Circulating HBV RNA and hepatitis B core-related antigen trajectories in persons with HIV/HBV coinfection and HBsAg loss on tenofovir therapy.
HBV RNA
HIV
Hepatitis B Core-related Antigen
Hepatitis B cure
Hepatitis B virus
Kinetics
Tenofovir
Journal
The Journal of infectious diseases
ISSN: 1537-6613
Titre abrégé: J Infect Dis
Pays: United States
ID NLM: 0413675
Informations de publication
Date de publication:
16 Apr 2024
16 Apr 2024
Historique:
received:
02
11
2023
revised:
28
02
2024
accepted:
09
04
2024
medline:
16
4
2024
pubmed:
16
4
2024
entrez:
16
4
2024
Statut:
aheadofprint
Résumé
We evaluated long-term trajectories of circulating hepatitis B virus (HBV)-RNA and hepatitis B core-related antigen (HBcrAg) in persons with and without hepatitis B surface antigen (HBsAg) loss during tenofovir therapy in the Swiss HIV Cohort Study. We included 29 persons with HIV (PWH) with HBsAg loss and 29 matched PWH without loss. We compared HBV-RNA and HBcrAg decline and assessed the cumulative proportions with undetectable HBV-RNA and HBcrAg levels during tenofovir therapy using Kaplan-Meier estimates. HBsAg loss occurred after a median of 4 years (IQR 1 - 8). All participants with HBsAg loss achieved suppressed HBV-DNA and undetectable HBV-RNA preceding undetectable qHBsAg levels, whereas 79% achieved negative HBcrAg. In comparison, 79% of the participants without HBsAg loss achieved undetectable HBV-RNA and 48% negative HBcrAg. After two years on tenofovir, an HBV RNA decline ≥1 log10 copies/ml had 100% sensitivity and 36.4% specificity for HBsAg loss, whereas an HBcrAg decline ≥1 log10 U/ml had 91.0% sensitivity and 64.5% specificity. HBV-RNA suppression preceded undetectable qHBsAg levels, and had high sensitivity but low specificity for HBsAg loss during tenofovir therapy in PWH. HBcrAg remained detectable in approximately 20% of persons with, and 50% of persons without HBsAg loss.
Sections du résumé
BACKGROUND
BACKGROUND
We evaluated long-term trajectories of circulating hepatitis B virus (HBV)-RNA and hepatitis B core-related antigen (HBcrAg) in persons with and without hepatitis B surface antigen (HBsAg) loss during tenofovir therapy in the Swiss HIV Cohort Study.
METHODS
METHODS
We included 29 persons with HIV (PWH) with HBsAg loss and 29 matched PWH without loss. We compared HBV-RNA and HBcrAg decline and assessed the cumulative proportions with undetectable HBV-RNA and HBcrAg levels during tenofovir therapy using Kaplan-Meier estimates.
RESULTS
RESULTS
HBsAg loss occurred after a median of 4 years (IQR 1 - 8). All participants with HBsAg loss achieved suppressed HBV-DNA and undetectable HBV-RNA preceding undetectable qHBsAg levels, whereas 79% achieved negative HBcrAg. In comparison, 79% of the participants without HBsAg loss achieved undetectable HBV-RNA and 48% negative HBcrAg. After two years on tenofovir, an HBV RNA decline ≥1 log10 copies/ml had 100% sensitivity and 36.4% specificity for HBsAg loss, whereas an HBcrAg decline ≥1 log10 U/ml had 91.0% sensitivity and 64.5% specificity.
CONCLUSIONS
CONCLUSIONS
HBV-RNA suppression preceded undetectable qHBsAg levels, and had high sensitivity but low specificity for HBsAg loss during tenofovir therapy in PWH. HBcrAg remained detectable in approximately 20% of persons with, and 50% of persons without HBsAg loss.
Identifiants
pubmed: 38626170
pii: 7646749
doi: 10.1093/infdis/jiae189
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Investigateurs
I Abela
(I)
K Aebi-Popp
(K)
A Anagnostopoulos
(A)
M Battegay
(M)
E Bernasconi
(E)
D L Braun
(DL)
H C Bucher
(HC)
A Calmy
(A)
M Cavassini
(M)
A Ciuffi
(A)
G Dollenmaier
(G)
M Egger
(M)
L Elzi
(L)
J Fehr
(J)
J Fellay
(J)
H Furrer
(H)
C A Fux
(CA)
H F Günthard
(HF)
A Hachfeld
(A)
D Haerry
(D)
B Hasse
(B)
H H Hirsch
(HH)
M Hoffmann
(M)
I Hösli
(I)
M Huber
(M)
D Jackson-Perry
(D)
C R Kahlert
(CR)
O Keiser
(O)
T Klimkait
(T)
R D Kouyos
(RD)
H Kovari
(H)
K Kusejko
(K)
N Labhardt
(N)
K Leuzinger
(K)
B Martinez de Tejada
(BM)
C Marzolini
(C)
K J Metzner
(KJ)
N Müller
(N)
J Nemeth
(J)
D Nicca
(D)
J Notter
(J)
P Paioni
(P)
G Pantaleo
(G)
M Perreau
(M)
A Rauch
(A)
L Salazar-Vizcaya
(L)
P Schmid
(P)
R Speck
(R)
M Stöckle
(M)
P Tarr
(P)
A Trkola
(A)
G Wandeler
(G)
M Weisser
(M)
S Yerly
(S)
Informations de copyright
© The Author(s) 2024. Published by Oxford University Press on behalf of Infectious Diseases Society of America.