The Syphilis and Candida sections has been updated! For a summary of changes, see the What's New section.
Type your search term(s) in the text box. Users can only search one guideline at a time. To search for an exact phrase, use quotation marks (i.e. "what to start"). To narrow your search, add additional relevant terms. If you are not finding what you need, try searching similar terms (i.e. perinatal OR pregnancy) to broaden your search.
Guidelines for the Prevention and Treatment of Opportunistic Infections in HIV-Infected Adults and Adolescents
Hepatitis C Virus Infection
(Last updated: October 28, 2014; last reviewed: October 28, 2014)
Hepatitis C virus (HCV) is a single-stranded RNA virus; the estimated worldwide prevalence of HCV infection is 2% to 3%, which translates to an estimated 170 million infected individuals of whom approximately 3.2 million live in the United States.1 Seven distinct HCV genotypes have been described.2 Genotype 1 infection accounts for approximately 75% of infections in the United States and approximately 90% of infections among blacks.3,4 Both HIV and HCV can be transmitted by percutaneous exposure to blood or blood products, through sexual intercourse, and from a mother to her infant; however, the relative efficiency of transmission by these routes varies substantially. Approximately, 20% to 30% of HIV-infected patients in the United States are coinfected with HCV.5,6
HCV is approximately 10 times more infectious than HIV through percutaneous blood exposures and has been shown to survive for weeks in syringes.7-9 Transmission via injection drug use remains the most common mode of acquisition in the United States while transmission through contaminated blood products is now rare. Health care-associated transmission of HCV also can occur as a result of improper reuse of parenteral medications and equipment.10-12 Other factors that have been associated with HCV infection include accidental occupation-related needlestick injuries, intranasal cocaine use, chronic hemodialysis, and tattoo placement.
Heterosexual transmission of HCV is uncommon but more likely in those whose partners are coinfected with HIV and HCV.13,14 Existing data also suggest that sexual contact is a relatively inefficient mode of transmission between HIV seronegative men who have sex with men (MSM).15 However, in HIV-infected MSM, multiple outbreaks of acute HCV infection demonstrate that sexual transmission is an important mode of acquisition in this population.16 Risk factors include unprotected receptive anal intercourse, use of sex toys, non-injection recreational drug use, and concurrent sexually transmitted diseases (STDs).15,17-19,20,21 Temporally, the increase in the incidence of sexual transmission of HCV among HIV-infected MSMs coincides with an increase in high-risk sexual behaviors following the introduction of antiretroviral therapy (ART).22,23
Mother-to-child transmission of HCV infection occurs in approximately 1% to 3% of infants born to HCV-seropositive mothers without and 4% to 7% of infants born to HCV-seropositive mothers with detectable plasma HCV RNA levels.24-27 Incidence of mother-to-child HCV transmission is increased when mothers are HIV-coinfected, reaching rates of 10% to 20%.28,29
Both acute and chronic HCV infections are usually minimally symptomatic or asymptomatic. Fewer than 20% of patients with acute infection have characteristic symptoms, including low-grade fever, mild right-upper-quadrant pain, nausea, vomiting, anorexia, dark urine, and jaundice. Unexplained elevations in serum alanine aminotransferase (ALT) or aspartate aminotransferase (AST) levels may be the only laboratory finding during acute and chronic infection. Recognition of acute HCV infection in patients with new-onset liver enzyme elevations is clinically important since HCV treatment during the early phases of infection is more efficacious than treatment during the chronic phase.30,31
Cirrhosis develops in approximately 20% of patients with chronic HCV infection within 20 years after infection, although the risk for an individual is highly variable.32,33 Risk factors for development of significant liver disease include older age at the time of infection, male sex, obesity, and concomitant alcohol use.33,34 HIV coinfection adversely affects the course of HCV infection, resulting in significantly accelerated progression of liver disease to cirrhosis, particularly in those with advanced immunodeficiency (CD4 T-lymphocyte [CD4] count <200 cells/mm3).35,36 Further, coinfected patients with cirrhosis progress more rapidly to life-limiting outcomes such as end-stage liver disease and hepatocellular carcinoma (HCC) than do those who are HCV-monoinfected.37,38 Because of its high prevalence and accelerated progression, HCV disease is a leading non-AIDS cause of death in HIV-infected individuals.39-41 In addition to liver disease, HCV may be associated with symptomatic vasculitis due to cryoglobulinemia (largely affecting the skin), renal disease (membranoproliferative glomerulonephritis), and porphyria cutanea tarda.
On entry into HIV care, all HIV-infected patients should undergo routine HCV screening. Initial testing for HCV should be performed using the most sensitive immunoassays licensed for detection of antibody to HCV (anti-HCV) in blood.42 For at risk HCV-seronegative individuals, HCV antibody testing is recommended annually or as indicated by risk exposure.
False-negative anti-HCV antibody results are possible but are uncommon (<1%) in HIV-infected patients with advanced immunosuppression.43,44 In addition, negative anti-HCV antibody results can occur during acute infection. Following acute HCV infection, the duration of the window period prior to seroconversion is highly variable, ranging from 2 weeks to 12 weeks. Serum ALT levels are frequently elevated early in the course of acute infection and high ALT levels should prompt testing for HCV RNA if serologic test results are negative or indeterminate in individuals at risk of HCV infection.45
Individuals who test positive for HCV antibody should undergo confirmatory testing by using a sensitive quantitative assay to measure plasma HCV RNA level. Importantly, plasma HCV RNA viral load does not correlate with HCV disease severity, and therefore, should not be monitored serially in patients not taking HCV treatment. Plasma HCV RNA levels do provide important prognostic information about the likelihood of response to HCV treatment.
The primary route of HCV transmission is drug injection via a syringe or other injection paraphernalia (i.e., “cookers,” filters, or water) previously used by an infected person. HCV-seronegative injection drug users should be encouraged to stop using injection drugs by entering a substance abuse treatment program or, if they are unwilling or unable to stop, to reduce the risk of transmission by never sharing needles or injection equipment.46-48 HCV also can be transmitted sexually, especially between HIV-infected MSM. HCV-seronegative patients must be counseled regarding the risk of sexual acquisition. The effectiveness of male condoms in reducing HCV transmission is unknown, nonetheless, barrier precautions are strongly recommended to reduce the risk of STDs, including HCV (BIII).49
There is no vaccine or recommended post-exposure prophylaxis to prevent HCV infection. Following acute HCV infection, chronic infection may be prevented within the first 6 to 12 months after infection through antiviral treatment; relatively high rates of viral clearance have been observed with HCV treatment during the acute phase of infection.50,51 However, patients also have the potential for spontaneous clearance after acute infection; as such, some experts recommend observation of acutely infected patients—particularly those whose infection (e.g., those with C/C IL28B genotype) is more likely to resolve—for approximately 3 to 6 months before initiating HCV treatment.52 In the setting of evolving data, recommendations for management of acute HCV infection in HIV-infected patients are expected to change rapidly. Clinicians should refer to the most recent HCV treatment guidelines (http://www.hcvguidelines.org) for the most up-to-date guidance.
HCV-infected individuals should be counseled about methods to prevent liver damage by avoiding any alcohol consumption (as alcohol accelerates progression of liver disease), limiting ingestion of potentially hepatotoxic medications (e.g., acetaminophen should be limited to <2 g/day), and avoiding iron supplementation in the absence of documented iron deficiency.53 HCV-infected patients should be tested for previous or concurrent hepatitis B virus (HBV) infection because co-infection with HBV is associated with increased morbidity. Those without evidence of immunity to HBV should be vaccinated (see Hepatitis B Virus Infection section). Likewise, because acute hepatitis A virus (HAV) infection is more likely to be fulminant in HCV-infected individuals, these patients should be screened for immunity (HAV IgG or antibody total) and those susceptible should be vaccinated (BIII).
Coinfected patients with cirrhosis are at risk of life-threatening complications and should be managed in consultation with a gastroenterologist or hepatologist. In particular, individuals with cirrhosis should undergo serial screening for HCC;54 some experts recommend performing ultrasonography at 6- to 12-month intervals, although the optimal screening strategy is unknown. Because of its relatively poor specificity and sensitivity, alfa-fetoprotein should not be the sole screening method. HIV infection is not an absolute contraindication to liver transplantation; accordingly, coinfected patients with decompensated liver disease and/or early HCC may be considered for transplantation at specialized transplant centers.
Although earlier studies focused on the potential for antiretroviral (ARV)-associated liver injury with certain agents, more recent studies have found that effective HIV treatment is associated with reduced risk of liver disease progression. Coinfected patients should be treated with ART in accordance with the Guidelines for the Use of Antiretroviral Agents in HIV-1-Infected Adults and Adolescents developed by the Department of Health and Human Services Panel.55 Dose adjustment of certain ARV agents may be needed in patients with decompensated cirrhosis.
In general, the goals of therapy, treatment regimen, and monitoring parameters for HIV/HCV coinfected patients are similar to those recommended for HCV monoinfected patients. The field of HCV drug development is evolving rapidly. The armamenarium of approved drugs is likely to expand considerably in the next few years. Clinicians should refer to the most recent HCV treatment guidelines (http://www.hcvguidelines.org) for the most up-to-date recommendations.
Special Considerations During Pregnancy
Pregnant HIV-infected women should be tested for HCV infection to allow appropriate management for the mothers during pregnancy and after delivery, and also for their infants.56 HCV treatment with PegIFN and ribavirin is contraindicated during pregnancy (AII). IFNs are abortifacient at high doses in monkeys and should not be used in pregnant women because of their direct antigrowth and antiproliferative effects.57 Ribavirin is an FDA category X drug because of its teratogenicity at low doses in multiple animal species. Defects noted in animals include limb abnormalities, craniofacial defects, exencephaly, and anophthalmia. Ribavirin should not be used during pregnancy (AII). Women of childbearing potential and men receiving ribavirin should be counseled about the risks and need for consistent contraceptive use during and for 6 months after completion of ribavirin therapy (AIII). Inadvertent pregnancy during paternal exposure was not associated with adverse events in two newborns.58 Pregnancies that occur in women taking ribavirin or those in women whose male partner is taking the drug should be reported to the Ribavirin Pregnancy Registry (800-593-2214 or http://www.ribavirinpregnancyregistry.com). Telaprevir, boceprevir, and sofosbuvir are Pregnancy Category B and simeprevir is Pregnancy Category C; however, these agents are often used in combination with PegIFN/ribavirin, which are not recommended in pregnancy. The FDA category assignment for these novel drugs, though, is based on safety in animal studies as there are no human data available.
Evaluation of HCV-infected pregnant women, including liver biopsy, can be delayed until >3 months after delivery to allow potential pregnancy-related changes in disease activity to resolve. HAV and HBV vaccines can be administered during pregnancy and women who have not previously been vaccinated should receive them. Several studies have reported that perinatal transmission of HCV occurs more frequently in women with HIV/HCV-coinfection than in those with HCV monoinfection. However, data are limited regarding the role of medical or surgical interventions to reduce the risk of perinatal HCV transmission. Nearly all studies, including those in HIV-uninfected and HIV-infected women, have found that elective cesarean delivery does not reduce the risk of perinatal HCV transmission.26,59-61 Moreover, there is an increased risk of maternal morbidity associated with cesarean compared with vaginal delivery, particularly in the setting of maternal HIV infection.62-65 Thus, while elective cesarean delivery in HIV/HCV-coinfected women can be considered based on HIV-related indications, data are insufficient to support its routine use for prevention of HCV transmission.
Alter MJ. Epidemiology of hepatitis C virus infection. World J Gastroenterol. 2007;13(17):2436-2441. Available at http://www.ncbi.nlm.nih.gov/pubmed/17552026.
Scott JD, Gretch DR. Molecular diagnostics of hepatitis C virus infection: a systematic review. JAMA. 2007;297(7):724-732. Available at http://www.ncbi.nlm.nih.gov/pubmed/17312292.
Armstrong GL, Wasley A, Simard EP, McQuillan GM, Kuhnert WL, Alter MJ. The prevalence of hepatitis C virus infection in the United States, 1999 through 2002. Ann Intern Med. 2006;144(10):705-714. Available at http://www.ncbi.nlm.nih.gov/pubmed/16702586.
Blatt LM, Mutchnick MG, Tong MJ, et al. Assessment of hepatitis C virus RNA and genotype from 6807 patients with chronic hepatitis C in the United States. J Viral Hepat. 2000;7(3):196-202. Available at http://www.ncbi.nlm.nih.gov/pubmed/10849261.
Staples CT, Jr., Rimland D, Dudas D. Hepatitis C in the HIV (human immunodeficiency virus) Atlanta V.A. (Veterans Affairs Medical Center) Cohort Study (HAVACS): the effect of coinfection on survival. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 1999;29(1):150-154. Available at http://www.ncbi.nlm.nih.gov/pubmed/10433578.
Sherman KE, Rouster SD, Chung RT, Rajicic N. Hepatitis C Virus prevalence among patients infected with Human Immunodeficiency Virus: a cross-sectional analysis of the US adult AIDS Clinical Trials Group. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 2002;34(6):831-837. Available at http://www.ncbi.nlm.nih.gov/pubmed/11833007.
Sulkowski MS, Moore RD, Mehta SH, Chaisson RE, Thomas DL. Hepatitis C and progression of HIV disease. JAMA. 2002;288(2):199-206. Available at http://www.ncbi.nlm.nih.gov/pubmed/12095384.
Ciesek S, Friesland M, Steinmann J, et al. How stable is the hepatitis C virus (HCV)? Environmental stability of HCV and its susceptibility to chemical biocides. J Infect Dis. 2010;201(12):1859-1866. Available at http://www.ncbi.nlm.nih.gov/pubmed/20441517.
Paintsil E, He H, Peters C, Lindenbach BD, Heimer R. Survival of hepatitis C virus in syringes: implication for transmission among injection drug users. J Infect Dis. 2010;202(7):984-990. Available at http://www.ncbi.nlm.nih.gov/pubmed/20726768.
Prati D. Transmission of hepatitis C virus by blood transfusions and other medical procedures: a global review. J Hepatol. 2006;45(4):607-616. Available at http://www.ncbi.nlm.nih.gov/pubmed/16901579.
Alter MJ. Healthcare should not be a vehicle for transmission of hepatitis C virus. J Hepatol. 2008;48(1):2-4. Available at http://www.ncbi.nlm.nih.gov/pubmed/18023493.
Centers for Disease C, Prevention. Acute hepatitis C virus infections attributed to unsafe injection practices at an endoscopy clinic--Nevada, 2007. MMWR. Morbidity and mortality weekly report. 2008;57(19):513-517. Available at http://www.ncbi.nlm.nih.gov/pubmed/18480743.
Eyster ME, Alter HJ, Aledort LM, Quan S, Hatzakis A, Goedert JJ. Heterosexual co-transmission of hepatitis C virus (HCV) and human immunodeficiency virus (HIV). Ann Intern Med. 1991;115(10):764-768. Available at http://www.ncbi.nlm.nih.gov/pubmed/1656825.
Lissen E, Alter HJ, Abad MA, et al. Hepatitis C virus infection among sexually promiscuous groups and the heterosexual partners of hepatitis C virus infected index cases. Eur J Clin Microbiol Infect Dis. 1993;12(11):827-831. Available at http://www.ncbi.nlm.nih.gov/pubmed/7509282.
van de Laar TJ, van der Bij AK, Prins M, et al. Increase in HCV incidence among men who have sex with men in Amsterdam most likely caused by sexual transmission. J Infect Dis. 2007;196(2):230-238. Available at http://www.ncbi.nlm.nih.gov/pubmed/17570110.
van de Laar TJ, Matthews GV, Prins M, Danta M. Acute hepatitis C in HIV-infected men who have sex with men: an emerging sexually transmitted infection. AIDS. 2010;24(12):1799-1812. Available at http://www.ncbi.nlm.nih.gov/pubmed/20601854.
Rauch A, Rickenbach M, Weber R, et al. Unsafe sex and increased incidence of hepatitis C virus infection among HIV-infected men who have sex with men: the Swiss HIV Cohort Study. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 2005;41(3):395-402. Available at http://www.ncbi.nlm.nih.gov/pubmed/16007539.
Danta M, Brown D, Bhagani S, et al. Recent epidemic of acute hepatitis C virus in HIV-positive men who have sex with men linked to high-risk sexual behaviours. AIDS. 2007;21(8):983-991. Available at http://www.ncbi.nlm.nih.gov/pubmed/17457092.
van de Laar T, Pybus O, Bruisten S, et al. Evidence of a large, international network of HCV transmission in HIV-positive men who have sex with men. Gastroenterology. 2009;136(5):1609-1617. Available at http://www.ncbi.nlm.nih.gov/pubmed/19422083.
Fierer DS, Uriel AJ, Carriero DC, et al. Liver fibrosis during an outbreak of acute hepatitis C virus infection in HIV-infected men: a prospective cohort study. J Infect Dis. 2008;198(5):683-686. Available at http://www.ncbi.nlm.nih.gov/pubmed/18627270.
Taylor LE, Holubar M, Wu K, et al. Incident hepatitis C virus infection among US HIV-infected men enrolled in clinical trials. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 2011;52(6):812-818. Available at http://www.ncbi.nlm.nih.gov/pubmed/21282184.
Crepaz N, Hart TA, Marks G. Highly active antiretroviral therapy and sexual risk behavior: a meta-analytic review. JAMA. 2004;292(2):224-236. Available at http://www.ncbi.nlm.nih.gov/pubmed/15249572.
Stolte IG, Dukers NH, Geskus RB, Coutinho RA, de Wit JB. Homosexual men change to risky sex when perceiving less threat of HIV/AIDS since availability of highly active antiretroviral therapy: a longitudinal study. AIDS. 2004;18(2):303-309. Available at http://www.ncbi.nlm.nih.gov/pubmed/15075549.
Ohto H, Terazawa S, Sasaki N, et al. Transmission of hepatitis C virus from mothers to infants. The Vertical Transmission of Hepatitis C Virus Collaborative Study Group. The New England Journal of Medicine. 1994;330(11):744-750. Available at http://www.ncbi.nlm.nih.gov/pubmed/8107740.
Roberts EA, Yeung L. Maternal-infant transmission of hepatitis C virus infection. Hepatology. 2002;36(5 Suppl 1):S106-113. Available at http://www.ncbi.nlm.nih.gov/pubmed/12407583.
McMenamin MB, Jackson AD, Lambert J, et al. Obstetric management of hepatitis C-positive mothers: analysis of vertical transmission in 559 mother-infant pairs. Am J Obstet Gynecol. 2008;199(3):315 e311-315. Available at http://www.ncbi.nlm.nih.gov/pubmed/18771997.
Valladares G, Chacaltana A, Sjogren MH. The management of HCV-infected pregnant women. Ann Hepatol. 2010;9 Suppl:92-97. Available at http://www.ncbi.nlm.nih.gov/pubmed/20714003.
Mast EE, Hwang LY, Seto DS, et al. Risk factors for perinatal transmission of hepatitis C virus (HCV) and the natural history of HCV infection acquired in infancy. J Infect Dis. 2005;192(11):1880-1889. Available at http://www.ncbi.nlm.nih.gov/pubmed/16267758.
Alter MJ. Epidemiology of viral hepatitis and HIV co-infection. J Hepatol. 2006;44(1 Suppl):S6-9. Available at http://www.ncbi.nlm.nih.gov/pubmed/16352363.
Jaeckel E, Cornberg M, Wedemeyer H, et al. Treatment of acute hepatitis C with interferon alfa-2b. The New England Journal of Medicine. 2001;345(20):1452-1457. Available at http://www.ncbi.nlm.nih.gov/pubmed/11794193.
Kamal SM, Fouly AE, Kamel RR, et al. Peginterferon alfa-2b therapy in acute hepatitis C: impact of onset of therapy on sustained virologic response. Gastroenterology. 2006;130(3):632-638. Available at http://www.ncbi.nlm.nih.gov/pubmed/16530503.
Tong MJ, el-Farra NS, Reikes AR, Co RL. Clinical outcomes after transfusion-associated hepatitis C. The New England Journal of Medicine. 1995;332(22):1463-1466. Available at http://www.ncbi.nlm.nih.gov/pubmed/7739682.
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. 1997;349(9055):825-832. Available at http://www.ncbi.nlm.nih.gov/pubmed/9121257.
Sulkowski MS, Thomas DL, Chaisson RE, Moore RD. Elevated liver enzymes following initiation of antiretroviral therapy. JAMA. 2000;283(19):2526-2527. Available at http://www.ncbi.nlm.nih.gov/pubmed/10815113.
Benhamou Y, Bochet M, Di Martino V, et al. Liver fibrosis progression in human immunodeficiency virus and hepatitis C virus coinfected patients. The Multivirc Group. Hepatology. 1999;30(4):1054-1058. Available at http://www.ncbi.nlm.nih.gov/pubmed/10498659.
Di Martino V, Rufat P, Boyer N, et al. The influence of human immunodeficiency virus coinfection on chronic hepatitis C in injection drug users: a long-term retrospective cohort study. Hepatology. 2001;34(6):1193-1199. Available at http://www.ncbi.nlm.nih.gov/pubmed/11732009.
Pineda JA, Romero-Gomez M, Diaz-Garcia F, et al. HIV coinfection shortens the survival of patients with hepatitis C virus-related decompensated cirrhosis. Hepatology. 2005;41(4):779-789. Available at http://www.ncbi.nlm.nih.gov/pubmed/15800956.
Ragni MV, Eghtesad B, Schlesinger KW, Dvorchik I, Fung JJ. Pretransplant survival is shorter in HIV-positive than HIV-negative subjects with end-stage liver disease. Liver Transpl. 2005;11(11):1425-1430. Available at http://www.ncbi.nlm.nih.gov/pubmed/16237709.
Salmon-Ceron D, Lewden C, Morlat P, et al. Liver disease as a major cause of death among HIV infected patients: role of hepatitis C and B viruses and alcohol. J Hepatol. 2005;42(6):799-805. Available at http://www.ncbi.nlm.nih.gov/pubmed/15973779.
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. 2006;166(15):1632-1641. Available at http://www.ncbi.nlm.nih.gov/pubmed/16908797.
Smith JA, Aberle JH, Fleming VM, et al. Dynamic coinfection with multiple viral subtypes in acute hepatitis C. J Infect Dis. 2010;202(12):1770-1779. Available at http://www.ncbi.nlm.nih.gov/pubmed/21067369.
National Institutes of Health Consensus Development Conference Statement: Management of hepatitis C: 2002--June 10-12, 2002. Hepatology. 2002;36(5 Suppl 1):S3-20. Available at http://www.ncbi.nlm.nih.gov/pubmed/12407572.
Chamot E, Hirschel B, Wintsch J, et al. Loss of antibodies against hepatitis C virus in HIV-seropositive intravenous drug users. AIDS. 1990;4(12):1275-1277. Available at http://www.ncbi.nlm.nih.gov/pubmed/1965126.
Thio CL, Nolt KR, Astemborski J, Vlahov D, Nelson KE, Thomas DL. Screening for hepatitis C virus in human immunodeficiency virus-infected individuals. J Clin Microbiol. 2000;38(2):575-577. Available at http://www.ncbi.nlm.nih.gov/pubmed/10655348.
Sulkowski MS, Thomas DL. Hepatitis C in the HIV-infected patient. Clin Liver Dis. 2003;7(1):179-194. Available at http://www.ncbi.nlm.nih.gov/pubmed/12691466.
Hagan H, Jarlais DC, Friedman SR, Purchase D, Alter MJ. Reduced risk of hepatitis B and hepatitis C among injection drug users in the Tacoma syringe exchange program. Am J Public Health. 1995;85(11):1531-1537. Available at http://www.ncbi.nlm.nih.gov/pubmed/7485666.
Hagan H, McGough JP, Thiede H, Weiss NS, Hopkins S, Alexander ER. Syringe exchange and risk of infection with hepatitis B and C viruses. Am J Epidemiol. 1999;149(3):203-213. Available at http://www.ncbi.nlm.nih.gov/pubmed/9927214.
Vlahov D, Junge B, Brookmeyer R, et al. Reductions in high-risk drug use behaviors among participants in the Baltimore needle exchange program. J Acquir Immune Defic Syndr Hum Retrovirol. 1997;16(5):400-406. Available at http://www.ncbi.nlm.nih.gov/pubmed/9420320.
Centers for Disease C, Prevention. Sexual transmission of hepatitis C virus among HIV-infected men who have sex with men--New York City, 2005-2010. MMWR. Morbidity and mortality weekly report. 2011;60(28):945-950. Available at http://www.ncbi.nlm.nih.gov/pubmed/21775948.
Lambers FA, Brinkman K, Schinkel J, et al. Treatment of acute hepatitis C virus infection in HIV-infected MSM: the effect of treatment duration. AIDS. 2011;25(10):1333-1336. Available at http://www.ncbi.nlm.nih.gov/pubmed/21516025.
Piroth L, Larsen C, Binquet C, et al. Treatment of acute hepatitis C in human immunodeficiency virus-infected patients: the HEPAIG study. Hepatology. 2010;52(6):1915-1921. Available at http://www.ncbi.nlm.nih.gov/pubmed/21064156.
Grebely J, Petoumenos K, Hellard M, et al. Potential role for interleukin-28B genotype in treatment decision-making in recent hepatitis C virus infection. Hepatology. 2010;52(4):1216-1224. Available at http://www.ncbi.nlm.nih.gov/pubmed/20803561.
Wiley TE, McCarthy M, Breidi L, McCarthy M, Layden TJ. Impact of alcohol on the histological and clinical progression of hepatitis C infection. Hepatology. 1998;28(3):805-809. Available at http://www.ncbi.nlm.nih.gov/pubmed/9731576.
Forns X, Bruix J. Treating hepatitis C in patients with cirrhosis: the effort is worth it. J Hepatol. 2010;52(5):624-626. Available at http://www.ncbi.nlm.nih.gov/pubmed/20334945.
Panel on Antiretroviral Guidelines for Adults and Adolescents. Guidelines for the use of antiretroviral agents in HIV-1-infected adults and adolescents. Department of Health and Human Services. Available at https://aidsinfo.nih.gov/ContentFiles/lvguidelines/AdultandAdolescentGL.pdf. Accessed June 1, 2012
ACOG educational bulletin. Viral hepatitis in pregnancy. Number 248, July 1998 (replaces No. 174, November 1992). American College of Obstetricians and Gynecologists. Int J Gynaecol Obstet. 1998;63(2):195-202. Available at http://www.ncbi.nlm.nih.gov/pubmed/9856330.
Boskovic R, Wide R, Wolpin J, Bauer DJ, Koren G. The reproductive effects of beta interferon therapy in pregnancy: a longitudinal cohort. Neurology. 2005;65(6):807-811. Available at http://www.ncbi.nlm.nih.gov/pubmed/16186517.
Hegenbarth K, Maurer U, Kroisel PM, Fickert P, Trauner M, Stauber RE. No evidence for mutagenic effects of ribavirin: report of two normal pregnancies. The American Journal of Gastroenterology. 2001;96(7):2286-2287. Available at http://www.ncbi.nlm.nih.gov/pubmed/11467687.
Ghamar Chehreh ME, Tabatabaei SV, Khazanehdari S, Alavian SM. Effect of cesarean section on the risk of perinatal transmission of hepatitis C virus from HCV-RNA+/HIV- mothers: a meta-analysis. Arch Gynecol Obstet. 2011;283(2):255-260. Available at http://www.ncbi.nlm.nih.gov/pubmed/20652289.
Marine-Barjoan E, Berrebi A, Giordanengo V, et al. HCV/HIV co-infection, HCV viral load and mode of delivery: risk factors for mother-to-child transmission of hepatitis C virus? AIDS. 2007;21(13):1811-1815. Available at http://www.ncbi.nlm.nih.gov/pubmed/17690581.
European Paediatric Hepatitis CVN. A significant sex--but not elective cesarean section--effect on mother-to-child transmission of hepatitis C virus infection. J Infect Dis. 2005;192(11):1872-1879. Available at http://www.ncbi.nlm.nih.gov/pubmed/16267757.
Read JS, Tuomala R, Kpamegan E, et al. Mode of delivery and postpartum morbidity among HIV-infected women: the women and infants transmission study. J Acquir Immune Defic Syndr. 2001;26(3):236-245. Available at http://www.ncbi.nlm.nih.gov/pubmed/11242196.
Grubert TA, Reindell D, Kastner R, et al. Rates of postoperative complications among human immunodeficiency virus-infected women who have undergone obstetric and gynecologic surgical procedures. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 2002;34(6):822-830. Available at http://www.ncbi.nlm.nih.gov/pubmed/11850864.
Grubert TA, Reindell D, Kastner R, Lutz-Friedrich R, Belohradsky BH, Dathe O. Complications after caesarean section in HIV-1-infected women not taking antiretroviral treatment. Lancet. 1999;354(9190):1612-1613. Available at http://www.ncbi.nlm.nih.gov/pubmed/10560681.
Fiore S, Newell ML, Thorne C, European HIViOG. Higher rates of post-partum complications in HIV-infected than in uninfected women irrespective of mode of delivery. AIDS. 2004;18(6):933-938. Available at http://www.ncbi.nlm.nih.gov/pubmed/15060441.