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Epidemiology and transmission of hepatitis C virus infection

Epidemiology and transmission of hepatitis C virus infection
Author:
Arthur Y Kim, MD, FIDSA
Section Editor:
Adrian M Di Bisceglie, MD
Deputy Editor:
Allyson Bloom, MD
Literature review current through: Feb 2022. | This topic last updated: Jun 12, 2019.

INTRODUCTION — Chronic hepatitis C virus (HCV) infection is one of the most common chronic liver diseases; in the United States, it accounts for at least 19,000 deaths each year and is the leading underlying etiology for liver transplantation.

This topic will review the epidemiology and transmission of HCV. Screening for HCV, the approach to patients with acute HCV, and the clinical features, diagnosis, natural history, and management of patients with chronic HCV are discussed separately:

(See "Clinical manifestations, diagnosis, and treatment of acute hepatitis C virus infection in adults".)

(See "Screening and diagnosis of chronic hepatitis C virus infection".)

(See "Clinical manifestations and natural history of chronic hepatitis C virus infection".)

(See "Extrahepatic manifestations of hepatitis C virus infection".)

(See "Overview of the management of chronic hepatitis C virus infection".)

(See "Treatment regimens for chronic hepatitis C virus genotype 1 infection in adults".)

(See "Treatment regimens for chronic hepatitis C virus genotypes 2 and 3 infection in adults".)

(See "Hepatitis C virus infection in liver transplant candidates and recipients".)

EPIDEMIOLOGY

Global distribution — The World Health Organization (WHO) estimated that in 2015, approximately 100 million people globally had serologic evidence of HCV exposure and 71 million people had chronic HCV infection (prevalence of 1 percent) (figure 1) [1].

The area with the highest prevalence (>2 percent) was:

Eastern Mediterranean region

Moderate prevalence rates (1 to 2 percent) were noted in:

Africa

European region

Low prevalence rates (<1 percent) were noted in:

Americas

South-East Asian region

Western Pacific region

Within these regions, there are differences in the prevalence of HCV by country; as examples, prevalence is higher in Eastern Europe compared with Western Europe and is higher in West Africa compared with East Africa (figure 1) [2]. Egypt has the highest known prevalence in the world, due to health care-associated transmission [3] (see 'Health care-associated' below). The four countries with the highest burden of cases are China, Pakistan, India, and Egypt because of high overall population, high prevalence, or both [2].

United States

Incidence and prevalence — Although the number of cases of acute HCV infection in the United States has decreased from approximately 230,000 per year in the 1980s, the incidence has fluctuated more recently and remains high. In 2016, there were an estimated 41,200 new HCV infections, representing a fourfold increase since 2005 (figure 2) [4]. This estimate was adjusted for case ascertainment and under-reporting, although it may still underestimate the actual incidence of acute HCV infection given the difficulties in diagnosis and narrow national case definitions [5].

Specifically, HCV infection rates have increased substantially among young adults over the past decade [6,7]. In one surveillance study, the incidence of acute HCV infection in young adults rose faster in nonurban than urban counties, and the majority of infected individuals were White (85 percent) with an even sex distribution [6]. These trends likely reflect the epidemic of opioid and injection drug use in the United States. The number of cases of transfusion-associated acute HCV infection decreased significantly after 1985 and has been reduced almost to zero [8]. Thus, transfusion-associated hepatitis has had little impact on the recent change in the incidence of HCV infection.

The prevalence of chronic HCV infection in the United States has been estimated by analyses of the National Health and Nutrition Examination Survey (NHANES), in which participants, chosen according to an algorithm to produce a representative sample of the noninstitutionalized population of the United States, are tested for antibodies to HCV and viral RNA if positive [9,10]. Between 2013 and 2016, the estimated prevalence of antibodies to HCV was 1.5 percent (reflecting an approximate 3.7 million people with past or current HCV infection), and the estimated prevalence of HCV RNA positivity was 0.9 percent (reflecting approximately 2 million people with current HCV infection) [10,11]. The peak prevalence was observed among individuals born between 1945 and 1965, although subsequent studies have suggested that the prevalence in younger individuals may be surpassing that [7]. (See 'Characteristics associated with infection' below.)

One major limitation of the using the NHANES data to extrapolate HCV prevalence is that they do not include individuals who are homeless or incarcerated and thus underestimate the overall prevalence [12]. Based on other surveys, it is estimated that 16 to 41 percent of adult prison inmates have serologic evidence of HCV infection, and that 12 to 35 percent are chronically infected [13,14].

Characteristics associated with infection — Injection drug use is the most important risk factor for HCV acquisition in the United States. As an example, the increasing incidence of HCV infections among young individuals in various urban, suburban, and rural settings has mirrored the epidemic of injection prescription opioid and subsequently heroin use in these areas [15-17]. (See 'Injection drug use' below and "Opioid use disorder: Epidemiology, pharmacology, clinical manifestations, course, screening, assessment, and diagnosis".)

Historically, birth between 1945 and 1965 has been associated with HCV infection in the United States. In an NHANES survey from 2003 to 2010, approximately 80 percent of patients with chronic HCV in the United States were born between 1945 and 1965; the prevalence of HCV among this group was 2.6 percent, which was sixfold the prevalence among all other adults [18]. This observation was the rationale for the recommendation by the United States Centers for Disease Control and Prevention (CDC) and the US Preventive Services Task Force to routinely screen all patients in this baby boomer birth cohort for HCV [19]. (See "Screening and diagnosis of chronic hepatitis C virus infection", section on 'Limitations of birth-cohort screening'.)

Other characteristics associated with chronic HCV infection include male sex, being of a non-Hispanic Black population, low income, high school education or less, a history of incarceration, marginal housing, and a history of at least 10 lifetime sexual partners.

Clinical consequences — Most cases of acute HCV infection are anicteric and asymptomatic, with fewer than 25 percent being clinically apparent. Fulminant hepatitis C is rare. Of those who go on to have chronic infection, a substantial proportion will develop cirrhosis, and a subset of those develop hepatocellular carcinoma. These are discussed in more detail elsewhere. (See "Clinical manifestations and natural history of chronic hepatitis C virus infection" and "Epidemiology and risk factors for hepatocellular carcinoma".)

Costs — In 2013, the total cost of chronic HCV in the United States was estimated at $6.5 billion that year and projected to peak in 2024 at $9.1 billion [20]. The majority of the peak costs were related to cirrhosis (66 percent) and hepatocellular carcinoma (16 percent). The lifetime cost of an individual infected with HCV in 2011 was estimated at $64,490.

TRANSMISSION — Most patients infected with HCV in the United States and Europe acquired the disease through intravenous drug use or blood transfusion, the latter of which has become rare since routine testing of the blood supply for HCV was begun in 1990 (see 'Blood transfusion' below). Other types of parenteral exposure are important in specific regions in the world [3].

Data from the early 1990s indicated that no identifiable risk factors for HCV infection during the previous six months could be identified in up to 44 percent of cases with new infections [21]. This rate was similar to that seen with acute hepatitis A or B infection. However, after careful questioning, most of these patients give a past history of high-risk behavior (such as injection drug use), and many are from low socioeconomic strata, which is known to be associated with a greater risk of hepatitis. Some of these risk factors were elucidated in a case control study from the United States involving 2316 HCV positive blood donors in whom the following HCV risk factors were identified [22]:

Intravenous drug use – odds ratio 49.6

Blood transfusion – odds ratio 10.9

Sex with an intravenous drug user – odds ratio 6.3

Having been in jail more than three days – odds ratio 2.9

Religious scarification – odds ratio 2.8

Having been struck or cut with a bloody object – odds ratio 2.1

Pierced ears or body parts – odds ratio 2.0

Immunoglobulin injection – odds ratio 1.6

Injection drug use — Parenteral exposure to the hepatitis C virus is the most efficient means of transmission. Viable virus has been recovered from the inside of syringes up to nine weeks after contamination [23]. Thus, it is not surprising that injection drug use with shared needles or other paraphernalia has been the most common identifiable source of acute HCV infection (figure 3). Worldwide, 25 countries have reported that 60 to 80 percent of injection drug users have reactive anti-HCV antibody; in 12 countries, the prevalence is over 80 percent [24].

The efficiency of transmission via this route is evidenced by the high rate of anti-HCV antibodies observed in short-term injectors and outbreaks of HCV among injection drug users. As an example, in a systematic review, the mean prevalence of anti-HCV reactivity after one year of injection drug use was 32 percent in resource-rich settings and 59 percent in resource-limited settings [25]. The prevalence estimated from studies in resource-rich settings prior to 1995 was higher and comparable with that from resource-limited settings; the subsequent decrease likely reflects public health efforts to stem transmission, such as needle and syringe exchanges. As an example, in one meta-analysis of predominantly observational studies, opioid agonist therapy was associated with a 50 percent reduction of HCV incidence alone and a 74 percent reduction when combined with high coverage of needle and syringe exchanges [26]. Without preventive measures, widespread transmission of HCV can occur rapidly within injection drug communities, as reflected by publicized outbreaks of HIV and HCV among over 100 prescription opioid injectors in a small rural county in the Midwestern United States and in an urban area in the Northeast [27,28].

HCV infection also has been associated with a history of intranasal drug use, presumably due to blood on shared straws [29,30].

Blood transfusion — Blood transfusion was a major risk factor for acute infection in the past, with more than 10 percent of transfusion recipients acquiring infection in some studies [31]. The screening of blood donors for historical risk factors, serologic evidence of hepatitis B infection (HBsAg and anti-HBc), and elevated serum ALT caused a striking reduction in the rates of non-A, non-B post-transfusion hepatitis, even before HCV was identified (figure 4). The subsequent initiation of donor screening for anti-HCV antibodies in 1990 has nearly eliminated the risk of post-transfusion acute HCV infection. The estimated risk is now less than one in a million per unit transfused [32].

In the spring of 1999, another blood donor HCV testing technology, nucleic acid testing (NAT), was introduced [33]. This technology, which detects HCV genetic material rather than later-appearing antibodies, has further decreased the risk of transfusion-transmitted HCV to less than one per million. As a result, a history of blood product transfusion is much more common in patients presenting with chronic HCV (remote infection) than with acute infection. (See "Blood donor screening: Laboratory testing", section on 'Hepatitis C virus'.)

Multiply transfused patients, including those with thalassemia or hemophilia, have been at particularly high risk of developing hepatitis C. The prevalence of anti-HCV in hemophiliacs who regularly received concentrates of clotting factors before adequate procedures were used to inactivate viruses (eg, heat inactivation or pasteurization) was 84 to 100 percent [34]. Since the use of treated or recombinant clotting factors has become routine, new cases of hepatitis C infection have become uncommon in these patients. The continued high prevalence of anti-HCV in this population is due to past exposure to untreated concentrates [34,35].

Health care workers — Issues related to HCV in health care workers are presented separately. (See "Prevention of hepatitis B virus and hepatitis C virus infection among health care providers".)

Health care-associated — Nosocomial transmission of HCV has been documented in several health care settings [36-38]. A study from Spain suggested that hospitalization itself was an important cause of acute HCV infection [36]. Hospitalization was believed to account for 73 of 109 cases (67 percent) of acute HCV cases documented in 18 Spanish hospitals, which accounted for more cases than intravenous drug use (8 percent), needle stick injury (6 percent), and sexual contact (5 percent). Of these patients, 33 had undergone surgery, 24 were admitted to a medical emergency unit or ward, and the remaining had undergone diagnostic or therapeutic procedures. In another study from Spain, hospitalization for longer than 10 days in a liver unit was associated with an increased risk of HCV transmission from infected patients (typically roommates) [39].

In the United States, where there are stringent infection control protocols to prevent transmission, particularly through unsafe medication injection practices, nosocomial transmission has still been reported, generally because of breaches in protocol. Rare sources of transmission of HCV include contaminated equipment used during the performance of procedures and other breakdowns of infection control procedures or aseptic techniques leading to person-to-person transmission [40-48]. As an example, an outbreak of acute HCV was identified in three hospitalized patients who received saline flushes from a multidose saline vial [42]. Another outbreak of six cases of HCV (along with six cases of hepatitis B) was linked to the inappropriate reuse of syringes and single-patient-use vials of propofol by a single anesthesiologist [47]. Other cases of nosocomial transmission or outbreaks are associated with health care personnel tampering with (diverting, self-injecting, and substituting) injectable opioids intended for medical use [49]. In one outbreak, 32 HCV infections were linked to drug diversion by a technician in a cardiac catheterization laboratory [50].

Organ transplantation — Transplant recipients who receive organs from HCV-positive donors have a high risk of acquiring HCV infection and liver disease [51-53]. Some studies have shown nearly universal transmission; in one report, 75 percent of the 29 recipients of organs (19 kidneys, 6 hearts, 4 livers) from 13 anti-HCV positive donors became anti-HCV or HCV-RNA positive [51]. Others have not found quite as strong an association; only 13 of 46 (29 percent) recipients of RIBA-positive donors developed post-transplant liver disease in a second series, although HCV-RNA was not checked [53].

The potential to successfully treat HCV infection acquired through organ donation with direct-acting antiviral regimens is changing the approach to utilization of organs from HCV-infected donors. (See "Kidney transplantation in adults: Hepatitis C virus infection in kidney donors" and "Kidney transplantation in adults: Hepatitis C infection in kidney transplant candidates and recipients".)

Sexual or household contact — The efficiency of HCV transmission by sexual or household contact is low. The majority of the data does not support transmission to nonsexual partners [54-56].

Sexual transmission of HCV can occur, although the risk appears to be low [57-60]. The seroprevalence of anti-HCV is increased among heterosexuals with many partners and men who have sex with men (MSM), groups which serve as an epidemiologic barometer of sexual transmission risk [60-62]. The risk of transmission from index cases who are not infected with HIV appears to be similar among straight and gay partners. Among MSM, rectal shedding of HCV in infected individuals has been reported and certain sexual practices may carry a higher risk of transmission [60,63,64]. In a study of 5310 MSM followed for a median of seven years, unprotected receptive anal sex with more than one partner was independently associated with incident HCV infection among both HIV-infected and uninfected participants, whereas unprotected insertive anal sex with multiple partners was not [63].

The risk of transmission of HCV infection between monogamous sexual partners has been difficult to demonstrate in prospective studies. One of the largest studies to examine rates of transmission in detail (reported in preliminary form) focused on 500 monogamous, heterosexual couples who had had sexual contact for a median of 15 years [56]. Only 17 percent reported regular or frequent use of condoms. A total of 20 partners (4 percent) had HCV antibodies. However, 40 percent of these patients had discordant genotypes/serotypes suggesting that they had acquired HCV through other routes of transmission. In addition, of those with concordant genotypes, phylogenetic evaluation found that the viral isolates from both members of the couple were highly related in three of the couples (0.6 percent of the total population studied), consistent with transmission of the virus within the couple. The overall incidence of HCV transmission by sex was estimated to be 0.07 percent per year.

Another large, prospective study included 895 monogamous, heterosexual partners of HCV infected individuals who were followed for 10 years [59]. The average weekly rate of sexual intercourse was 1.8. All couples denied practicing anal intercourse, having sex during menstruation, or use of condoms. During follow-up, three patients developed HCV infection; however, molecular analysis showed that none had acquired it from their spouse.

Other, retrospective studies estimate the likelihood of transmission under these circumstances to be approximately 0.1 percent annually [55]. A potential mechanism of nonsexual transmission in these instances is mucosal exposure to infectious blood or to body fluids containing blood, or unapparent percutaneous exposure through personal hygiene items (eg, shared razors or toothbrushes). In many situations, it is difficult to rule out the possibility that transmission resulted from common exposure to risk factors other than sexual exposure [65].

The risk of sexual transmission may be higher if the index case is coinfected with HIV [60]. In one report, for example, the anti-HCV prevalence in stable heterosexual partners of HCV-positive/HIV-positive index cases was 2.2 times higher than in stable heterosexual partners of index cases reactive for anti-HCV only (9.2 versus 4.1 percent) [62]. Other factors associated with anti-HCV positivity included greater numbers of sexual partners, history of sexually transmitted diseases, and failure to use a condom. (See "Epidemiology, natural history, and diagnosis of hepatitis C in patients with HIV".)

Patients with acute or chronic HCV infection should be advised that transmission to sexual or household contacts is a possibility, although the risk is relatively low. It is likely that the use of condoms will lower the risk of sexual transmission further, similar to the case with hepatitis B virus and HIV. However, the United States Public Health Service and a consensus statement issued by the National Institutes of Health have not recommended barrier precautions between stable monogamous sexual partners.

Perinatal transmission — Perinatal transmission of HCV occurs at the time of birth in about 5 to 6 percent of infants born to anti-HCV positive women [66,67]. The risk of infection is approximately twofold higher in infants born to women coinfected with HCV and HIV [68]. Transmission occurs almost exclusively from mothers who are HCV-RNA positive (as opposed to those who are anti-HCV positive but HCV-RNA negative) [69]. As an increasing number of women of childbearing age in the United States are infected with HCV due to the opioid epidemic, an estimated 1700 infants are predicted to be infected annually [7]. The risk of perinatal HCV infection is discussed in detail elsewhere. (See "Vertical transmission of hepatitis C virus".)

Hemodialysis — HCV infection is more common among patients on dialysis than in the general population. Although the incidence of HCV infection has been declining among dialysis patients, the relatively high incidence of anti-HCV seropositivity in this population remains a concern and intermittent outbreaks in dialysis units continue to occur [70]. A number of risk factors have been identified for HCV infection among dialysis patients, including blood transfusions, the duration of end-stage kidney disease (and dialysis), the type of dialysis (risk is highest with in-hospital hemodialysis and lowest with peritoneal dialysis), and the prevalence of HCV infection in the dialysis unit. HCV infection among patients on dialysis is discussed in detail elsewhere. (See "Hepatitis C virus infection in patients on maintenance dialysis".)

Other — Procedures involved in traditional medicine, folk medicine (eg, scarification, cupping), tattooing, body piercing, and commercial barbering may also transmit HCV on rare occasions.

Tattooing and body piercing have the potential to transmit HCV. However, the extent to which they contribute to the disease burden of HCV is uncertain. In a case-control study that utilized questionnaires to assess risk factors for infection, having one or more tattoos was more common among 1930 HCV infected compared with 1941 HCV uninfected participants (35 versus 13 percent) [71]. A history of tattoo receipt was associated with HCV infection even after adjustment for age, race, sex, and other behaviors associated with transmission (OR 3.7 95% CI 3.0-4.7) and exclusion of patients with a history of intravenous drug use or transfusion (OR 3.8, 95% CI 3.0-4.9). It remains unknown whether the transmission risk is from the tattooing itself or from some other associated risk not accounted for or reported on the questionnaire.

Surprisingly high rates of HCV infection (approximately 30 percent) have been found in patients with alcohol abuse, even in the absence of other risk factors for infection [72-74]. HCV may accelerate the liver injury in patients who drink heavily [75], alcohol use appears to decrease the efficacy of interferon therapy for HCV [76], and patients with alcohol and HCV-induced liver injury have a greater risk for hepatocellular carcinoma [77,78]. (See "Hepatitis C and alcohol".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Hepatitis C virus infection".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topic (see "Patient education: Hepatitis C (The Basics)")

Beyond the Basics topic (see "Patient education: Hepatitis C (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

The global prevalence of chronic hepatitis C virus (HCV) infection, as reflected by anti-HCV antibody positivity, is approximately 1 percent. Areas with relatively high prevalence include the Eastern Mediterranean region, West Africa, and Eastern Europe (figure 1). (See 'Global distribution' above.)

The prevalence of antibodies to hepatitis C virus (anti-HCV) in the United States is approximately 1.3 percent (reflecting an approximate 3.6 million people with past or current HCV infection), while the prevalence of positive HCV RNA is approximately 1.0 percent (reflecting an approximate 2.7 million people with chronic HCV infection). The peak prevalence has been observed among persons born between 1945 and 1965, although the prevalence among younger individuals is increasing.

As a result of the opioid epidemic, HCV incidence has risen, with increasing numbers of acute cases reported. Since an increasing number of women of childbearing age are infected with HCV, more infants are being exposed. (See 'United States' above.)

Multiple risk factors for the transmission of HCV have been identified. (See 'Transmission' above.)

Intravenous drug use

Receipt of blood-derived products before routine screening of donors or blood supply

Health care exposures in the setting of suboptimal infection control practices

Organ transplantation from a donor with HCV viremia

Sexual transmission, particularly among men with HIV infection who have sex with men

Perinatal exposure to a mother with HCV viremia

Hemodialysis

Procedures such as scarification, tattooing, body piercing, and commercial barbering with suboptimal infection control practices

These risk factors for transmission define target populations for screening and testing. (See "Screening and diagnosis of chronic hepatitis C virus infection".)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Sanjiv Chopra, MD, MACP, who contributed to an earlier version of this topic review.

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  53. Roth D, Zucker K, Cirocco R, et al. The impact of hepatitis C virus infection on renal allograft recipients. Kidney Int 1994; 45:238.
  54. Everhart JE, Di Bisceglie AM, Murray LM, et al. Risk for non-A, non-B (type C) hepatitis through sexual or household contact with chronic carriers. Ann Intern Med 1990; 112:544.
  55. Dienstag JL. Sexual and perinatal transmission of hepatitis C. Hepatology 1997; 26:66S.
  56. Terrault NA, Dodge JL, Murphy EL, et al. Sexual transmission of hepatitis C virus among monogamous heterosexual couples: the HCV partners study. Hepatology 2013; 57:881.
  57. Alter MJ, Coleman PJ, Alexander WJ, et al. Importance of heterosexual activity in the transmission of hepatitis B and non-A, non-B hepatitis. JAMA 1989; 262:1201.
  58. Stroffolini T, Lorenzoni U, Menniti-Ippolito F, et al. Hepatitis C virus infection in spouses: sexual transmission or common exposure to the same risk factors? Am J Gastroenterol 2001; 96:3138.
  59. Vandelli C, Renzo F, Romanò L, et al. Lack of evidence of sexual transmission of hepatitis C among monogamous couples: results of a 10-year prospective follow-up study. Am J Gastroenterol 2004; 99:855.
  60. Tohme RA, Holmberg SD. Is sexual contact a major mode of hepatitis C virus transmission? Hepatology 2010; 52:1497.
  61. Alter MJ, Kruszon-Moran D, Nainan OV, et al. The prevalence of hepatitis C virus infection in the United States, 1988 through 1994. N Engl J Med 1999; 341:556.
  62. 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; 12:827.
  63. Witt MD, Seaberg EC, Darilay A, et al. Incident hepatitis C virus infection in men who have sex with men: a prospective cohort analysis, 1984-2011. Clin Infect Dis 2013; 57:77.
  64. Foster AL, Gaisa MM, Hijdra RM, et al. Shedding of Hepatitis C Virus Into the Rectum of HIV-infected Men Who Have Sex With Men. Clin Infect Dis 2017; 64:284.
  65. Zylberberg H, Thiers V, Lagorce D, et al. Epidemiological and virological analysis of couples infected with hepatitis C virus. Gut 1999; 45:112.
  66. 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. N Engl J Med 1994; 330:744.
  67. Benova L, Mohamoud YA, Calvert C, Abu-Raddad LJ. Vertical transmission of hepatitis C virus: systematic review and meta-analysis. Clin Infect Dis 2014; 59:765.
  68. Zanetti AR, Tanzi E, Paccagnini S, et al. Mother-to-infant transmission of hepatitis C virus. Lombardy Study Group on Vertical HCV Transmission. Lancet 1995; 345:289.
  69. Resti M, Azzari C, Mannelli F, et al. Mother to child transmission of hepatitis C virus: prospective study of risk factors and timing of infection in children born to women seronegative for HIV-1. Tuscany Study Group on Hepatitis C Virus Infection. BMJ 1998; 317:437.
  70. Fabrizi F, Messa P. Transmission of hepatitis C virus in dialysis units: a systematic review of reports on outbreaks. Int J Artif Organs 2015; 38:471.
  71. Carney K, Dhalla S, Aytaman A, et al. Association of tattooing and hepatitis C virus infection: a multicenter case-control study. Hepatology 2013; 57:2117.
  72. Haley RW, Fischer RP. Commercial tattooing as a potentially important source of hepatitis C infection. Clinical epidemiology of 626 consecutive patients unaware of their hepatitis C serologic status. Medicine (Baltimore) 2001; 80:134.
  73. Parés A, Barrera JM, Caballería J, et al. Hepatitis C virus antibodies in chronic alcoholic patients: association with severity of liver injury. Hepatology 1990; 12:1295.
  74. Mendenhall CL, Moritz T, Rouster S, et al. Epidemiology of hepatitis C among veterans with alcoholic liver disease. The VA Cooperative Study Group 275. Am J Gastroenterol 1993; 88:1022.
  75. Koff RS, Dienstag JL. Extrahepatic manifestations of hepatitis C and the association with alcoholic liver disease. Semin Liver Dis 1995; 15:101.
  76. Okazaki T, Yoshihara H, Suzuki K, et al. Efficacy of interferon therapy in patients with chronic hepatitis C. Comparison between non-drinkers and drinkers. Scand J Gastroenterol 1994; 29:1039.
  77. Nalpas B, Driss F, Pol S, et al. Association between HCV and HBV infection in hepatocellular carcinoma and alcoholic liver disease. J Hepatol 1991; 12:70.
  78. Bruix J, Barrera JM, Calvet X, et al. Prevalence of antibodies to hepatitis C virus in Spanish patients with hepatocellular carcinoma and hepatic cirrhosis. Lancet 1989; 2:1004.
Topic 3675 Version 37.0

References

1 : World Health Organization. Web Annex B. WHO estimates of the prevalence and incidence of hepatitis C virus infection by WHO region, 2015. In: Global hepatitis report 2017. https://apps.who.int/iris/bitstream/handle/10665/277005/WHO-CDS-HIV-18.46-eng.pdf (Accessed on May 21, 2019).

2 : Global prevalence and genotype distribution of hepatitis C virus infection in 2015: a modelling study.

3 : The role of parenteral antischistosomal therapy in the spread of hepatitis C virus in Egypt.

4 : The role of parenteral antischistosomal therapy in the spread of hepatitis C virus in Egypt.

5 : Underascertainment of acute hepatitis C virus infections in the U.S. surveillance system: a case series and chart review.

6 : Emerging epidemic of hepatitis C virus infections among young nonurban persons who inject drugs in the United States, 2006-2012.

7 : Hepatitis C Virus Infection Among Reproductive-Aged Women and Children in the United States, 2006 to 2014.

8 : Epidemiology of hepatitis C.

9 : The prevalence of hepatitis C virus infection in the United States, 1999 through 2002.

10 : Estimating Prevalence of Hepatitis C Virus Infection in the United States, 2013-2016.

11 : Prevalence of Hepatitis C Virus Infection in US States and the District of Columbia, 2013 to 2016.

12 : Toward a more accurate estimate of the prevalence of hepatitis C in the United States.

13 : Prevention and control of infections with hepatitis viruses in correctional settings. Centers for Disease Control and Prevention.

14 : Letter to the Editor: Hepatitis C Virus Prevalence Estimates Among Incarcerated Persons.

15 : Increases in hepatitis C virus infection related to injection drug use among persons aged≤30 years - Kentucky, Tennessee, Virginia, and West Virginia, 2006-2012.

16 : Notes from the field: risk factors for hepatitis C virus infections among young adults--Massachusetts, 2010.

17 : Notes from the field : hepatitis C virus infections among young adults--rural Wisconsin, 2010.

18 : Chronic hepatitis C virus infection in the United States, National Health and Nutrition Examination Survey 2003 to 2010.

19 : Previous exposure to HCV among persons born during 1945-1965: prevalence and predictors, United States, 1999-2008.

20 : Chronic hepatitis C virus (HCV) disease burden and cost in the United States.

21 : Sporadic non-A, non-B hepatitis: frequency and epidemiology in an urban U.S. population.

22 : Risk factors for hepatitis C virus infection in United States blood donors. NHLBI Retrovirus Epidemiology Donor Study (REDS)

23 : Survival of hepatitis C virus in syringes: implication for transmission among injection drug users.

24 : Global epidemiology of hepatitis B and hepatitis C in people who inject drugs: results of systematic reviews.

25 : Meta-regression of hepatitis C virus infection in relation to time since onset of illicit drug injection: the influence of time and place.

26 : Needle syringe programmes and opioid substitution therapy for preventing hepatitis C transmission in people who inject drugs.

27 : Community Outbreak of HIV Infection Linked to Injection Drug Use of Oxymorphone--Indiana, 2015.

28 : Notes from the Field: HIV Diagnoses Among Persons Who Inject Drugs - Northeastern Massachusetts, 2015-2018.

29 : Intranasal transmission of hepatitis C virus: virological and clinical evidence.

30 : Sharing of Snorting Straws and Hepatitis C Virus Infection in Pregnant Women.

31 : Detection of antibody to hepatitis C virus in prospectively followed transfusion recipients with acute and chronic non-A, non-B hepatitis.

32 : Risks of transfusion-transmitted infections: 2003.

33 : NAT screening of blood and plasma donations: evolution of technology and regulatory policy.

34 : Hepatitis C infection and viremia in Dutch hemophilia patients.

35 : A multicenter study of viral hepatitis in a United States hemophilic population.

36 : Hospital admission is a relevant source of hepatitis C virus acquisition in Spain.

37 : Healthcare should not be a vehicle for transmission of hepatitis C virus.

38 : Case-control study of hepatitis B and hepatitis C in older adults: Do healthcare exposures contribute to burden of new infections?

39 : Nosocomial transmission of HCV in the liver unit of a tertiary care center.

40 : National surveillance of dialysis-associated diseases in the United States, 1989.

41 : Nosocomial transmission of hepatitis C virus from an anesthesiologist to three patients--epidemiologic and molecular evidence.

42 : Nosocomial transmission of hepatitis C virus associated with the use of multidose saline vials.

43 : Nosocomial transmission of hepatitis C virus.

44 : Nonhospital health care-associated hepatitis B and C virus transmission: United States, 1998-2008.

45 : Epidemiologic and molecular investigation of outbreaks of hepatitis C virus infection on a pediatric oncology service.

46 : Transmission of hepatitis C virus in a gynecological surgery setting.

47 : Multiple clusters of hepatitis virus infections associated with anesthesia for outpatient endoscopy procedures.

48 : Transmission of hepatitis C virus associated with surgical procedures - New Jersey 2010 and Wisconsin 2011.

49 : Nosocomial hepatitis C virus transmission from tampering with injectable anesthetic opioids.

50 : Large Outbreak of Hepatitis C Virus Associated With Drug Diversion by a Healthcare Technician.

51 : Transmission of hepatitis C virus by organ transplantation.

52 : Hepatitis C transmission and infection by orthotopic heart transplantation.

53 : The impact of hepatitis C virus infection on renal allograft recipients.

54 : Risk for non-A, non-B (type C) hepatitis through sexual or household contact with chronic carriers.

55 : Sexual and perinatal transmission of hepatitis C.

56 : Sexual transmission of hepatitis C virus among monogamous heterosexual couples: the HCV partners study.

57 : Importance of heterosexual activity in the transmission of hepatitis B and non-A, non-B hepatitis.

58 : Hepatitis C virus infection in spouses: sexual transmission or common exposure to the same risk factors?

59 : Lack of evidence of sexual transmission of hepatitis C among monogamous couples: results of a 10-year prospective follow-up study.

60 : Is sexual contact a major mode of hepatitis C virus transmission?

61 : The prevalence of hepatitis C virus infection in the United States, 1988 through 1994.

62 : Hepatitis C virus infection among sexually promiscuous groups and the heterosexual partners of hepatitis C virus infected index cases.

63 : Incident hepatitis C virus infection in men who have sex with men: a prospective cohort analysis, 1984-2011.

64 : Shedding of Hepatitis C Virus Into the Rectum of HIV-infected Men Who Have Sex With Men.

65 : Epidemiological and virological analysis of couples infected with hepatitis C virus.

66 : Transmission of hepatitis C virus from mothers to infants. The Vertical Transmission of Hepatitis C Virus Collaborative Study Group.

67 : Vertical transmission of hepatitis C virus: systematic review and meta-analysis.

68 : Mother-to-infant transmission of hepatitis C virus. Lombardy Study Group on Vertical HCV Transmission.

69 : Mother to child transmission of hepatitis C virus: prospective study of risk factors and timing of infection in children born to women seronegative for HIV-1. Tuscany Study Group on Hepatitis C Virus Infection.

70 : Transmission of hepatitis C virus in dialysis units: a systematic review of reports on outbreaks.

71 : Association of tattooing and hepatitis C virus infection: a multicenter case-control study.

72 : Commercial tattooing as a potentially important source of hepatitis C infection. Clinical epidemiology of 626 consecutive patients unaware of their hepatitis C serologic status.

73 : Hepatitis C virus antibodies in chronic alcoholic patients: association with severity of liver injury.

74 : Epidemiology of hepatitis C among veterans with alcoholic liver disease. The VA Cooperative Study Group 275.

75 : Extrahepatic manifestations of hepatitis C and the association with alcoholic liver disease.

76 : Efficacy of interferon therapy in patients with chronic hepatitis C. Comparison between non-drinkers and drinkers.

77 : Association between HCV and HBV infection in hepatocellular carcinoma and alcoholic liver disease.

78 : Prevalence of antibodies to hepatitis C virus in Spanish patients with hepatocellular carcinoma and hepatic cirrhosis.