Virologic and serologic outcomes of mono versus dual HBV therapy and characterization of HIV/HBV coinfection in a US cohort.
OBJECTIVE
To characterize HIV/hepatitis B virus (HBV) coinfection in the AIDS Clinical Trials Group Longitudinal Linked Randomized Trials cohort and compare long-term HBV outcomes between regimens with 1 (MONO) or 2 (DUAL) anti-HBV agents.


METHODS
A retrospective study of coinfected AIDS Clinical Trials Group Longitudinal Linked Randomized Trials subjects who received regimens containing anti-HBV agent(s).


METHODS
Stored samples at baseline and weeks 16, 32, 48, 144, and 240 were tested for HBV DNA, HBV e antigen (HBeAg), HBV e antibody (HBeAb), and hepatitis D virus (HDV) antibody. Resistance and genotype were tested in samples with HBV DNA >600 IU/mL. MONO versus DUAL analyses were limited to HBV treatment-naive subjects (Naive-MONO, Naive-DUAL).


RESULTS
Of 150 study subjects, median age was 40 years, 96% were male; 57% white, 26% black, 13% Hispanic. Baseline median CD4 was 224 cells per cubic millimeter, HIV RNA 4.48 log10 copies/mL, HBV DNA 6.30 log10 IU/mL; 59% HBeAg positive and 65% HBeAb negative; HBV genotypes A = 69%, G = 18%, D = 7%, <2% for A/G, B, C, F, H. Coinfection with HDV was 2%. There were 49 Naive-MONO (lamivudine) and 22 Naive-DUAL (11 lamivudine + tenofovir, 11 emtricitabine + tenofovir) with detectable HBV DNA. In the 240-week follow-up, HBV DNA suppression was not significantly higher in Naive-DUAL (P = 0.14); lower baseline HBV DNA (P < 0.01) was associated with suppression. Among 32 Naive-MONO subjects with detectable HBV DNA at baseline and results at week 48, 41% suppressed; among such 15 Naive-DUAL subjects, 53% suppressed. HBeAg and HBeAb analyses showed similar trends.


CONCLUSIONS
While consistent trends toward increased HBV DNA suppression, HBeAg loss and HBeAb seroconversion were observed in Naive-DUAL compared with Naive-MONO, they were not statistically significant. Overall, HDV coinfection was low.
*Center for Biostatistics in AIDS Research, Harvard School of Public Health, Boston, MA; †Department of Medicine, Division of Infectious Diseases, New York University, New York, NY; ‡Division of Infectious Diseases, Ohio State University, Columbus, OH; and §Department of Epidemiology and Biostatistics, George Washington University Milken Institute, School of Public Health, Washington, DC.
Minhee
M
Kang
Kimberly
K
Hollabaugh
Vinh
V
Pham
Susan L
SL
Koletar
Kunling
K
Wu
Marlene
M
Smurzynski
Judith A
JA
Aberg
D000225:Adenine / Q000031:analogs & derivatives / Q000627:therapeutic use; D000328:Adult; D000914:Antibodies, Viral / Q000097:blood; D023241:Antiretroviral Therapy, Highly Active; D000998:Antiviral Agents / Q000627:therapeutic use*; D018791:CD4 Lymphocyte Count; D060085:Coinfection / Q000188:drug therapy* / Q000821:virology; D004279:DNA, Viral / Q000097:blood; D003841:Deoxycytidine / Q000031:analogs & derivatives / Q000627:therapeutic use; D000068679:Emtricitabine; D005260:Female; D005500:Follow-Up Studies; D015658:HIV Infections / Q000188:drug therapy*; D006509:Hepatitis B / Q000188:drug therapy*; D006513:Hepatitis B e Antigens / Q000097:blood; D006801:Humans; D019259:Lamivudine / Q000627:therapeutic use; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D063065:Organophosphonates / Q000627:therapeutic use; D016032:Randomized Controlled Trials as Topic; D012189:Retrospective Studies; D000068698:Tenofovir; D014481:United States
D000914:Antibodies, Viral; D000998:Antiviral Agents; D004279:DNA, Viral; D006513:Hepatitis B e Antigens; D063065:Organophosphonates; D003841:Deoxycytidine; D019259:Lamivudine; D000068698:Tenofovir; D000068679:Emtricitabine; D000225:Adenine