infection Prevention Collaboration Among Healthcare Facility Networks." Infection Control & Hospital Epidemiology 41, S1 (October 2020): s187. http://dx.doi.org/10.1017/ice.2020.725.

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Background: Antimicrobial resistance (AR), including Clostridioides difficile infection (CDI), can spread across the healthcare continuum when patients move between facilities. In 2015, the CDC recommended that healthcare facilities (HCFs) and local public health departments (LPH) coordinate their efforts to prevent the spread of AR and CDI. Accordingly, the California Department of Public Health (CDPH) Healthcare-Associated Infections (HAI) Program developed a model for implementing regionally based AR/CDI prevention collaboratives within HCF networks. Methods: The CDPH HAI Program began identifying regions in California with high AR/CDI incidence or risk for AR/CDI emergence using NHSN data. During 2015–2019, we organized AR/CDI prevention collaboratives in these regions. We recruited HCFs for participation by presenting at local professional organization meetings and engaging skilled nursing facility corporate leadership. HAI Program infection preventionists conducted onsite infection prevention assessments at each participating HCF. HAI Program and LPH staff convened quarterly in-person learning and discussion sessions focused on infection prevention and antimicrobial stewardship best practices. Participating HCFs committed to facility-tailored process improvement plans and conducted self-assessments to evaluate infection prevention practice changes at the conclusion of the collaborative. For CDI-focused collaboratives, we used data reported to CDPH via NHSN to assess changes in hospital- and community-onset CDI incidence among participating hospitals before and after the collaboratives. Results: Since 2015, 205 HCFs in 15 LPH jurisdictions have participated in 6 regional AR/CDI prevention collaboratives. Participating HCFs reported improved implementation of AR/CDI prevention strategies. For CDI-focused collaboratives, hospital-onset CDI incidence decreased by ~3% per month among participating hospitals. The collaboratives created forums for communication and relationship building, which previously did not exist among LPH and the HCF networks. We used our experience and feedback from partners to develop an HAI Program AR Prevention Collaborative Tool Kit to help LPHs and healthcare organizations develop and implement regional AR/CDI prevention collaboratives in other at-risk or high AR/CDI prevalence areas in California. The tool kit includes materials developed for each of our collaboratives, which may be adapted to meet local needs. Conclusions: Regionally coordinated AR/CDI prevention initiatives among LPHs and HCFs can contribute to increased AR awareness, improved AR prevention practices, and decreased AR/CDI incidence. The effectiveness of regional AR/CDI prevention collaboratives may be the result of concurrent efforts to improve AR prevention practices both within individual HCFs and across patient sharing networks.Funding: NoneDisclosures: None

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Li, Shuang, Zhibin Geng, Xiyang Wang, Xiaoru Ren, Jinghai Liu, Xiangyan Hou, Yu Sun, Wei Zhang, Keke Huang, and Shouhua Feng. "Optimizing the surface state of cobalt-iron bimetallic phosphide via regulating phosphorus vacancies." Chemical Communications 56, no. 17 (2020): 2602–5. http://dx.doi.org/10.1039/c9cc09741d.

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