HIV coinfection with hepatitis b medical therapy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Goals of Treatment

HIV: Treatment for HIV has resulted in a marked reduction in AIDS-related mortality. As a result, liver disease from HBV and HCV is now becoming a major cause of morbidity and mortality in HIV infected patients.[1] Therefore the goal of treatment is to optimize anti-HIV therapy in HIV/HBV coinfected patients to improve and/or preserve immune function and reduce HIV associated morbidity and mortality.

HBV: In mono-infected patients, HBV therapy can reduce the risk of developing complications of liver disease.[2] [3] Natural history studies of chronically infected individuals have linked the risk of progression to cirrhosis and HCC to ongoing HBV replication.[4][5][6] In addition, treatment for HBV has been directed at reducing replicating virus. It has been demonstrated that the degree of HBV viral suppression achieved during treatment appears to be the most important determinant of treatment outcomes [7][8], but HBV DNA levels as low as 2000 IU/mL is still associated with disease progression.[9][10] Recent recommendations have advocated for undetectable HBV DNA as the therapeutic goal with the overall goal of therapy being to reduce 5 progression to cirrhosis, liver failure, HCC and need for liver transplantation.[11][12]

Medical Therapy

Treatment is most beneficial for those in the immunoactive phase of chronic hepatitis B (characterized by liver enzyme elevations, fluctuating HBV DNA levels and pronounced hepatic necro-inflammation) [13]

Patient characteristics that favour treatment success are [14]

  • Low HBV DNA levels.
  • HBeAg positivity.
  • Evidence of liver inflammation based on liver biopsy findings.
  • Liver enzyme elevations.

It is unknown, if this applies to HIV coinfected individuals who have higher HBV DNA and lower liver enzyme elevations but more cirrhosis, and therefore the optimum time to commence treatment in HIV-HBV coinfected individuals is unclear at present.

The treatment and management of coinfected individuals requires modification in resource poor countries due to limited availability of some HBV tests as well as therapeutic agents for treatment of HIV and HBV. 3TC is widely available and tenofovir and adefovir have limited availability.

Current Regimen

There are several agents presently used for the treatment of HBV and HIV coinfection including interferon and nucleoside or nucleotide analogs.[15] Decisions regarding when to initiate anti-HBV therapy require assessment of HIV status prior to initiation of treatment as several of these agents (tenofovir, lamivudine, emtricitabine, adefovir and entecavir) have activity against both HIV and HBV.

Telbivudine, a newer agent used to treat HBV, has not been shown to have activity against HIV.

Treatment decisions should be based on a combination of these factors:[13]

  1. Which virus needs treatment.
  2. The type of antiviral agents used in the concurrent anti-HIV regimen.
  3. The presence of 3TC-resistant HBV.
  4. The potential effect of drug resistance on the long term management of HIV and HBV infection.

If ART is to be initiated, then first line therapy should include TDF and 3TC/FTC as the nucleoside backbone.

Current WHO criteria for commencing ART in HIV infected individuals are based on a combination of WHO Clinical Stage and CD4 count.

Lamivudine/emtricitabine (3TC/FTC)

Dore et al demonstrated the efficacy of 3TC in persons coinfected with HIV and hepatitis B virus in the CAESAR study, a randomized placebo-controlled trial assessing the addition of 3TC or 3TC (150 mg 2x/day) plus loviride (100 mg 3x/day) to zidovudine-containing background antiretroviral treatment.[16] Baseline HBsAg was positive in 122 (6.8%) of 1790 subjects. At weeks 12 and 52, median log10 HBV DNA change was -2.0 and -2.7, respectively, in the lamivudine arms, compared with no reduction among placebo recipients (P<.001).

A trend to lower ALT level, and delayed progression of HIV disease (relative hazard, 0.26; 95% confidence interval, 0.08-0.80) were also seen in the 3TC arms, compared with the placebo group. 3TC used as monotherapy however, results in the development of resistance at rates of 14-32% annually, exceeding 70% after 49 months of treatment and plateauing at > 90% in HIV-coinfected patients at 4-5 years.[17][18]

Since 3TC has been widely used as part of ARV regimens in coinfected persons, with HBV Pol mutations observed in 94% of viremic patients who have been on treatment for at least four years.[18]

FTC possesses similar characteristics to 3TC, although FTC has a longer half-life and is more potent in monotherapy in treatment naive patients.[19]

3TC/FTC are interchangeable agents according to current treatment guidelines.

Tenofovir (TDF) with or without 3TC/FTC

There is now significant data supporting the use of TDF in coinfected patients. TDF is highly effective in suppressing HBV replication in HBV mono-infected patients with 3TC resistant HBV.[20][21] TDF has also demonstrated potent anti-HBV efficacy in the setting of HIV coinfection. [22][23] [24] [25]

Various studies have been conducted, as listed below:

  • Dore did a substudy analysis of two phase 3 randomized, double-blind, placebo-controlled trials recently examined the safety and efficacy of tenofovir DF among antiretroviral therapy-experienced (.study 907) and -naive (study 903) HIV-1-infected patients.[22] Substudies of study 907 and study 903 were undertaken to examine the safety and efficacy of tenofovir DF among antiretroviral therapy-experienced and -naive HIV-HBV-coinfected individuals.
    • Individuals in study 907 were randomized to receive TDF or placebo, and individuals in study 903 were randomized to receive antiretroviral therapy regimens that included lamivudine plus tenofovir. Among individuals co infected with HIV and HBV in these 2 randomized controlled trials, therapy with TDF demonstrated anti-HBV virologic efficacy.
    • During 48 weeks of therapy with TDF, a mean reduction of 4 -5 log, copies/mL in the HBV DNA level was seen in antiretroviral therapy-experienced HIV-HBV-co infected individuals with or without resistance to lamivudine.
    • During the 48 weeks of the study, a similar reduction in the HBV DNA level was seen in antiretroviral therapy-naive HIV-HBV-co infected individuals who received combination therapy with lamivudine and TDF as a component of their initial 3-drug HAART regimen.
    • A trend toward greater suppression of HBV DNA as well as reduced YMDD resistance in HIV-HBV-co infected individuals who were receiving lamivudine and TDF, compared with lamivudine alone.
  • Van Bommel et al evaluated 52 patients with HBV infection, 21 coinfected with HIV and compared TDF with adefovir (ADV) in 3TC resistant HBV. All TDF treated patients (n=35) showed a strong and early suppression of HBV DNA within a few weeks as compared to ADV. At week 48, TDF treated individuals had a higher reduction in viral load (5.5 log10 copies/ml for TDF vs 2.8 log10 copies/ml with ADV) and 100% TDF were undetectable vs 44% with ADV. There was no resistance in TDF treated patients at 130 weeks. [21]
  • Benhamou evaluated the efficacy and tolerability of TDF in 3TC naïve and 3TC refractory coinfected patients in a retrospective study. Of 65 coinfected patients (54 HBeAg positive and 11 HBeAg negative) with serum HBV DNA > 2.3 copies/ml were started on TDF therapy.[26] 68% were 3TC refractory. Over 12 months, the median reduction in HBV DNA as 4.56 log10 copies/ml in HBeAg positive patients and 2.53 log10 copies/ml in HBeAg negative individuals. At the end of the study (median follow up of 12 months), 30% of HBeAg positive and 82% of HBeAg negative had undetectable HBV DNA. No TDF mutations were detected in this study.
  • Lacombe evaluated 85 HIV-HBV co infected patients in an open label study initiating an ARV regimen including either TDF or ADV.[27] The decline in HBV DNA was more pronounced in patients treated with TDF than with ADV at 12 months (66% versus 53%, p=00001). Patients receiving TDF had a steeper rate of decline and mean time to undetectable HBV DNA was 19 months with TDF compared to 26 months with ADV.

The combination of TDF and 3TC has also been evaluated in a multi centre European study. Schmutz et al compared the efficacy of TDF plus 3TC with that of sequential therapy with TDF in HIV infected individuals with 3TC resistant HBV. In this study, 50 patients received TDF as the only active HBV agent subsequent to 3TC therapy and 25 received ART containing TDF plus 3TC. At 116 weeks, 84% treated with TDF had undetectable HBV DNA < 1000 copies/ml compared to 76% receiving TDF plus 3TC; this was not a statistically significant difference (p=0.53). The rates of loss of HBeAg and HBsAg were similar in both arms. This study indicates that TDF plus 3TC are no more efficacious than TDF alone. Sheldon reported the development of resistance to TDF in 2 of 43 HIV-HBV co infected patients treated for longer than 12 months.[28]

  • Matthews et al evaluated 36 HIV-HBV co-infected patients in Thailand; subjects were randomized to receive either 3TC, TDF or both.[29] At the end of 48 weeks, the average decline in HBV DNA was similar in all three arms, ranging from 4.07-4.73 log10 copies/ml. However, suppression of HBV DNA levels to < 1000 copies/ml was more frequent in subjects receiving TDF (92% and 91% compared to 46% in 3TC arm). Again, adding 3TC to TDF is no more efficacious than TDF alone. Drug resistance developed in 2 subjects both in 3TC only arm.
  • In a study in Australia, Matthews evaluated a cross sectional cohort of 3TC experienced HIV-HBV co infected patients. Individuals receiving TDF plus either 3TC or FTC were more likely to have undetectable HBV DNA (<100IU/ML) than those receiving either TDF or 3TC monotherapy. The combination group was also less likely to have high HBV DNA levels (>200,000 IU/ML). Despite the limitations of a cross sectional study, this study does provide some evidence that TDF-3TC/FTC combination therapy is superior to TDF or 3TC monotherapy in HIV-HBV co infected individuals with 3TC resistant HBV. However, confounders were not controlled for.[30]
  • Alvarez-Uria reported on their experience in the UK in a retrospective observational study to investigate the long term efficacy of TDF against HBV in a cohort of HIV co infected patients. Median duration of follow up was 34 months and 41 (79%) were HBeAg positive and 35 had received previous 3TC therapy for a median duration of 32 months. Nadir CD4 cell count was 110 cells/mm3 in individuals experiencing virologic breakthrough. At the end of the follow up period, HBV DNA was < 1000 copies/ml in 42 (81%) patients and < 200 copies/ml in 31 (60%) patients. In the 3TC experienced group, longer duration of 3TC was associated with failure to achieve HBV DNA < 200 copies/ml (p=0.036). Adding 3TC or FTC did not improve virologic suppression. Of 39 patients who achieved HBV DNA of < 200 copies/ml during TDF treatment, virologic breakthrough was seen in 2 (5% patients) after a median follow up of 40 months.[31]

Entecavir (ETV)

Entecavir (ETV) has been shown to be superior to 3TC with superior histological improvement, greater mean reduction in HBV DNA and normalization of serum ALT levels and large RCT have demonstrated efficacy up to 96 weeks.[32] Entecavir is associated with lower rates of development of resistance as compared with 3TC. Entecavir is associated with lower rates of development of resistance as compared with 3TC. Entecavir monotherapy is now considered contra-indicated as anti-HIV activity has been described and monotherapy has led to the development of HIV resistance mutation (M184V0) which are relevant for HIV therapy.[33] There is one RCT of ETV in 68 HIV/HBV coinfected patients comparing ETV to placebo while continuing 3TC containing ART for 24 weeks followed by ETV open-label.[34] ETV was given at 1.0mg dose. At 24 weeks, 6% of 51 patients had HBV DNA < 300 copies/ml and at 48 weeks, 8% had HBV DNA < 300 copies/ml. Mean decline in HBV DNA was 3.65 log10 copies/ml.

Telbivudine

Telbivudine is not known to be active against HIV but one drawback is that HBV resistance may develop if this drug is used a single agent; in the GLOBE trial comparing 3TC vs telbivudine for mono-infected patients, resistance developed in 25% patients receiving telbivudine vs 40% those treated with 3TC.[8]

Adefovir (ADV)

Of agents with activity against HBV, adefovir is the least potent. In addition, adefovir at low doses (10mg) does not have activity against HIV but higher doses do have activity against HIV.[12] Adefovir has been studied in 35 co-infected patients continuing on 3TC and after 144 weeks of therapy, 45% achieved HBV DNA < 1000 copies/ml (vs 56% in HBV mono-infection).[35] [26] Resistance also develops less frequently than with 3TC in HBV mono-infected patients with HBeAg negative CHB: 2% after 2 years, 11% after 3 years, 18% after 4 years and 29% after 5 years.[36]

Interferon

Pegylated interferon-alpha has not been studied as HBV treatment in HIV co infected individuals and as such its efficacy in this setting is unknown. [13] However, in HIV-uninfected individuals, it has been demonstrated to be more effective than short acting interferon. One small study of 18 coinfected patients who were HBeAg positive, with documented 3TC resistance to HBV and on ART containing 3TC evaluated the use of ADV and pegylated interferon alpha2a for 48 weeks and achieved a median decline in HBV DNA of 3.6 log10 copies/ml at 48 weeks and 1.4 log10 copies./ml at 72 weeks. None of the patients became HBeAg negative. On treatment response was not maintained off therapy.

National Institute of Health recommendations

  • Prior to initiation of antiretroviral therapy (ART), all patients who test positive for hepatitis B surface antigen (HBsAg) should be tested for hepatitis B virus (HBV) DNA using a quantitative assay to determine the level of HBV replicatio (AIII).
  • Because emtricitabine (FTC), lamivudine (3TC), and tenofovir (TDF) have activity against both HIV and HBV, if HBV or HIV treatment is needed, ART should be initiated with the combination of TDF + FTC or TDF + 3TC as the nucleoside reverse transcriptase inhibitor (NRTI) backbone of a fully suppressive antiretroviral (ARV) regimen (AI)
  • If HBV treatment is needed and TDF cannot safely be used, the alternative recommended HBV therapy is entecavir in addition to a fully suppressive ARV regimen (BI). Other HBV treatment regimens include peginterferon alfa monotherapy or adefovir in combination with 3TC or FTC or telbivudine in addition to a fully suppressive ARV regimen (BII).
  • Entecavir has activity against HIV; its use for HBV treatment without ART in patients with dual infection may result in the selection of the M184V mutation that confers HIV resistance to 3TC and FTC. Therefore, entecavir must be used in addition to a fully suppressive ARV regimen when used in HIV/HBV-coinfected patients (AII)
  • Discontinuation of agents with anti-HBV activity may cause serious hepatocellular damage resulting from reactivation of HBV; patients should be advised against self-discontinuation and carefully monitored during interruptions in HBV treatment (AII).
  • If ART needs to be modified due to HIV virologic failure and the patient has adequate HBV suppression, the ARV drugs active against HBV should be continued for HBV treatment in combination with other suitable ARV agents to achieve HIV suppression (AIII).

References

  1. ↑ Puoti M, Spinetti A, Ghezzi A, Donato F, Zaltron S, Putzolu V, Quiros-Roldan E, Zanini B, Casari S, Carosi G (2000). "Mortality for liver disease in patients with HIV infection: a cohort study". J. Acquir. Immune Defic. Syndr. 24 (3): 211–7. PMID 10969344. Retrieved 2012-03-29. Unknown parameter |month= ignored (help)
  2. ↑ Niederau C, Heintges T, Lange S, Goldmann G, Niederau CM, Mohr L, Häussinger D (1996). "Long-term follow-up of HBeAg-positive patients treated with interferon alfa for chronic hepatitis B". N. Engl. J. Med. 334 (22): 1422–7. doi:10.1056/NEJM199605303342202. PMID 8618580. Retrieved 2012-03-30. Unknown parameter |month= ignored (help)
  3. ↑ Yao FY, Terrault NA, Freise C, Maslow L, Bass NM (2001). "Lamivudine treatment is beneficial in patients with severely decompensated cirrhosis and actively replicating hepatitis B infection awaiting liver transplantation: a comparative study using a matched, untreated cohort". Hepatology. 34 (2): 411–6. doi:10.1053/jhep.2001.26512. PMID 11481627. Retrieved 2012-03-30. Unknown parameter |month= ignored (help)
  4. ↑ Chen CJ, Yang HI, Su J, Jen CL, You SL, Lu SN, Huang GT, Iloeje UH (2006). "Risk of hepatocellular carcinoma across a biological gradient of serum hepatitis B virus DNA level". JAMA. 295 (1): 65–73. doi:10.1001/jama.295.1.65. PMID 16391218. Retrieved 2012-03-30. Unknown parameter |month= ignored (help)
  5. ↑ Chen G, Lin W, Shen F, Iloeje UH, London WT, Evans AA (2006). "Past HBV viral load as predictor of mortality and morbidity from HCC and chronic liver disease in a prospective study". Am. J. Gastroenterol. 101 (8): 1797–803. doi:10.1111/j.1572-0241.2006.00647.x. PMID 16817842. Retrieved 2012-03-30. Unknown parameter |month= ignored (help)
  6. ↑ Iloeje UH, Yang HI, Su J, Jen CL, You SL, Chen CJ (2006). "Predicting cirrhosis risk based on the level of circulating hepatitis B viral load". Gastroenterology. 130 (3): 678–86. doi:10.1053/j.gastro.2005.11.016. PMID 16530509. Retrieved 2012-03-30. Unknown parameter |month= ignored (help)
  7. ↑ Liaw YF (2005). "The current management of HBV drug resistance". J. Clin. Virol. 34 Suppl 1: S143–6. PMID 16461216. Retrieved 2012-03-30. Unknown parameter |month= ignored (help)
  8. ↑ 8.0 8.1 Liaw YF (2006). "Hepatitis B virus replication and liver disease progression: the impact of antiviral therapy". Antivir. Ther. (Lond.). 11 (6): 669–79. PMID 17310811. |access-date= requires |url= (help)
  9. ↑ Yuan HJ, Yuen MF, Ka-Ho Wong D, Sablon E, Lai CL (2005). "The relationship between HBV-DNA levels and cirrhosis-related complications in Chinese with chronic hepatitis B". J. Viral Hepat. 12 (4): 373–9. doi:10.1111/j.1365-2893.2005.00603.x. PMID 15985007. Retrieved 2012-03-30. Unknown parameter |month= ignored (help)
  10. ↑ Yuen MF, Yuan HJ, Wong DK, Yuen JC, Wong WM, Chan AO, Wong BC, Lai KC, Lai CL (2005). "Prognostic determinants for chronic hepatitis B in Asians: therapeutic implications". Gut. 54 (11): 1610–4. doi:10.1136/gut.2005.065136. PMC 1774768. PMID 15871997. Retrieved 2012-03-30. Unknown parameter |month= ignored (help)
  11. ↑ Keeffe EB, Zeuzem S, Koff RS, Dieterich DT, Esteban-Mur R, Gane EJ, Jacobson IM, Lim SG, Naoumov N, Marcellin P, Piratvisuth T, Zoulim F (2007). "Report of an international workshop: Roadmap for management of patients receiving oral therapy for chronic hepatitis B". Clin. Gastroenterol. Hepatol. 5 (8): 890–7. doi:10.1016/j.cgh.2007.05.004. PMID 17632041. Retrieved 2012-03-30. Unknown parameter |month= ignored (help)
  12. ↑ 12.0 12.1 Keeffe EB, Dieterich DT, Han SH, Jacobson IM, Martin P, Schiff ER, Tobias H (2008). "A treatment algorithm for the management of chronic hepatitis B virus infection in the United States: 2008 update". Clin. Gastroenterol. Hepatol. 6 (12): 1315–41, quiz 1286. doi:10.1016/j.cgh.2008.08.021. PMID 18845489. Retrieved 2012-03-30. Unknown parameter |month= ignored (help)
  13. ↑ 13.0 13.1 13.2 Hoffmann CJ, Thio CL (2007). "Clinical implications of HIV and hepatitis B coinfection in Asia and Africa". Lancet Infect Dis. 7 (6): 402–9. doi:10.1016/S1473-3099(07)70135-4. PMID 17521593. Retrieved 2012-03-29. Unknown parameter |month= ignored (help)
  14. ↑ Soriano V, Puoti M, Bonacini M, Brook G, Cargnel A, Rockstroh J, Thio C, Benhamou Y (2005). "Care of patients with chronic hepatitis B and HIV coinfection: recommendations from an HIV-HBV International Panel". AIDS. 19 (3): 221–40. PMID 15718833. Retrieved 2012-03-30. Unknown parameter |month= ignored (help)
  15. ↑ Soriano V, Barreiro P, Nuñez M (2006). "Management of chronic hepatitis B and C in HIV-coinfected patients". J. Antimicrob. Chemother. 57 (5): 815–8. doi:10.1093/jac/dkl068. PMID 16556638. Retrieved 2012-03-30. Unknown parameter |month= ignored (help)
  16. ↑ Dore GJ, Cooper DA, Barrett C, Goh LE, Thakrar B, Atkins M (1999). "Dual efficacy of lamivudine treatment in human immunodeficiency virus/hepatitis B virus-coinfected persons in a randomized, controlled study (CAESAR). The CAESAR Coordinating Committee". J. Infect. Dis. 180 (3): 607–13. doi:10.1086/314942. PMID 10438346. Retrieved 2012-03-30. Unknown parameter |month= ignored (help)
  17. ↑ Benhamou Y, Katlama C, Lunel F, Coutellier A, Dohin E, Hamm N, Tubiana R, Herson S, Poynard T, Opolon P (1996). "Effects of lamivudine on replication of hepatitis B virus in HIV-infected men". Ann. Intern. Med. 125 (9): 705–12. PMID 8929003. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  18. ↑ 18.0 18.1 Matthews GV, Bartholomeusz A, Locarnini S, Ayres A, Sasaduesz J, Seaberg E, Cooper DA, Lewin S, Dore GJ, Thio CL (2006). "Characteristics of drug resistant HBV in an international collaborative study of HIV-HBV-infected individuals on extended lamivudine therapy". AIDS. 20 (6): 863–70. doi:10.1097/01.aids.0000218550.85081.59. PMID 16549970. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  19. ↑ Rousseau FS, Wakeford C, Mommeja-Marin H, Sanne I, Moxham C, Harris J, Hulett L, Wang LH, Quinn JB, Barry DW (2003). "Prospective randomized trial of emtricitabine versus lamivudine short-term monotherapy in human immunodeficiency virus-infected patients". J. Infect. Dis. 188 (11): 1652–8. doi:10.1086/379667. PMID 14639535. Retrieved 2012-03-30. Unknown parameter |month= ignored (help)
  20. ↑ van Bömmel F, Zöllner B, Sarrazin C, Spengler U, Hüppe D, Möller B, Feucht HH, Wiedenmann B, Berg T (2006). "Tenofovir for patients with lamivudine-resistant hepatitis B virus (HBV) infection and high HBV DNA level during adefovir therapy". Hepatology. 44 (2): 318–25. doi:10.1002/hep.21253. PMID 16871563. Retrieved 2012-03-30. Unknown parameter |month= ignored (help)
  21. ↑ 21.0 21.1 van Bömmel F, Wünsche T, Mauss S, Reinke P, Bergk A, Schürmann D, Wiedenmann B, Berg T (2004). "Comparison of adefovir and tenofovir in the treatment of lamivudine-resistant hepatitis B virus infection". Hepatology. 40 (6): 1421–5. doi:10.1002/hep.20464. PMID 15565615. Retrieved 2012-03-30. Unknown parameter |month= ignored (help)
  22. ↑ 22.0 22.1 Dore GJ, Cooper DA, Pozniak AL, DeJesus E, Zhong L, Miller MD, Lu B, Cheng AK (2004). "Efficacy of tenofovir disoproxil fumarate in antiretroviral therapy-naive and -experienced patients coinfected with HIV-1 and hepatitis B virus". J. Infect. Dis. 189 (7): 1185–92. doi:10.1086/380398. PMID 15031786. Retrieved 2012-03-30. Unknown parameter |month= ignored (help)
  23. ↑ Núñez M, Pérez-Olmeda M, Díaz B, Ríos P, González-Lahoz J, Soriano V (2002). "Activity of tenofovir on hepatitis B virus replication in HIV-co-infected patients failing or partially responding to lamivudine". AIDS. 16 (17): 2352–4. PMID 12441815. Retrieved 2012-03-30. Unknown parameter |month= ignored (help)
  24. ↑ Ristig MB, Crippin J, Aberg JA, Powderly WG, Lisker-Melman M, Kessels L, Tebas P (2002). "Tenofovir disoproxil fumarate therapy for chronic hepatitis B in human immunodeficiency virus/hepatitis B virus-coinfected individuals for whom interferon-alpha and lamivudine therapy have failed". J. Infect. Dis. 186 (12): 1844–7. doi:10.1086/345770. PMID 12447773. Retrieved 2012-03-30. Unknown parameter |month= ignored (help)
  25. ↑ Stephan C, Berger A, Carlebach A, Lutz T, Bickel M, Klauke S, Staszewski S, Stuermer M (2005). "Impact of tenofovir-containing antiretroviral therapy on chronic hepatitis B in a cohort co-infected with human immunodeficiency virus". J. Antimicrob. Chemother. 56 (6): 1087–93. doi:10.1093/jac/dki396. PMID 16269552. Retrieved 2012-03-30. Unknown parameter |month= ignored (help)
  26. ↑ 26.0 26.1 Benhamou Y, Fleury H, Trimoulet P, Pellegrin I, Urbinelli R, Katlama C, Rozenbaum W, Le Teuff G, Trylesinski A, Piketty C (2006). "Anti-hepatitis B virus efficacy of tenofovir disoproxil fumarate in HIV-infected patients". Hepatology. 43 (3): 548–55. doi:10.1002/hep.21055. PMID 16496322. Retrieved 2012-03-30. Unknown parameter |month= ignored (help)
  27. ↑ Lacombe K, Gozlan J, Boyd A, Boelle PY, Bonnard P, Molina JM, Miailhes P, Lascoux-Combe C, Serfaty L, Zoulim F, Girard PM (2008). "Comparison of the antiviral activity of adefovir and tenofovir on hepatitis B virus in HIV-HBV-coinfected patients". Antivir. Ther. (Lond.). 13 (5): 705–13. PMC 2665195. PMID 18771054. |access-date= requires |url= (help)
  28. ↑ Sheldon J, Camino N, Rodés B, Bartholomeusz A, Kuiper M, Tacke F, Núñez M, Mauss S, Lutz T, Klausen G, Locarnini S, Soriano V (2005). "Selection of hepatitis B virus polymerase mutations in HIV-coinfected patients treated with tenofovir". Antivir. Ther. (Lond.). 10 (6): 727–34. PMID 16218172. |access-date= requires |url= (help)
  29. ↑ Matthews GV, Avihingsanon A, Lewin SR, Amin J, Rerknimitr R, Petcharapirat P, Marks P, Sasadeusz J, Cooper DA, Bowden S, Locarnini S, Ruxrungtham K, Dore GJ (2008). "A randomized trial of combination hepatitis B therapy in HIV/HBV coinfected antiretroviral naïve individuals in Thailand". Hepatology. 48 (4): 1062–9. doi:10.1002/hep.22462. PMID 18697216. Retrieved 2012-03-30. Unknown parameter |month= ignored (help)
  30. ↑ Matthews GV, Seaberg E, Dore GJ, Bowden S, Lewin SR, Sasadeusz J, Marks P, Goodman Z, Philp FH, Tang Y, Locarnini S, Thio CL (2009). "Combination HBV therapy is linked to greater HBV DNA suppression in a cohort of lamivudine-experienced HIV/HBV coinfected individuals". AIDS. 23 (13): 1707–15. doi:10.1097/QAD.0b013e32832b43f2. PMC 2918388. PMID 19584701. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  31. ↑ Alvarez-Uria G, Ratcliffe L, Vilar J (2009). "Long-term outcome of tenofovir disoproxil fumarate use against hepatitis B in an HIV-coinfected cohort". HIV Med. 10 (5): 269–73. doi:10.1111/j.1468-1293.2008.00683.x. PMID 19210695. Retrieved 2012-04-01. Unknown parameter |month= ignored (help)
  32. ↑ Chang TT, Chao YC, Gorbakov VV, Han KH, Gish RG, de Man R, Cheinquer H, Bessone F, Brett-Smith H, Tamez R (2009). "Results of up to 2 years of entecavir vs lamivudine therapy in nucleoside-naïve HBeAg-positive patients with chronic hepatitis B". J. Viral Hepat. 16 (11): 784–9. doi:10.1111/j.1365-2893.2009.01142.x. PMID 19457141. Retrieved 2012-04-01. Unknown parameter |month= ignored (help)
  33. ↑ McMahon MA, Jilek BL, Brennan TP, Shen L, Zhou Y, Wind-Rotolo M, Xing S, Bhat S, Hale B, Hegarty R, Chong CR, Liu JO, Siliciano RF, Thio CL (2007). "The HBV drug entecavir - effects on HIV-1 replication and resistance". N. Engl. J. Med. 356 (25): 2614–21. doi:10.1056/NEJMoa067710. PMC 3069686. PMID 17582071. Retrieved 2012-04-01. Unknown parameter |month= ignored (help)
  34. ↑ Pessôa MG, Gazzard B, Huang AK, Brandão-Mello CE, Cassetti I, Mendes-Corrêa MC, Soriano V, Phiri P, Hall A, Brett-Smith H (2008). "Efficacy and safety of entecavir for chronic HBV in HIV/HBV coinfected patients receiving lamivudine as part of antiretroviral therapy". AIDS. 22 (14): 1779–87. doi:10.1097/QAD.0b013e32830b3ab5. PMID 18753861. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  35. ↑ Marcellin P, Chang TT, Lim SG, Tong MJ, Sievert W, Shiffman ML, Jeffers L, Goodman Z, Wulfsohn MS, Xiong S, Fry J, Brosgart CL (2003). "Adefovir dipivoxil for the treatment of hepatitis B e antigen-positive chronic hepatitis B". N. Engl. J. Med. 348 (9): 808–16. doi:10.1056/NEJMoa020681. PMID 12606735. Retrieved 2012-04-01. Unknown parameter |month= ignored (help)
  36. ↑ Hadziyannis SJ, Tassopoulos NC, Heathcote EJ, Chang TT, Kitis G, Rizzetto M, Marcellin P, Lim SG, Goodman Z, Ma J, Arterburn S, Xiong S, Currie G, Brosgart CL (2005). "Long-term therapy with adefovir dipivoxil for HBeAg-negative chronic hepatitis B". N. Engl. J. Med. 352 (26): 2673–81. doi:10.1056/NEJMoa042957. PMID 15987916. Retrieved 2012-04-01. Unknown parameter |month= ignored (help)
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