Hepatitis C Virus (HCV)/HIV Co-infection

(Last updated:14/7/2016; last reviewed:14/7/2016)

Panel recommendations

  • All HIV-infected patients should be screened for hepatitis C virus (HCV) infection. Patients at high risk of HCV infection should be screened annually and whenever HCV infection is suspected.
  • Antiretroviral therapy (ART) may slow the progression of liver disease by preserving or restoring immune function and reducing HIVrelated immune activation and inflammation. For most HCV/HIV-coinfected patients, including those with cirrhosis, the benefits of ART outweigh concerns regarding drug-induced liver injury. Therefore, ART should be initiated in all HCV/HIV-coinfected patients, regardless of CD4 T lymphocyte (CD4) cell count (AI).
  • Initial ART regimens recommended for most HCV/HIV-coinfected patients are the same as those recommended for individuals without HCV infection. However, when treatment for both HIV and HCV is indicated, the regimen should be selected with special considerations of potential drug-drug interactions and overlapping toxicities with the HCV treatment regimen (see discussion in the text below and in Table 12).
  • Combined treatment of HIV and HCV can be complicated by drug-drug interactions, increased pill burden, and toxicities. Although ART should be initiated for all HCV/HIV-coinfected patients regardless of CD4 cell count, in ART-naive patients with CD4 counts >500 cells/mm3 some clinicians may choose to defer ART until HCV treatment is completed (CIII).
  • In patients with lower CD4 counts (eg, <200 cells/mm3), ART should be initiated promptly (AI) and HCV therapy may be delayed until the patient is stable on HIV treatment (CIII).

Rating of Recommendations:
  A = Strong; B = Moderate; C = Optional
Rating of Evidence:  I = data from randomized controlled trials; II = data from well-designed nonrandomized trials or observational cohort studies with long-term clinical outcomes; III = expert opinion

#1538 HIV/Hepatitis C Virus Coinfection
October 2017 - Feedback

In Australia, the PBS now lists the following all-oral regimens for treatment of chronic hepatitis C infection in Australia, regardless of liver disease stage or ongoing drug and alcohol use:

For genotype 1 – sofosbuvir plus ledipasvir OR sofosbuvir plus daclatasvir ± ribavirin OR grazoprevir plus elbasvir ± ribavirin
For genotype 2 – sofosbuvir plus ribavirin
For genotype 3 – sofosbuvir plus daclatasvir OR sofosbuvir plus ribavirin
For genotype 4 – sofosbuvir plus PEG-IFN (and) ribavirin OR grazoprevir plus elbasvir ± ribavirin
For genotype 5-6 – sofosbuvir plus PEG-IFN (and) ribavirin

Guidelines and resources for the management of Hepatitis C are available at and a treatment guideline is available at 

Treatment with these regimens from clinical trials is expected to produce sustained virological response (SVR) rates similar to mono-infected patients.

Clinically significant Drug-drug interactions relevant to HIV treatments should be considered and a drug interaction search can be undertaken at An interaction between efavirenz and daclatasvir means that daclatasvir requires higher dosing (90 mg vs standard 60 mg once daily), while another interaction between ritonavir-boosted atazanavir and daclatasvir means that daclatasvir is dosed at a lower level (30 mg vs 60 mg once daily). Paritaprevir-ritonavir/ombitasvir/dasabuvir has significant drug-drug interactions, many resulting from the inclusion of ritonavir in the regimen and is uncommonly chosen because of pill burden and drug interactions. Sofosbuvir/daclatasvir has the advantage of being pangenotypic (activity against genotypes 1-6, although only PBS listed for genotypes 1 and 3), whereas sofosbuvir/ledipasvir has poorer activity against genotypes 2-3.

#1510 - When to start
October 2017 - Feedback  

The ASHM Sub-Committee for Guidance on HIV Management in Australia has developed clinical guidance for the Australian context in regards to this topic.  Please see "When to start antiretroviral therapy in people with HIV".

The treatment of hepatitis C virus (HCV) infection is rapidly evolving. Data suggest that HCV/HIVcoinfected patients treated with all-oral HCV regimens have sustained virologic response rates comparable to those of HCV-monoinfected patients. The purpose of this section is to discuss hepatic safety and drug-drug interaction issues related to HCV/HIV coinfection and the concomitant use of antiretroviral (ARV) agents and HCV drugs. For specific guidance on HCV treatment, please refer to

Among patients with chronic HCV infection, approximately one-third progress to cirrhosis, at a median time of less than 20 years.1,2 The rate of progression increases with older age, alcoholism, male sex, and HIV infection.3-6 A meta-analysis found that HCV/HIV-coinfected patients had a three-fold greater risk of progression to cirrhosis or decompensated liver disease than HCV-monoinfected patients.5 The risk of progression is even greater in HCV/HIV-coinfected patients with low CD4 T lymphocyte (CD4) cell counts. Although antiretroviral therapy (ART) appears to slow the rate of HCV disease progression in HCV/HIV coinfected patients, several studies have demonstrated that the rate continues to exceed that observed in patients without HIV infection.7,8 Whether HCV infection accelerates HIV progression, as measured by AIDS-related opportunistic infections (OIs) or death,9 is unclear. Although some older ARV drugs that are no longer commonly used have been associated with higher rates of hepatotoxicity in patients with chronic HCV infection,10,11 newer ARV agents currently in use appear to be less hepatotoxic.

For more than a decade, the mainstay of treatment for HCV infection was a combination regimen of peginterferon and ribavirin (PegIFN/RBV), but this regimen was associated with a poor rate of sustained virologic response (SVR), especially in HCV/HIV-coinfected patients. Rapid advances in HCV drug development led to the discovery of new classes of direct-acting antiviral (DAA) agents that target the HCV replication cycle. Recently approved DAA agents are used with or without RBV and have higher SVR rates, reduced pill burden, less frequent dosing, fewer side effects, and shorter durations of therapy than earlier approved agents.12-16 Guidance on the treatment and management of HCV in HIV-infected and HIV-uninfected adults can be found at

Assessment of HIV/Hepatitis C Virus Coinfection Before Initiation of Antiretroviral Therapy

  • All HIV-infected patients should be screened for HCV infection using sensitive immunoassays licensed for detection of antibody to HCV in blood16. HCV-seronegative patients at risk for the aquistion of HCV infection should undergo repeat testing annually. HCV-seropositive patients should be tested for HCV RNA using a qualitative or quantitative assay to confirm the presence of active infection17.
  • Patients with HIV/HCV coinfection should be counseled to avoid consuming alcohol and to use appropriate precautions to prevent transmission of HIV and/or HCV to others. HIV/HCV-coinfected patients who are susceptible to hepatitis A virus (HAV) or hepatitis B virus (HBV) infection should be vaccinated against these viruses.
  • All patients with HIV/HCV coinfection should be evaluated for HCV therapy.

Antiretroviral Therapy in HIV/Hepatitis C Virus Coinfection

When to start antiretroviral therapy
The rate of liver disease (liver fibrosis) progression is accelerated in HCV/HIV-coinfected patients, particularly in individuals with low CD4 counts (≤350 cells/mm3). Data largely from retrospective cohort studies are inconsistent regarding the effect of ART on the natural history of HCV disease;6,19,20 however, some studies suggest that ART may slow the progression of liver disease by preserving or restoring immune function and by reducing HIV-related immune activation and inflammation.21-23 Therefore, ART should be initiated in all HCV/HIV-coinfected patients, regardless of CD4 count (AI). However, in HIV treatment naive patients with CD4 counts >500 cells/mm3, some clinicians may choose to defer ART until HCV treatment is completed to avoid drug-drug interactions (CIII). Compared to patients with CD4 counts >350 cells/mm3, those with CD4 counts <200 cells/mm3 had lower HCV treatment response rates and higher rates of toxicity due to PegIFN/RBV.24 There is a lack of data regarding HCV treatment response to combination therapy with DAA agents in those with advanced immunosuppression. For patients with lower CD4 counts (eg, <200 cells/mm3), ART should be initiated promptly (AI) and HCV therapy may be delayed until the patient is stable on HIV treatment (CIII).25-28

Antiretroviral Drugs to Start and Avoid

Initial ARV combination regimens recommended for most HIV treatment-naive patients with HCV are the same as those recommended for patients without HCV infection. Special considerations for ARV selection in HCV/HIV-coinfected patients include the folllowing:

  • When both HIV and HCV treatments are indicated, the ARV regimen should be selected with careful consideration of potential drug-drug interactions (see Table 12) and overlapping toxicities with the HCV treatment regimen.
  • Cirrhotic patients should be carefully evaluated by an expert in advanced liver disease for signs of liver decompensation according to the Child-Turcotte-Pugh classification system. This assessment is necessary because hepatically metabolized ARV and HCV DAA drugs may be contraindicated or require dose modification in patients with Child-Pugh class B and C disease (see Appendix B, Table 7).


Drug-induced liver injury (DILI) following the initiation of ART is more common in HCV/HIV-coinfected patients than in those with HIV monoinfection. HVC/HIV coinfected individuals with advanced liver disease (eg, cirrhosis, end-stage liver disease) are at greatest risk for DILI.29 Eradicating HCV infection with treatment may decrease the likelihood of ARV-associated DILI.30

  • Given the substantial heterogeneity in patient populations and drug regimens, comparison of DILI incidence rates for individual ARV agents across clinical trials is difficult. The incidence of significant elevations in liver enzyme levels (more than 5 times the upper limit of the normal laboratory reference range) is low with currently recommended ART regimens. Hypersensitivity (or allergic) reactions associated with rash and elevations in liver enzymes can occur with certain ARVs. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels should be monitored 2 to 8 weeks after initiation of ART and every 3 to 6 months thereafter. Mild to moderate fluctuations in ALT and/or AST are typical in individuals with chronic HCV infection. In the absence of signs and/or symptoms of liver disease or increases in bilirubin, these fluctuations do not warrant interruption of ART. Patients with significant ALT and/or AST elevation should be carefully evaluated for signs and symptoms of liver insufficiency and for alternative causes of liver injury (eg, acute HAV or HBV infection, hepatobiliary disease, or alcoholic hepatitis). Short-term interruption of the ART regimen or of the specific drug suspected of causing the DILI may be required.31

Concurrent Treatment of HIV and Hepatitis C Virus Infection

Concurrent treatment of HIV and HCV is feasible, but treatment may be complicated by pill burden, drug-drug interactions, and toxicities. In this context, the stage of HCV disease should be assessed to determine the medical need for HCV treatment and to inform the decision on when to start treatment. Additional guidance on the treatment and management of HCV in HIV-infected and uninfected adults can be found at If the decision is to treat HCV, the ART regimen may need to be modified before HCV treatment is initiated to reduce the potential for drug-drug interactions and/or toxicities that may develop during the period of concurrent HIV and HCV treatment. See Table 12 for recommendations on the concomitant use of selected drugs for treatment of HCV and HIV infection. In patients with suppressed plasma HIV RNA and modified ART, HIV RNA should be measured within 4 to 8 weeks after changing HIV therapy to confirm the effectiveness of the new regimen. After HCV treatment is completed, the modified ART regimen should be continued for at least 2 weeks before reinitiating the original regimen. Continued use of the modified regimen is necessary because of the prolonged half-life of some HCV drugs and the potential risk of drug-drug interactions if a prior HIV regimen is resumed soon after HCV treatment is completed.

Antiretroviral and Hepatitis C Virus Drug-Drug Interactions

Considerations for the concurrent use of ART and recommended HCV agents (per are discussed below. Table 12 provides recommendations on the concomitant use of selected drugs for treatment of HCV and HIV infection.

  • Sofosbuvir is an HCV NS5B nucleotide polymerase inhibitor that is not metabolized by the cytochrome P450 enzyme system and, therefore, can be used in combination with most ARV drugs. Sofosbuvir is a substrate of p-glycoprotein (P-gp). P-gp inducers, such as tipranavir (TPV), may decrease sofosbuvir plasma concentrations and should not be coadministered with sofosbuvir. No other clinicially significant pharmocokinetic interactions between sofosbuvir and ARVs have been identified.

  • Ledipasvir is an HCV NS5A inhibitor and is part of a fixed-dose drug combination of sofosbuvir and ledipasvir.32 Similar to sofosbuvir, ledipasvir is not metabolized by the cytochrome P (CYP) 450 system of enzymes and is a substrate for P-gp. Ledipasvir inhibits the drug transporters P-gp and breast cancer resistance protein (BCRP) and may increase intestinal absorption of coadministered substrates for these transporters. The use of P-gp inducers is not recommended with ledipasivir/sofosbuvir. Coadministering ledipasvir/sofosbuvir and ARV regimens containing tenofovir disoproxil fumarate (TDF) is associated with increased exposure to TDF, especially when TDF is taken with an HIV protease inhibitor (PI) boosted with either ritonavir (RTV) or cobicistat (COBI). In some patients, alternative HCV or ARV drugs should be considered to avoid increases in TDF exposures. If the drugs are coadministered, the patient should be monitored for potential TDF-associated renal injury by assessing measurements of renal function (ie, estimated creatinine clearance, serum phosphorus, urine glucose, and urine protein) before HCV treatment initiation and periodically during treatment.

  • Daclatasvir is an HCV NS5A inhibitor that is approved for use with sofosbuvir.33 Daclatasvir is a substrate of CYP3A and an inhibitor of P-gp, OATP1B1/3, and BCRP. Moderate or strong inducers of CYP3A, such as efavirenz (EFV), etravirine (ETR), and nevirapine (NVP), may decrease plasma levels of daclatasvir and reduce the drug’s therapeutic effect. In this case, the daclatasvir dosage should be increased from 60 mg once daily to 90 mg once daily. By contrast, strong CYP3A inhibitors may increase plasma levels of daclatasvir, in which case the daclatasvir dosage should be reduced to 30 mg once daily. Clinically relevant interactions between daclatasvir and TDF have not been observed. Because daclatasvir also is an inhibitor of P-gp, OATP1B1/3, and BCRP, administration of daclatasvir may increase systemic e posure to medications that are substrates of these transporters and proteins, which could increase or prolong the therapeutic or adverse effects of that medication.

  • Elbasvir (a NS5A inhibitor) and grazoprevir (an HCV PI) are available in combination as a fixed-dose tablet. Both elbasvir and grazoprevir are substrates of CYP3A and P-gp.34 In addition, grazoprevir is a substrate of OATP1B1/3 transporters. Coadministration of the elbasvir and grazoprevir combination with strong CYP3A inducers, such as EFV, is contraindicated because elbasvir and grazoprevir concentrations may be decreased. Coadministration of strong CYP3A4 inhibitors with elbasvir and grazoprevir is also contraindicated or not recommended bcause elbasvir and grazoprevir concentrations may increase. Elbasvir and grazoprevir are also inhibitors of the drug transporter BCRP and may increase plasma concentrations of coadministered BCRP substrates.

  • The fixed-dose drug combination of ombitasvir (a NS5A inhibitor), paritaprevir (an HCV PI), and RTV (a pharmacokinetic [PK] enhancer) is copackaged with or without dasabuvir, an NS5B inhibitor.35,36

    • Paritaprevir is a substrate and inhibitor of the CYP3A4 enzymes and therefore may have significant interactions with certain ARVs that are metabolized by, or may induce or inhibit, the same pathways. Paritaprevir is also a substrate and inhibitor of OATP1B1/3.

    • Both ombitasvir and paritaprevir are inhibitors of UGT1A1 and also substrates of P-gp and BCRP.

    • Dasabuvir is primarily metabolized by the CYP2C8 enzymes. It is also an inhibitor of UGT1A1 and a substrate of P-gp and BCRP.

    • Coadministration of ombitasvir/paritaprevir/RTV with drugs that are substrates or inhibitors of the enzymes and drug transporters noted may result in increased plasma concentrations of either the HCV drugs or the coadministered drug. Given that several CYP enzymes and drug transporters are involved in the metabolism of ombitasvir, paritaprevir, and RTV, complex drug-drug interactions are likely. Therefore, clinicians need to consider all coadministered drugs for potential drug-drug interactions.

    • If a patient’s ART regimen contains RTV- or COBI-boosted atazanavir (ATV), the boosting agent should be discontinued during therapy with ombitasvir/paritaprevir/RTV and ATV should be taken in the morning at the same time as the HCV therapy. RTV or COBI should be restarted after completion of HCV treatment. HIV-infected patients not on ART should be placed on an alternative HCV regimen because RTV has activity against HIV.
  • Simeprevir is an HCV NS3/4A PI that is approved for use with sofosbuvir. Simeprevir is a substrate and inhibitor of CYP3A4 and P gp enzymes, and therefore has significant interactions with ARVs that are metabolized by the same pathways (eg, HIV PIs, EFV, ETR). Simeprevir is also an inhibitor of the drug transporter OATP1B1/3.

Given that the treatment of HCV is rapidly evolving, this section will be updated when new HCV drugs that may impact the treatment of HIV are approved. For guidance on the treatment of HCV infection, refer to

Table 12. Concomitant Use of Selected HIV Drugs and FDA-Approved HCV Drugs for Treatment ofHCV in HIV-Infected Adults

The recommendations in this table for concomitant use of selected HIV drugs with FDA-approved HCV direct-acting antiviral (DAA) drugs are based on available pharmacokinetics interaction data or predictions based on the known metabolic pathway of the agents. In some cases, there are not enough data to make any recommendations, and these instances are indicated in the table. In all cases where HIV and HCV drugs are used concomitantly, patients should be closely monitored for HIV and HCV virologic efficacy and potential toxicities. As the field of HCV therapy is rapidly evolving, readers should also refer to the latest drug product labels and HCV guidelines ( for updated information.

Changes in 2016 Guidelines
  • The text and Table 12 in this section were updated with information regarding the potential pharmacokinetic (PK) interactions between different ARV drugs and the recently approved hepatitis C drugs daclatasvir and the fixed-dose combination product of elbasvir and grazoprevir.
  • Peginterferon alfa and ribavirin were removed from Table 12, as these agents do not have significant PK interactions with ARV drugs.
  1. Alter MJ, Margolis HS, Krawczynski K, et al. The natural history of community-acquired hepatitis C in the United States.The Sentinel Counties Chronic non-A, non-B Hepatitis Study Team. N Engl J Med. Dec 31 1992;327(27):1899-1905. Available at;db=PubMed&dopt=Citation&list_uids=1280771.
  2. Thomas DL, Astemborski J, Rai RM, et al. The natural history of hepatitis C virus infection: host, viral, and environmental factors. JAMA. Jul 26 2000;284(4):450-456. Available at;db=PubMed&dopt=Citation&list_uids=10904508.
  3. Poynard T, Bedossa P, Opolon P. Natural history of liver fibrosis progression in patients with chronic hepatitis C. The OBSVIRC, METAVIR, CLINIVIR, and DOSVIRC groups. Lancet. Mar 22 1997;349(9055):825-832. Available at;db=PubMed&dopt=Citation&list_uids=9121257.
  4. Wiley TE, McCarthy M, Breidi L, Layden TJ. Impact of alcohol on the histological and clinical progression of hepatitis C infection. Hepatology. Sep 1998;28(3):805-809. Available at;db=PubMed&dopt=Citation&list_uids=9731576.
  5. Graham CS, Baden LR, Yu E, et al. Influence of human immunodeficiency virus infection on the course of hepatitis C virus infection: a meta-analysis. Clin Infect Dis. Aug 15 2001;33(4):562-569. Available at;db=PubMed&dopt=Citation&list_uids=11462196.
  6. Thein HH, Yi Q, Dore GJ, Krahn MD. Natural history of hepatitis C virus infection in HIV-infected individuals and the impact of HIV in the era of highly active antiretroviral therapy: a meta-analysis. AIDS. Oct 1 2008;22(15):1979-1991. Available at;db=PubMed&dopt=Citation&list_uids=18784461.
  7. Weber R, Sabin CA, Friis-Moller N, et al. Liver-related deaths in persons infected with the human immunodeficiency virus: the D:A:D study. Arch Intern Med. Aug 14-28 2006;166(15):1632-1641. Available at;db=PubMed&dopt=Citation&list_uids=16908797.
  8. Kitahata MM, Gange SJ, Abraham AG, et al. Effect of early versus deferred antiretroviral therapy for HIV on survival. N Engl J Med. Apr 30 2009;360(18):1815-1826. Available at;db=PubMed&dopt=Citation&list_uids=19339714.
  9. Greub G, Ledergerber B, Battegay M, et al. Clinical progression, survival, and immune recovery during antiretroviral therapy in patients with HIV-1 and hepatitis C virus coinfection: the Swiss HIV Cohort Study. Lancet. Nov 25 2000;356(9244):1800-1805. Available at;db=PubMed&dopt=Citation&list_uids=11117912.
  10. Sulkowski MS, Thomas DL, Chaisson RE, Moore RD. Hepatotoxicity associated with antiretroviral therapy in adults infected with human immunodeficiency virus and the role of hepatitis C or B virus infection. JAMA. Jan 5 2000;283(1):74-80. Available at;db=PubMed&dopt=Citation&list_uids=10632283.
  11. Sulkowski MS, Thomas DL, Mehta SH, et al. Hepatotoxicity associated with nevirapine or efavirenz-containing antiretroviral therapy: role of hepatitis C and B infections. Hepatology. 2002;35(1):182-189. Available at;db=PubMed&list_uids=11786975&dopt=Abstract.
  12. Afdhal N, Zeuzem S, Kwo P, et al. Ledipasvir and sofosbuvir for untreated HCV genotype 1 infection. N Engl J Med. May 15 2014;370(20):1889-1898. Available at
  13. Kowdley KV, Gordon SC, Reddy KR, et al. Ledipasvir and sofosbuvir for 8 or 12 weeks for chronic HCV without cirrhosis. N Engl J Med. May 15 2014;370(20):1879-1888. Available at
  14. Sulkowski MS, Gardiner DF, Rodriguez-Torres M, et al. Daclatasvir plus sofosbuvir for previously treated or untreated chronic HCV infection. N Engl J Med. Jan 16 2014;370(3):211-221. Available at
  15. Feld JJ, Kowdley KV, Coakley E, et al. Treatment of HCV with ABT-450/r-ombitasvir and dasabuvir with ribavirin. N Engl J Med. Apr 24 2014;370(17):1594-1603. Available at
  16. Zeuzem S, Andreone P, Pol S, et al. Telaprevir for retreatment of HCV infection. N Engl J Med. Jun 23 2011;364(25):2417-2428. Available at
  17. AASLD-IDSA. Recommendations for testing, managing, and treating hepatitis C. Available at
  18. Panel on Opportunistic Infections in HIV-Infected Adults and Adolescents. Guidelines for the prevention and treatment of opportunistic infections in HIV-infected adults and adolescents: recommendations from the Centers for Disease Control and Prevention, the National Institutes of Health, and the HIV Medicine Association of the Infectious Diseases Society of America. Available at Accessed July 6, 2016.
  19. Sulkowski MS, Mehta SH, Torbenson MS, et al. Rapid fibrosis progression among HIV/hepatitis C virus-co-infected adults. AIDS. Oct 18 2007;21(16):2209-2216. Available at;db=PubMed&dopt=Citation&list_uids=18090048.
  20. Brau N, Salvatore M, Rios-Bedoya CF, et al. Slower fibrosis progression in HIV/HCV-coinfected patients with successful HIV suppression using antiretroviral therapy. J Hepatol. Jan 2006;44(1):47-55. Available at;db=PubMed&dopt=Citation&list_uids=16182404.
  21. Macias J, Berenguer J, Japon MA, et al. Fast fibrosis progression between repeated liver biopsies in patients coinfected with human immunodeficiency virus/hepatitis C virus. Hepatology. Oct 2009;50(4):1056-1063. Available at;db=PubMed&dopt=Citation&list_uids=19670415.
  22. Verma S, Goldin RD, Main J. Hepatic steatosis in patients with HIV-Hepatitis C Virus coinfection: is it associated with antiretroviral therapy and more advanced hepatic fibrosis? BMC Res Notes. 2008;1:46. Available at;db=PubMed&dopt=Citation&list_uids=18710499.
  23. Ragni MV, Nalesnik MA, Schillo R, Dang Q. Highly active antiretroviral therapy improves ESLD-free survival in HIV-HCV co-infection. Haemophilia. Mar 2009;15(2):552-558. Available at;db=PubMed&dopt=Citation&list_uids=19347994.
  24. Opravil M, Sasadeusz J, Cooper DA, et al. Effect of baseline CD4 cell count on the efficacy and safety of peginterferon Alfa- 2a (40KD) plus ribavirin in patients with HIV/hepatitis C virus coinfection. J Acquir Immune Defic Syndr. Jan 1 2008;47(1):36-49. Available at;db=PubMed&dopt=Citation&list_uids=18156990.
  25. Ghany MG, Strader DB, Thomas DL, Seeff LB. Diagnosis, management, and treatment of hepatitis C: an update. Hepatology. Apr 2009;49(4):1335-1374. Available at;db=PubMed&dopt=Citation&list_uids=19330875.
  26. Soriano V, Puoti M, Sulkowski M, et al. Care of patients coinfected with HIV and hepatitis C virus: 2007 updated recommendations from the HCV-HIV International Panel. AIDS. May 31 2007;21(9):1073-1089. Available at;db=PubMed&dopt=Citation&list_uids=17502718.
  27. Tien PC. Management and treatment of hepatitis C virus infection in HIV-infected adults: recommendations from the Veterans Affairs Hepatitis C Resource Center Program and National Hepatitis C Program Office. Am J Gastroenterol. Oct 2005;100(10):2338-2354. Available at;db=PubMed&dopt=Citation&list_uids=16181388.
  28. Avidan NU, Goldstein D, Rozenberg L, et al. Hepatitis C viral kinetics during treatment with peg IFN-alpha-2b in HIV/HCV coinfected patients as a function of baseline CD4+ T-cell counts. J Acquir Immune Defic Syndr. Dec 1 2009;52(4):452-458. Available at;db=PubMed&dopt=Citation&list_uids=19797971.
  29. Aranzabal L, Casado JL, Moya J, et al. Influence of liver fibrosis on highly active antiretroviral therapy-associated hepatotoxicity in patients with HIV and hepatitis C virus coinfection. Clin Infect Dis. Feb 15 2005;40(4):588-593. Available at;db=PubMed&dopt=Citation&list_uids=15712082.
  30. Labarga P, Soriano V, Vispo ME, et al. Hepatotoxicity of antiretroviral drugs is reduced after successful treatment of chronic hepatitis C in HIV-infected patients. J Infect Dis. Sep 1 2007;196(5):670-676. Available at;db=PubMed&dopt=Citation&list_uids=17674307.
  31. Sulkowski MS, Thomas DL. Hepatitis C in the HIV-infected patient. Clin Liver Dis. Feb 2003;7(1):179-194. Available at;db=PubMed&dopt=Citation&list_uids=12691466.
  32. Ledipasvir/sofobuvir (Harvoni) [package insert]. Gilead. 2016. Available at Accessed July 6, 2016.
  33. Daclatasvir (Daklinza) [package insert] Bristol Myers Squibb. 2016. Available at Accessed July 6, 2016.
  34. Elbasavir/grazoprevir (Zapatier) [package insert]. 2016. Available at Accessed July 6, 2016.
  35. Ombitasvir/paritaprevir/ritonavir (Technivie) [package insert]. AbbVie. 2016. Available at Available at July 6, 2016.
  36. Ombitasvir/paritaprevir/ritonavir/dasabuvir (Viekira) [package insert]. Food and Drug Administration. 2014. Available at Accessed July 6, 2016.

ASHM - Supporting the HIV, Viral Hepatitis and Sexual Health Workforce