Hepatitis C virus drives increased type I interferon-associated impairments associated with fibrosis severity in antiretroviral treatment-treated HIV-1-hepatitis C virus-coinfected individuals

Morgane Griesbeck (1) , Marc-Antoine Valantin (2) , Karine Lacombe (3) , Assia Samri-Hassimi (4) , Julie Bottero (5) , Catherine Blanc (6) , Zineb Sbihi (1) , Rima Zoorob (7) , Christine Katlama (3) , Marguerite Guiguet (3) , Marcus Altfeld (8) , Brigitte Autran (9)

1 CIMI - Centre d'Immunologie et de Maladies Infectieuses
2 CHU Pitié-Salpêtrière [AP-HP]
3 iPLESP - Institut Pierre Louis d'Epidémiologie et de Santé Publique
4 Immunité et Infection
5 iPLESP - Institut Pierre Louis d'Epidémiologie et de Santé Publique
6 UMS LUMIC - Unité Mixte de Service d'Imagerie et de Cytométrie
7 GMIFC - Génétique moléculaire et intégration des fonctions cellulaires
8 Ragon Institute of MGH, MIT and Harvard
9 CIMI - Centre d'Immunologie et des Maladies Infectieuses

On behalf of the HepACT-VIH study group - Viral coinfections might contribute to the increased immune activation and inflammation that persist in antiretroviral treatment (ART)-treated HIV-1 patients. We investigated whether the hepatitis C virus (HCV) coinfection contributes to such alterations by impairing the plasmacytoid dendritic cell (pDC) IFNa/TLR7 pathway in a highly homogeneous group of ART-treated HIV-1-HCV-coinfected patients.

Domains: Immunology

Morgane Griesbeck, Marc-Antoine Valantin, Karine Lacombe, Assia Samri-Hassimi, Julie Bottero, et al.. Hepatitis C virus drives increased type I interferon-associated impairments associated with fibrosis severity in antiretroviral treatment-treated HIV-1-hepatitis C virus-coinfected individuals. HIV/AIDS surveillance report (Atlanta, Ga.), 2017, ⟨10.1097/QAD.0000000000001455⟩. ⟨hal-02548458⟩