IFNα induces CCR5 in CD4
Journal
Research square
Titre abrégé: Res Sq
Pays: United States
ID NLM: 101768035
Informations de publication
Date de publication:
11 May 2023
11 May 2023
Historique:
pubmed:
22
5
2023
medline:
22
5
2023
entrez:
22
5
2023
Statut:
epublish
Résumé
Like EC, we find that ART-treated patients control serum IFNα concentration and show few immune cell alterations enabling a healthy but fragile medical status. However, treatment interruption leads to elevated IFNα reflecting virus production indicating that like EC, ART does not achieve a virological cure. The immune system becomes overwhelmed by multiple immune cell abnormalities as found in untreated patients. These are chiefly mediated by elevated IFNα inducing signaling checkpoints abnormalities, including PD1, in cytotoxic immune cells. Importantly, during acute infection, elevated IFNα correlated with HIV load and we found that IFNα enhances CCR5, the HIV coreceptor in CD4
Identifiants
pubmed: 37214795
doi: 10.21203/rs.3.rs-2813616/v1
pmc: PMC10197818
pii:
doi:
Types de publication
Preprint
Langues
eng
Déclaration de conflit d'intérêts
Additional Declarations: There is NO Competing Interest.