Cathia Soulie1,2,3, Maxime Grudé1,2, Diane Descamps4,5, Corinne Amiel6, Laurence Morand-Joubert1,2,7, Stéphanie Raymond8, Coralie Pallier9, Pantxika Bellecave10,11, Sandrine Reigadas10,11, Mary-Anne Trabaud12, Constance Delaugerre13,14, Brigitte Montes15, Francis Barin16, Virginie Ferré17, Hélène Jeulin18,19, Chakib Alloui20, Sabine Yerly21, Anne Signori-Schmuck22, Aurélie Guigon23, Samira Fafi-Kremer24, Stéphanie Haïm-Boukobza9, Audrey Mirand25, Anne Maillard26, Sophie Vallet27, Catherine Roussel28, Lambert Assoumou1,2, Vincent Calvez1,2,3, Philippe Flandre1,2, Anne-Geneviève Marcelin1,2,3. 1. Sorbonne Universités, UPMC Univ. Paris 06-UMR_S 1136 Pierre Louis Institute of Epidemiology and Public Health, F-75005 Paris, France. 2. INSERM-UMR_S 1136 Pierre Louis Institute of Epidemiology and Public Health, F-75013 Paris, France. 3. AP-HP, Groupe hospitalier Pitié Salpêtrière, Laboratoire de Virologie, F-75013 Paris, France. 4. IAME, UMR 1137-Université Paris Diderot, Sorbonne Paris Cité, INSERM, F-75018 Paris, France. 5. AP-HP, Hôpital Bichat, Laboratoire de Virologie, F-75018 Paris, France. 6. Laboratoire de Virologie, AP-HP, Hôpital Tenon, Paris, France. 7. Laboratoire de Virologie, AP-HP, CHU Saint Antoine, Paris, France. 8. CHU de Toulouse, Laboratoire de Virologie, Toulouse, France. 9. CHU Paul Brousse, Laboratoire de Virologie, Villejuif, France. 10. CHU de Bordeaux, Laboratoire de Virologie, F-33000 Bordeaux, France. 11. Univ. Bordeaux, CNRS UMR 5234, F-33000 Bordeaux, France. 12. Hôpital de la Croix-Rousse, Hospices Civils de Lyon, Lyon, France. 13. INSERM U941-Université Paris Diderot, Sorbonne Paris Cité, INSERM, F-75010 Paris, France. 14. AP-HP, Hôpital Saint-Louis, Laboratoire de Virologie, F-75010 Paris, France. 15. Laboratoire de Virologie, CHU Montpellier, France. 16. CHU Tours, France. 17. CHU Nantes, France. 18. Laboratoire de Virologie, CHU de Nancy Brabois, Vandoeuvre les Nancy, France. 19. EA 7300, Université de Lorraine, Faculté de Médecine, Vandoeuvre les Nancy, France. 20. CHU Avicennes, Bobigny, France. 21. Laboratory of Virology, Geneva University Hospitals, Switzerland. 22. CHU Grenoble, France. 23. CHU Orléans, France. 24. Laboratoire de Virologie, CHU Strasbourg, France. 25. CHU Clermont-Ferrand, France. 26. CHU Rennes, France. 27. CHU Brest, France. 28. CHU Amiens, France.
Abstract
Background: HIV therapy reduces the CSF HIV RNA viral load (VL) and prevents disorders related to HIV encephalitis. However, these brain disorders may persist in some cases. A large population of antiretroviral-treated patients who had a VL > 1.7 log 10 copies/mL in CSF with detectable or undetectable VL in plasma associated with cognitive impairment was studied, in order to characterize discriminatory factors of these two patient populations. Methods: Blood and CSF samples were collected at the time of neurological disorders for 227 patients in 22 centres in France and 1 centre in Switzerland. Genotypic HIV resistance tests were performed on CSF. The genotypic susceptibility score was calculated according to the last Agence Nationale de Recherche sur le Sida et les hépatites virales Action Coordonnée 11 (ANRS AC11) genotype interpretation algorithm. Results: Among the 227 studied patients with VL > 1.7 log 10 copies/mL in CSF, 195 had VL detectable in plasma [median (IQR) HIV RNA was 3.7 (2.7-4.7) log 10 copies/mL] and 32 had discordant VL in plasma (VL < 1.7 log 10 copies/mL). The CSF VL was lower (median 2.8 versus 4.0 log 10 copies/mL; P < 0.001) and the CD4 cell count was higher (median 476 versus 214 cells/mm 3 ; P < 0.001) in the group of patients with VL < 1.7 log 10 copies/mL in plasma compared with patients with plasma VL > 1.7 log 10 copies/mL. Resistance to antiretrovirals was observed in CSF for the two groups of patients. Conclusions: Fourteen percent of this population of patients with cognitive impairment and detectable VL in CSF had well controlled VL in plasma. Thus, it is important to explore CSF HIV (VL and genotype) even if the HIV VL is controlled in plasma because HIV resistance may be observed.
Background: HIV therapy reduces the CSF HIV RNA viral load (VL) and prevents disorders related to HIV encephalitis. However, these brain disorders may persist in some cases. A large population of antiretroviral-treated patients who had a VL > 1.7 log 10 copies/mL in CSF with detectable or undetectable VL in plasma associated with cognitive impairment was studied, in order to characterize discriminatory factors of these two patient populations. Methods: Blood and CSF samples were collected at the time of neurological disorders for 227 patients in 22 centres in France and 1 centre in Switzerland. Genotypic HIV resistance tests were performed on CSF. The genotypic susceptibility score was calculated according to the last Agence Nationale de Recherche sur le Sida et les hépatites virales Action Coordonnée 11 (ANRS AC11) genotype interpretation algorithm. Results: Among the 227 studied patients with VL > 1.7 log 10 copies/mL in CSF, 195 had VL detectable in plasma [median (IQR) HIV RNA was 3.7 (2.7-4.7) log 10 copies/mL] and 32 had discordant VL in plasma (VL < 1.7 log 10 copies/mL). The CSF VL was lower (median 2.8 versus 4.0 log 10 copies/mL; P < 0.001) and the CD4 cell count was higher (median 476 versus 214 cells/mm 3 ; P < 0.001) in the group of patients with VL < 1.7 log 10 copies/mL in plasma compared with patients with plasma VL > 1.7 log 10 copies/mL. Resistance to antiretrovirals was observed in CSF for the two groups of patients. Conclusions: Fourteen percent of this population of patients with cognitive impairment and detectable VL in CSF had well controlled VL in plasma. Thus, it is important to explore CSF HIV (VL and genotype) even if the HIV VL is controlled in plasma because HIV resistance may be observed.
Authors: Olubusuyi Moses Adewumi; Elena Dukhovlinova; Nathan Y Shehu; Shuntai Zhou; Olivia D Council; Maxwell O Akanbi; Babafemi Taiwo; Adesola Ogunniyi; Kevin Robertson; Cecilia Kanyama; Mina C Hosseinipour; Ronald Swanstrom Journal: AIDS Res Hum Retroviruses Date: 2020-02-17 Impact factor: 2.205