Hepatitis C - Wikipedia

Human viral infection Medical condition

Hepatitis C
Electron micrograph of hepatitis C virus from cell culture (scale = 50 nanometers)
Specialty	Gastroenterology, infectious disease
Symptoms	Typically none[1]
Complications	Liver failure, liver cancer, esophageal and gastric varices[2]
Duration	Long term (80%)[1]
Causes	Hepatitis C virus usually spread by blood-to-blood contact[1][3]
Diagnostic method	Blood testing for antibodies or viral RNA[1]
Prevention	Sterile needles, testing donated blood[4]
Treatment	Medications, liver transplant[5]
Medication	Antivirals (sofosbuvir, simeprevir, others)[1][4]
Frequency	58 million (2019)[4]
Deaths	290,000 (2019)[4]

Hepatitis C is an infectious disease caused by the hepatitis C virus (HCV) that primarily affects the liver;[2] it is a type of viral hepatitis.[6] During the initial infection period, people often have mild or no symptoms.[1] Early symptoms can include fever, dark urine, abdominal pain, and yellow tinged skin.[1] The virus persists in the liver, becoming chronic, in about 70% of those initially infected.[4] Early on, chronic infection typically has no symptoms.[1] Over many years however, it often leads to liver disease and occasionally cirrhosis.[1] In some cases, those with cirrhosis will develop serious complications such as liver failure, liver cancer, or dilated blood vessels in the esophagus and stomach.[2]

HCV is spread primarily by blood-to-blood contact associated with injection drug use, poorly sterilized medical equipment, needlestick injuries in healthcare, and transfusions.[1][3] In regions where blood screening has been implemented, the risk of contracting HCV from a transfusion has dropped substantially to less than one per two million.[1] HCV may also be spread from an infected mother to her baby during birth.[1] It is not spread through breast milk, food, water or casual contact such as hugging, kissing and sharing food or drinks with an infected person.[4] It is one of five known hepatitis viruses: A, B, C, D, and E.[7] Diagnosis is by blood testing to look for either antibodies to the virus or viral RNA.[1] In the United States, screening for HCV infection is recommended in all adults age 18 to 79 years old.[8] There is no vaccine against hepatitis C.[1][9] Prevention includes harm reduction efforts among people who inject drugs, testing donated blood, and treatment of people with chronic infection.[4][10] Chronic infection can be cured more than 95% of the time with antiviral medications such as sofosbuvir or simeprevir.[1][4] Peginterferon and ribavirin were earlier generation treatments that proved successful in <50% of cases and caused greater side effects.[4]: 2015 version [11] While access to the newer treatments was expensive, by 2022 prices had dropped dramatically in many countries (primarily low-income and lower-middle-income countries) due to the introduction of generic versions of medicines.[4] Those who develop cirrhosis or liver cancer may require a liver transplant.[5] Hepatitis C is one of the leading reasons for liver transplantation, though the virus usually recurs after transplantation.[5]

An estimated 58 million people worldwide were infected with hepatitis C in 2019. Approximately 290,000 deaths from the virus, mainly from liver cancer and cirrhosis attributed to hepatitis C, also occurred in 2019.[12] The existence of hepatitis C – originally identifiable only as a type of non-A non-B hepatitis – was suggested in the 1970s and proven in 1989.[13] Hepatitis C infects only humans and chimpanzees.[14]

Signs and symptoms

[edit]

Acute infection

[edit]

Acute symptoms develop in some 20% of those infected.[4][1] When this occurs, it is generally 4–12 weeks following infection (but it may take from 2 weeks to 6 months for acute symptoms to appear).[1][4]

Symptoms are generally mild and vague, and may include fatigue, nausea and vomiting, fever, muscle or joint pains, abdominal pain, decreased appetite and weight loss, jaundice (occurs in ~25% of those infected), dark urine, and clay-coloured stools.[1][15][16] Acute liver failure due to acute hepatitis C is exceedingly rare.[17] Symptoms and laboratory findings suggestive of liver disease should prompt further tests and can thus help establish a diagnosis of hepatitis C infection early on.[16]

Following the acute phase, the infection may resolve spontaneously in 10–50% of affected people; this occurs more frequently in young people and females.[15]

Chronic infection

[edit]

About 70% of those exposed to the virus develop a chronic infection.[4] This is defined as the presence of detectable viral replication for at least six months. Though most experience minimal or no symptoms during the initial few decades of a chronic infection,[18] chronic hepatitis C can be associated with fatigue[19] and mild cognitive problems.[20] After several years, chronic infection may cause cirrhosis or liver cancer.[5] The liver enzymes measured from blood samples are normal in 7–53%.[21] (Elevated levels indicate liver cells are being damaged by the virus or other disease). Late relapses after apparent cure have been reported, but these can be difficult to distinguish from reinfection.[21]

Fatty changes to the liver occur in about half of those infected and are usually present before cirrhosis develops.[22][23] Usually (80% of the time) this change affects less than a third of the liver.[22] Worldwide hepatitis C is the cause of 27% of cirrhosis cases and 25% of hepatocellular carcinoma.[24] About 10–30% of those infected develop cirrhosis over 30 years.[5][16] Cirrhosis is more common in those also infected with hepatitis B, schistosoma, or HIV, in alcoholics, and in those of male sex.[16] In those with hepatitis C, excess alcohol increases the risk of developing cirrhosis 5-fold.[25] Those who develop cirrhosis have a 20-fold greater risk of hepatocellular carcinoma. This transformation occurs at a rate of 1–3% per year.[5][16] Being infected with hepatitis B in addition to hepatitis C increases this risk further.[26]

Liver cirrhosis may lead to portal hypertension, ascites (accumulation of fluid in the abdomen), easy bruising or bleeding, varices (enlarged veins, especially in the stomach and esophagus), jaundice, and a syndrome of cognitive impairment known as hepatic encephalopathy.[27] Ascites occurs at some stage in more than half of those who have a chronic infection.[28]

Extrahepatic complications

[edit]

The most common problem due to hepatitis C but not involving the liver is mixed cryoglobulinemia (usually the type II form) – an inflammation of small and medium-sized blood vessels.[29][30] Hepatitis C is also associated with autoimmune disorders such as Sjögren's syndrome, lichen planus, a low platelet count, porphyria cutanea tarda, necrolytic acral erythema, insulin resistance, diabetes mellitus, diabetic nephropathy, autoimmune thyroiditis, and B-cell lymphoproliferative disorders.[31][32] 20–30% of people infected have rheumatoid factor – a type of antibody.[33] Possible associations include Hyde's prurigo nodularis[34] and membranoproliferative glomerulonephritis.[19] Cardiomyopathy with associated abnormal heart rhythms has also been reported.[35] A variety of central and peripheral nervous system disorders has been reported.[36][37] Chronic infection seems to be associated with an increased risk of pancreatic cancer.[9][38] People may experience other issues in the mouth such as dryness, salivary duct stones, and crusted lesions around the mouth.[39][40][41]

Occult infection

[edit]

Persons who have been infected with hepatitis C may appear to clear the virus but remain infected.[42] The virus is not detectable with conventional testing but can be found with ultra-sensitive tests.[43] The original method of detection was by demonstrating the viral genome within liver biopsies, but newer methods include an antibody test for the virus' core protein and the detection of the viral genome after first concentrating the viral particles by ultracentrifugation.[44] A form of infection with persistently moderately elevated serum liver enzymes but without antibodies to hepatitis C has also been reported.[45] This form is known as cryptogenic occult infection.

Several clinical pictures have been associated with this type of infection.[46] It may be found in people with anti-hepatitis-C antibodies but with normal serum levels of liver enzymes; in antibody-negative people with ongoing elevated liver enzymes of unknown cause; in healthy populations without evidence of liver disease; and in groups at risk for HCV infection including those on hemodialysis or family members of people with occult HCV. The clinical relevance of this form of infection is under investigation.[47] The consequences of occult infection appear to be less severe than with chronic infection but can vary from minimal to hepatocellular carcinoma.[44]

The rate of occult infection in those apparently cured is controversial but appears to be low.[21] 40% of those with hepatitis but with both negative hepatitis C serology and the absence of detectable viral genome in the serum have hepatitis C virus in the liver on biopsy.[48] How commonly this occurs in children is unknown.[49]

Virology

[edit] Main article: Hepatitis C virus

The hepatitis C virus (HCV) is a small, enveloped, single-stranded, positive-sense RNA virus.[5] It is a member of the genus Hepacivirus in the family Flaviviridae.[19] There are seven major genotypes of HCV, which are known as genotypes one to seven.[50] The genotypes are divided into several subtypes with the number of subtypes depending on the genotype. In the United States, about 70% of cases are caused by genotype 1, 20% by genotype 2 and about 1% by each of the other genotypes.[16] Genotype 1 is also the most common in South America and Europe.[5]

The half life of the virus particles in the serum is around 3 hours and may be as short as 45 minutes.[51][52] In an infected person, about 1012 virus particles are produced each day.[51] In addition to replicating in the liver the virus can multiply in lymphocytes.[53]

Transmission

[edit]

Percutaneous contact with contaminated blood is responsible for most infections; however, the method of transmission is strongly dependent on both geographic region and economic status.[54] Indeed, the primary route of transmission in the developed world is injection drug use, while in the developing world the main methods are blood transfusions and unsafe medical procedures.[3] The cause of transmission remains unknown in 20% of cases;[55] however, many of these are believed to be accounted for by injection drug use.[15]

Body modification

[edit]

Tattooing is associated with two to threefold increased risk of hepatitis C.[56] This could be due to either improperly sterilized equipment or contamination of the dyes being used.[56] Tattoos or piercings performed either before the mid-1980s, "underground", or nonprofessionally are of particular concern, since sterile techniques in such settings may be lacking. The risk also appears to be greater for larger tattoos.[56] It is estimated that nearly half of prison inmates share unsterilized tattooing equipment.[56] It is rare for tattoos in a licensed facility to be directly associated with HCV infection.[57]

Drug use

[edit]

See also: Needle sharing

Injection drug use (IDU) is a major risk factor for hepatitis C in many parts of the world.[59] Of 77 countries reviewed, 25 (including the United States) were found to have a prevalence of hepatitis C of 60–80% among people who use injection drugs.[60][59] Twelve countries had rates greater than 80%.[60] It is believed that ten million intravenous drug users are infected with hepatitis C; China (1.6 million), the United States (1.5 million), and Russia (1.3 million) have the highest absolute totals.[60] Occurrence of hepatitis C among prison inmates in the United States is 10 to 20 times that of the occurrence observed in the general population; this has been attributed to high-risk behavior in prisons such as IDU and tattooing with non-sterile equipment.[61][62] Shared intranasal drug use may also be a risk factor.[63]

Fomites

[edit]

A fomite (/ˈfoʊmaɪt/) or fomes (/ˈfoʊmiːz/) is any inanimate object that, when contaminated with or exposed to infectious agents (such as pathogenic bacteria, viruses or fungi), can transfer disease to a new host.[64]

Personal-care items such as razors, toothbrushes, and manicuring or pedicuring equipment can be contaminated with blood. Sharing such items can potentially lead to exposure to HCV.[65][66] Appropriate caution should be taken regarding any medical condition that results in bleeding, such as cuts and sores.[66] HCV is not spread through casual contact, such as hugging, kissing, or sharing eating or cooking utensils,[66] nor is it transmitted through food or water.[67]

Healthcare exposure

[edit]

Blood transfusion, transfusion of blood products, or organ transplants without HCV screening carry significant risks of infection.[16] The United States instituted universal screening in 1992,[68] and Canada instituted universal screening in 1990.[69] This decreased the risk from one in 200 units[68] to between one in 10,000 to one in 10,000,000 per unit of blood.[15][55] This low risk remains as there is a period of about 11–70 days between the potential blood donor's acquiring hepatitis C and the blood's testing positive depending on the method.[55] Some countries do not screen for hepatitis C due to the cost.[24]

Those who have experienced a needle stick injury from someone who was HCV positive have about a 1.8% chance of subsequently contracting the disease themselves.[16] The risk is greater if the needle in question is hollow and the puncture wound is deep.[24] There is a risk from mucosal exposures to blood, but this risk is low, and there is no risk if blood exposure occurs on intact skin.[24]

Hospital equipment has also been documented as a method of transmission of hepatitis C, including reuse of needles and syringes, multiple-use medication vials, infusion bags, and improperly sterilized surgical equipment, among others.[24] Limitations in the implementation and enforcement of stringent standard precautions in public and private medical and dental facilities are known to have been the primary cause of the spread of HCV in Egypt, the country that had the highest rate of infection in the world in 2012, and currently

Egypt becomes the first country to achieve WHO validation on the path to elimination of hepatitis C.[70]

For more, see HONOReform (Hepatitis Outbreaks National Organization for Reform).

Mother-to-child transmission

[edit]

Mother-to-child transmission of hepatitis C occurs in fewer than 10% of pregnancies.[71] There are no measures that alter this risk.[71] It is not clear when transmission occurs during pregnancy, but it may occur both during gestation and at delivery.[55] A long labor is associated with a greater risk of transmission.[24] There is no evidence that breastfeeding spreads HCV; however, to be cautious, an infected mother is advised to avoid breastfeeding if her nipples are cracked and bleeding,[72] or if her viral loads are high.[55]

Sexual intercourse

[edit]

Sexual transmission of hepatitis C is uncommon.[11] Studies examining the risk of HCV transmission between heterosexual partners, when one is infected and the other is not, have found very low risks.[11] Sexual practices that involve higher levels of trauma to the anogenital mucosa, such as anal penetrative sex, or that occur when there is a concurrent sexually transmitted infection, including HIV or genital ulceration, present greater risks.[11][73] The United States Department of Veterans Affairs recommends condom use to prevent hepatitis C transmission in those with multiple partners, but not those in relationships that involve only a single partner.[74]

Diagnosis

[edit]

There are a number of diagnostic tests for hepatitis C, including HCV antibody enzyme immunoassay (ELISA), recombinant immunoblot assay, and quantitative HCV RNA polymerase chain reaction (PCR).[16] HCV RNA can be detected by PCR typically one to two weeks after infection, while antibodies can take substantially longer to form and thus be detected.[27]

Diagnosing patients is generally a challenge as patients with acute illness generally present with mild, non-specific flu-like symptoms,[75] while the transition from acute to chronic is sub-clinical.[76] Chronic hepatitis C is defined as infection with the hepatitis C virus persisting for more than six months based on the presence of its RNA.[18] Chronic infections are typically asymptomatic during the first few decades,[18] and thus are most commonly discovered following the investigation of elevated liver enzyme levels or during a routine screening of high-risk individuals. Testing is not able to distinguish between acute and chronic infections.[24] Diagnosis in infants is difficult as maternal antibodies may persist for up to 18 months.[49]

Serology

[edit]

Hepatitis C testing typically begins with blood testing to detect the presence of antibodies to the HCV, using an enzyme immunoassay.[16] If this test is positive, a confirmatory test is then performed to verify the immunoassay and to determine the viral load.[16] A recombinant immunoblot assay is used to verify the immunoassay and the viral load is determined by an HCV RNA polymerase chain reaction.[16] If there is no RNA and the immunoblot is positive, it means that the person tested had a previous infection but cleared it either with treatment or spontaneously; if the immunoblot is negative, it means that the immunoassay was wrong.[16] It takes about 6–8 weeks following infection before the immunoassay will test positive.[19] A number of tests are available as point-of-care testing (POCT), which can provide results within 30 minutes.[77]

Liver enzymes are variable during the initial part of the infection[18] and on average begin to rise at seven weeks after infection.[19] The elevation of liver enzymes does not closely follow disease severity.[19]

Biopsy

[edit]

Liver biopsies are used to determine the degree of liver damage present; however, there are risks from the procedure.[5] The typical changes seen are lymphocytes within the parenchyma, lymphoid follicles in portal triad, and changes to the bile ducts.[5] There are a number of blood tests available that try to determine the degree of hepatic fibrosis and alleviate the need for biopsy.[5]

Screening

[edit]

It is believed that only 5–50% of those infected in the United States and Canada are aware of their status.[56] Routine screening for those between the ages of 18 and 79 was recommended by the United States Preventive Services Task Force in 2020.[8] Previously, testing was recommended for those at high risk, including injection drug users, those who have received blood transfusions before 1992,[63] those who have been incarcerated, those on long-term hemodialysis,[63] and those with tattoos.[56] Screening is also recommended for those with elevated liver enzymes, as this is frequently the only sign of chronic hepatitis.[78] As of 2012[update], the U.S. Centers for Disease Control and Prevention (CDC) recommends a single screening test for those born between 1945 and 1965.[79][80][81][82] In Canada, a one-time screening is recommended for those born between 1945 and 1975.[83]

Prevention

[edit] See also: Hepatitis C vaccine

As of 2022, no approved vaccine protects against contracting hepatitis C.[84] A combination of harm reduction strategies, such as the provision of new needles and syringes and treatment of substance use, decreases the risk of hepatitis C in people using injection drugs by about 75%.[85] The screening of blood donors is important at a national level, as is adhering to universal precautions within healthcare facilities.[19] In countries where there is an insufficient supply of sterile syringes, medications should be given orally rather than via injection (when possible).[24] Recent research also suggests that treating people with active infection, thereby reducing the potential for transmission, may be an effective preventive measure.[10]

Hepatitis C vaccine phase 1 clinical trials are set to begin in the summer of 2023.[86]

Treatment

[edit]

Those with chronic hepatitis C are advised to avoid alcohol and medications that are toxic to the liver.[16] They should also be vaccinated against hepatitis A and hepatitis B due to the increased risk if also infected.[16] Use of acetaminophen is generally considered safe at reduced doses.[11] Nonsteroidal anti-inflammatory drugs (NSAIDs) are not recommended in those with advanced liver disease due to an increased risk of bleeding.[11] Ultrasound surveillance for hepatocellular carcinoma is recommended in those with accompanying cirrhosis.[16] Coffee consumption has been associated with[vague] a slower rate of liver scarring in those infected with HCV.[11]

Medications

[edit]

More than 95% of chronic cases clear with treatment.[4] Treatment with antiviral medication is recommended for all people with proven chronic hepatitis C who are not at high risk of death from other causes.[87] People with the highest complication risk, which is based on the degree of liver scarring, should be treated first.[87] The initial recommended treatment depends on the type of hepatitis C virus, if the person has received previous hepatitis C treatment, and whether the person has cirrhosis.[88] Direct-acting antivirals are the preferred treatment and have been validated by testing for virus particles in patients' blood.[89]

No prior treatment

[edit]

• HCV genotype 1a (no cirrhosis): 8 weeks of glecaprevir/pibrentasvir or ledipasvir/sofosbuvir (the latter for people who do not have HIV/AIDS, are not African-American, and have less than 6 million HCV viral copies per milliliter of blood) or 12 weeks of elbasvir/grazoprevir, ledipasvir/sofosbuvir, or sofosbuvir/velpatasvir.[90] Sofosbuvir with either daclatasvir or simeprevir may also be used.[88]
• HCV genotype 1a (with compensated cirrhosis): 8 weeks of glecaprevir/pibrentasvir or 12 weeks of elbasvir/grazoprevir, ledipasvir/sofosbuvir, or sofosbuvir/velpatasvir. An alternative treatment regimen of elbasvir/grazoprevir with weight-based ribavirin for 16 weeks can be used if the HCV is found to have antiviral resistance mutations against NS5A protease inhibitors.[91]
• HCV genotype 1b (no cirrhosis): 8 weeks of glecaprevir/pibrentasvir or ledipasvir/sofosbuvir (with the aforementioned limitations for the latter as above) or 12 weeks of elbasvir/grazoprevir, ledipasvir/sofosbuvir, or sofosbuvir/velpatasvir. Alternative regimens include 12 weeks of ombitasvir/paritaprevir/ritonavir with dasabuvir or 12 weeks of sofosbuvir with either daclatasvir or simeprevir.[92]
• HCV genotype 1b (with compensated cirrhosis): 8 weeks of glecaprevir/pibrentasvir or 12 weeks of elbasvir/grazoprevir, ledipasvir/sofosbuvir, or sofosbuvir/velpatasvir. A 12-week course of paritaprevir/ritonavir/ombitasvir with dasabuvir may also be used.[93]
• HCV genotype 2 (no cirrhosis): 8 weeks of glecaprevir/pibrentasvir or 12 weeks of sofosbuvir/velpatasvir. Alternatively, 12 weeks of sofosbuvir/daclatasvir can be used.[94]
• HCV genotype 2 (with compensated cirrhosis): 8 weeks of glecaprevir/pibrentasvir or 12 weeks of sofosbuvir/velpatasvir. An alternative regimen of sofosbuvir/daclatasvir can be used for 16–24 weeks.[95]
• HCV genotype 3 (no cirrhosis): 8 weeks of glecaprevir/pibrentasvir or 12 weeks of sofosbuvir/velpatasvir or sofosbuvir and daclatasvir.[96]
• HCV genotype 3 (with compensated cirrhosis): 8 weeks of glecaprevir/pibrentasvir or 12 weeks of sofosbuvir/velpatasvir, or if certain antiviral mutations are present, 12 weeks of sofosbuvir/velpatasvir/voxilaprevir (when certain antiviral mutations are present), or 24 weeks of sofosbuvir and daclatasvir.[97]
• HCV genotype 4 (no cirrhosis): 8 weeks of glecaprevir/pibrentasvir or 12 weeks of sofosbuvir/velpatasvir, elbasvir/grazoprevir, or ledipasvir/sofosbuvir. A 12-week regimen of ombitasvir/paritaprevir/ritonavir is also acceptable in combination with weight-based ribavirin.[98]
• HCV genotype 4 (with compensated cirrhosis): 8 weeks of glecaprevir/pibrentasvir or 12 weeks of sofosbuvir/velpatasvir, elbasvir/grazoprevir, or ledipasvir/sofosbuvir is recommended. A 12-week course of ombitasvir/paritaprevir/ritonavir with weight-based ribavirin is an acceptable alternative.[99]
• HCV genotype 5 or 6 (with or without compensated cirrhosis): 8 weeks of glecaprevir/pibrentasvir is recommended. If cirrhosis is present, then a 12-week course of sofosbuvir/velpatasvir, or ledipasvir/sofosbuvir is an alternative option.[100]

More than 95% of people with chronic infection can be cured when treated with medications;[101] this could be expensive, but by 2022 prices had dropped dramatically.[4] The combination of sofosbuvir, velpatasvir, and voxilaprevir may be used in those who have previously been treated with sofosbuvir or other drugs that inhibit NS5A and were not cured.[102]

Prior to 2011, treatments consisted of a combination of pegylated interferon alpha and ribavirin for a period of 24 or 48 weeks, depending on HCV genotype.[16] This treatment produces cure rates of 70–80% for genotype 2 and 3, respectively, and 45–70% for genotypes 1 and 4.[103] Adverse effects with these treatments were common, with 50–60% of those being treated experiencing flu-like symptoms and nearly a third experiencing depression or other emotional issues.[16] Treatment during the first six months of infection (the acute stage) is more effective than when hepatitis C has entered the chronic stage.[27] In those with chronic hepatitis B, treatment for hepatitis C results in reactivation of hepatitis B about 25% of the time.[104]

Surgery

[edit]

Cirrhosis due to hepatitis C is a common reason for liver transplantation,[27] though the virus usually (80–90% of cases) recurs afterwards.[5][105] Infection of the graft leads to 10–30% of people developing cirrhosis within five years.[106] Treatment with pegylated interferon and ribavirin post-transplant decreases the risk of recurrence to 70%.[107] A 2013 review found no clear evidence as to whether antiviral medication is useful if the graft became reinfected.[108]

Alternative medicine

[edit]

Several alternative therapies are claimed by their proponents to be helpful for hepatitis C, including milk thistle, ginseng, and colloidal silver.[109] However, no alternative therapy has been shown to improve outcomes for hepatitis C patients, and no evidence exists that alternative therapies have any effect on the virus.[109][110][111]

Prognosis

[edit]

The responses to treatment is measured by sustained viral response (SVR), defined as the absence of detectable RNA of the hepatitis C virus in blood serum for at least 24 weeks after discontinuing treatment,[112] and rapid virological response (RVR), defined as undetectable levels achieved within four weeks of treatment. Successful treatment decreases the future risk of hepatocellular carcinoma by 75%.[113]

Prior to 2012, sustained response occurred in about 40–50% of those with HCV genotype 1 who received 48 weeks of treatment.[5] A sustained response was seen in 70–80% of people with HCV genotypes 2 and 3 following 24 weeks of treatment.[5] A sustained response occurs for about 65% of those with genotype 4 after 48 weeks of treatment. For those with HCV genotype 6, a 48-week treatment protocol of pegylated interferon and ribavirin results in a higher rate of sustained responses than for genotype 1 (86% vs. 52%). Further studies are needed to determine results for shorter 24-week treatments and for those given at lower dosages.[114]

Spontaneous resolution

[edit]

Around 30% (15–45%) of those with acute HCV infections will spontaneously clear the virus within six months, before the infection is considered chronic.[4] Spontaneous resolution following acute infection appears more common in females and in patients who are younger, and may be influenced by certain genetic factors.[15] Chronic HCV infection may also resolve spontaneously months or years after the acute phase has passed, though this is unusual.[15]

Epidemiology

[edit]

This section needs to be updated. Please help update this article to reflect recent events or newly available information. (July 2020)

The World Health Organization estimated in a 2021 report that 58 million people globally were living with chronic hepatitis C as of 2019.[12] About 1.5 million people are infected per year, and about 290,000 people die yearly from hepatitis C–related diseases, mainly from liver cancer and cirrhosis.[4]

Hepatitis C infection rates increased substantially in the 20th century due to a combination of intravenous drug abuse and the reuse of poorly sterilized medical equipment.[24] However, advancements in treatment have led to notable declines in chronic infections and deaths from the virus. As a result, the number of chronic patients receiving treatment worldwide has grown from about 950,000 in 2015 to 9.4 million in 2019. During the same period, hepatitis C deaths declined from about 400,000 to 290,000.[4][12]

Previously, a 2013 study found high infection rates (>3.5% population infected) in Central and East Asia, North Africa and the Middle East, intermediate infection rates (1.5–3.5%) in South and Southeast Asia, sub-Saharan Africa, Andean, Central and Southern Latin America, Caribbean, Oceania, Australasia and Central, Eastern and Western Europe; and low infection rates (<1.5%) in Asia-Pacific, Tropical Latin America and North America.[115]

Among those chronically infected, the risk of cirrhosis after 20 years varies between studies but has been estimated at ~10–15% for men and ~1–5% for women. The reason for this difference is not known. Once cirrhosis is established, the rate of developing hepatocellular carcinoma is ~1–4% per year.[116] Rates of new infections have decreased in the Western world since the 1990s due to improved screening of blood before transfusion.[27]

In Egypt, following Egypt's 2030 Vision, the country managed to bring down the infection rates of hepatitis C from 22% in 2011 to just 2% in 2021.[117] It was believed that the high prevalence in Egypt was linked to a discontinued mass-treatment campaign for schistosomiasis, using improperly sterilized glass syringes.[24]

In the United States, about 2% of people have chronic hepatitis C.[16] In 2014, an estimated 30,500 new acute hepatitis C cases occurred (0.7 per 100,000 population), an increase from 2010 to 2012.[118] The number of deaths from hepatitis C has increased to 15,800 in 2008[119] having overtaken HIV/AIDS as a cause of death in the US in 2007.[120] In 2014, it was the single greatest cause of infectious death in the United States.[121] This mortality rate is expected to increase, as those infected by transfusion before HCV testing become apparent.[122] In Europe, the percentage of people with chronic infections has been estimated to be between 0.13 and 3.26%.[123]

In the United Kingdom, about 118,000 people were chronically infected in 2019.[124] About half of people using a needle exchange in London in 2017–18 tested positive for hepatitis C of which half were unaware that they had it.[125] As part of a bid to eradicate hepatitis C by 2025, NHS England conducted a large procurement exercise in 2019. Merck Sharp & Dohme, Gilead Sciences, and Abbvie were awarded contracts, which, together, are worth up to £1 billion over five years.[126]

The total number of people with this infection is higher in some countries in Africa and Asia.[127] Countries with particularly high rates of infection include Pakistan (4.8%) and China (3.2%).[128]

Since 2014, extremely effective treatments have been available to eradicate the disease within 8–12 weeks in most people.[129] In 2015, about 950,000 people were treated while 1.7 million new infections occurred, meaning that overall the number of people with HCV increased.[129] These numbers differ by country and improved in 2016, with some countries achieving higher cure rates than new infection rates (mostly high income countries).[129] By 2018, twelve countries are on track to achieve HCV elimination.[129] While antiviral agents will curb new infections, it is less clear whether they impact overall deaths and morbidity.[129] Furthermore, for them to be effective, people need to be aware of their infection – it is estimated that worldwide only 20% of infected people are aware of their infection (in the US, fewer than half were aware).[129]

History

[edit]

In the mid-1970s, Harvey J. Alter, Chief of the Infectious Disease Section in the Department of Transfusion Medicine at the National Institutes of Health, and his research team demonstrated how most post-transfusion hepatitis cases were not due to hepatitis A or B viruses. Despite this discovery, international research efforts to identify the virus, initially called non-A, non-B hepatitis (NANBH), failed for the next decade. In 1987, Michael Houghton, Qui-Lim Choo, and George Kuo at Chiron Corporation, collaborating with Daniel W. Bradley at the Centers for Disease Control and Prevention, used a novel molecular cloning approach to identify the unknown organism and develop a diagnostic test.[130] In 1988, Alter confirmed the virus by verifying its presence in a panel of NANBH specimens, and Chiron announced its discovery at a Washington, D.C. press conference in May 1988.

At the time, Chiron was in talks with the Japanese health ministry to sell a biotech version of the hepatitis B vaccine. Simultaneously, Emperor Hirohito had developed cancer and required numerous blood transfusions. The Japanese health ministry placed a screening order for Chiron's experimental NANBH test. Chiron's Japanese marketing subsidiary, Diagnostic Systems KK, introduced the term "Hepatitis C" in November 1988 in Tokyo news reports publicizing the testing of the emperor's blood.[131] Chiron sold a screening order to the Japanese health ministry in November 1988, earning the company US$60 million a year. However, because Chiron had not published any of its research and did not make a culture model available to other researchers to verify Chiron's discovery, hepatitis C earned the nickname "The Emperor's New Virus."

In April 1989, the "discovery" of HCV was published in two articles in the journal Science.[132][133] Chiron filed for several patents on the virus and its diagnosis.[134] A competing patent application by the CDC was dropped in 1990 after Chiron paid $1.9 million to the CDC and $337,500 to Bradley. In 1994, Bradley sued Chiron, seeking to invalidate the patent, have himself included as a co-inventor, and receive damages and royalty income. The court ruled against him, which was sustained on appeal in 1998.[135] Because of the unique molecular "isolation" of the hepatitis C virus, although Houghton and Kuo's team at Chiron had discovered strong biochemical markers for the virus and the test proved effective at reducing cases of post-transfusion hepatitis, the existence of a hepatitis C virus was essentially inferred.[136] In 1992, the San Francisco Chronicle reported that the virus had never been observed under an electron microscope.[137] In 1997, the American FDA approved the first hepatitis C drug on the basis of a surrogate marker called "Sustained Virological Response." In response, the pharmaceutical industry established a nationwide network of "Astro-Turf" patient advocacy groups to raise awareness (and fear) of the disease.[138]

Hepatitis C was finally "discovered" in 2005 when a Japanese team was able to propagate a molecular clone in a cell culture called Huh7.[139] This discovery enabled proper characterization of the viral particle and rapid research into the development of protease inhibitors replacing early interferon treatments. The first of these, sofosbuvir, was approved on December 6, 2013. These drugs are marketed as "cures;" however, because they were approved on the basis of surrogate markers and not clinical endpoints such as prolonging life or improving liver health, many experts question their value.[140][141]

After blood screening began, a notable hepatitis C prevalence was discovered in Egypt, which claimed six million individuals were infected by unsterile needles in a late 1970s mass chemotherapy campaign to eliminate schistosomiasis (snail fever).[142]

On October 5, 2020, Houghton and Alter, together with Charles M. Rice, were awarded the Nobel Prize in Physiology or Medicine for their work.[143][144]

Society and culture

[edit]

This section needs to be updated. Please help update this article to reflect recent events or newly available information. (July 2020)

See also: List of people with hepatitis C

World Hepatitis Day, held on July 28, is coordinated by the World Hepatitis Alliance.[145] The economic costs of hepatitis C are significant both to the individual and to society. In the United States, the average lifetime cost of the disease was estimated at US$33,407 in 2003[146] with the cost of a liver transplant as of 2011[update] costing approximately US$200,000.[147] In Canada, the cost of a course of antiviral treatment is as high as 30,000 CAD in 2003,[148] while the United States costs are between 9,200 and US$17,600 in 1998.[146] In many areas of the world, people are unable to afford treatment with antivirals as they either lack insurance coverage or the insurance they have will not pay for antivirals.[149] In the English National Health Service treatment rates for hepatitis C were higher among less deprived groups in 2010–2012.[150]

Hepatitis C–infected Spanish anaesthetist Juan Maeso was jailed for the maximum possible period of 20 years for infecting 275 patients between 1988 and 1997, as he used the same needles to give both himself and the patients opioids.[151][152]

Special populations

[edit]

Children and pregnancy

[edit] Main article: HCV in children and pregnancy

Compared with adults, infection in children is much less understood. Worldwide the prevalence of hepatitis C virus infection in pregnant women and children has been estimated to 1–8% and 0.05–5% respectively.[153] The vertical transmission rate has been estimated to be 3–5% and there is a high rate of spontaneous clearance (25–50%) in the children. Higher rates have been reported for both vertical transmission (18%, 6–36%, and 41%)[154][155] and prevalence in children (15%).[156]

In developed countries, transmission around the time of birth is now the leading cause of HCV infection. In the absence of virus in the mother's blood, transmission seems to be rare.[155] Factors associated with an increased rate of infection include membrane rupture of longer than 6 hours before delivery and procedures exposing the infant to maternal blood.[157] Cesarean sections are not recommended. Breastfeeding is considered safe if the nipples are not damaged. Infection around the time of birth in one child does not increase the risk in a subsequent pregnancy. All genotypes appear to have the same risk of transmission.

HCV infection is frequently found in children who have previously been presumed to have non-A, non-B hepatitis and cryptogenic liver disease.[158] The presentation in childhood may be asymptomatic or with elevated liver function tests.[159] While infection is commonly asymptomatic, both cirrhosis with liver failure and hepatocellular carcinoma may occur in childhood.

Immunosuppressed

[edit] See also: Hepatitis C and HIV coinfection

The rate of hepatitis C in immunosuppressed people is higher. This is particularly true in those with human immunodeficiency virus infection, recipients of organ transplants, and those with hypogammaglobulinemia.[160] Infection in these people is associated with an unusually rapid progression to cirrhosis. People with stable HIV who never received medication for HCV, may be treated with a combination of peginterferon plus ribavirin with caution to the possible side effects.[161]

Research

[edit]

As of 2011[update], there are about one hundred medications in development for hepatitis C.[147] These include vaccines to treat hepatitis, immunomodulators, and cyclophilin inhibitors, among others.[162] These potential new treatments have come about due to a better understanding of the hepatitis C virus.[163] There are a number of vaccines under development and some have shown encouraging results.[164]

The combination of sofosbuvir and velpatasvir in one trial (reported in 2015) resulted in cure rates of 99%.[165] More studies are needed to investigate the role of the preventive antiviral medication against HCV recurrence after transplantation.[166]

Animal models

[edit]

One barrier to finding treatments for hepatitis C is the lack of a suitable animal model. Despite moderate success, research highlights the need for pre-clinical testing in mammalian systems such as mouse, particularly for the development of vaccines in poorer communities. Chimpanzees remain the only available living system to study, yet their use has ethical concerns and regulatory restrictions. While scientists have made use of human cell culture systems such as hepatocytes, questions have been raised about their accuracy in reflecting the body's response to infection.[167]

One aspect of hepatitis research is to reproduce infections in mammalian models. A strategy is to introduce liver tissues from humans into mice, a technique known as xenotransplantation. This is done by generating chimeric mice and exposing the mice to HCV infection. This engineering process is known to create humanized mice, and provide opportunities to study hepatitis C within the 3D architectural design of the liver and evaluating antiviral compounds.[167] Alternatively, generating inbred mice with susceptibility to HCV would simplify the process of studying mouse models.

See also

[edit]

• PSI-6130, an experimental drug treatment

References

[edit]

1. ^ a b c d e f g h i j k l m n o p q r "Q&A for Health Professionals". Viral Hepatitis. Centers for Disease Control and Prevention. Retrieved 28 September 2020.
2. ^ a b c Ryan KJ, Ray CG, eds. (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. pp. 551–52. ISBN 978-0-8385-8529-0.
3. ^ a b c Maheshwari A, Thuluvath PJ (February 2010). "Management of acute hepatitis C". Clinics in Liver Disease. 14 (1): 169–76, x. doi:10.1016/j.cld.2009.11.007. PMID 20123448.
4. ^ a b c d e f g h i j k l m n o p q r "Hepatitis C Fact sheet". WHO. 24 June 2022. Archived from the original on 31 January 2016. Updated as required.
5. ^ a b c d e f g h i j k l m n Rosen HR (June 2011). "Clinical practice. Chronic hepatitis C infection". The New England Journal of Medicine. 364 (25): 2429–38. doi:10.1056/NEJMcp1006613. PMID 21696309. S2CID 19755395.
6. ^ "Hepatitis MedlinePlus". U.S. National Library of Medicine. Retrieved 2020-06-19.
7. ^ "Viral Hepatitis: A through E and Beyond". National Institute of Diabetes and Digestive and Kidney Diseases. April 2012. Archived from the original on 2 February 2016. Retrieved 4 February 2016.
8. ^ a b Owens DK, Davidson KW, Krist AH, Barry MJ, Cabana M, Caughey AB, et al. (March 2020). "Screening for Hepatitis C Virus Infection in Adolescents and Adults: US Preventive Services Task Force Recommendation Statement". JAMA. 323 (10): 970–975. doi:10.1001/jama.2020.1123. PMID 32119076.
9. ^ a b Webster DP, Klenerman P, Dusheiko GM (March 2015). "Hepatitis C". Lancet. 385 (9973): 1124–35. doi:10.1016/S0140-6736(14)62401-6. PMC 4878852. PMID 25687730.
10. ^ a b Zelenev A, Li J, Mazhnaya A, Basu S, Altice FL (February 2018). "Hepatitis C virus treatment as prevention in an extended network of people who inject drugs in the USA: a modelling study". The Lancet. Infectious Diseases. 18 (2): 215–224. doi:10.1016/S1473-3099(17)30676-X. PMC 5860640. PMID 29153265.
11. ^ a b c d e f g Kim A (September 2016). "Hepatitis C Virus". Annals of Internal Medicine (Review). 165 (5): ITC33–ITC48. doi:10.7326/AITC201609060. PMID 27595226. S2CID 95756.
12. ^ a b c "Global progress report on HIV, viral hepatitis and sexually transmitted infections, 2021". www.who.int. Retrieved 2022-01-19.
13. ^ Houghton M (November 2009). "The long and winding road leading to the identification of the hepatitis C virus". Journal of Hepatology. 51 (5): 939–48. doi:10.1016/j.jhep.2009.08.004. PMID 19781804.
14. ^ Shors T (2011). Understanding viruses (2nd ed.). Burlington, MA: Jones & Bartlett Learning. p. 535. ISBN 978-0-7637-8553-6. Archived from the original on 2016-05-15.
15. ^ a b c d e f Chronic Hepatitis C Virus Advances in Treatment, Promise for the Future. Springer Verlag. 2011. p. 14. ISBN 978-1-4614-1191-8. Archived from the original on 2016-06-17.
16. ^ a b c d e f g h i j k l m n o p q r s Wilkins T, Malcolm JK, Raina D, Schade RR (June 2010). "Hepatitis C: diagnosis and treatment" (PDF). American Family Physician. 81 (11): 1351–1357. PMID 20521755. Archived (PDF) from the original on 2013-05-21.
17. ^ Rao A, Rule JA, Cerro-Chiang G, Stravitz RT, McGuire BM, Lee G, et al. (January 2023). "Role of Hepatitis C Infection in Acute Liver Injury/Acute Liver Failure in North America". Digestive Diseases and Sciences. 68 (1): 304–311. doi:10.1007/s10620-022-07524-6. PMC 9094131. PMID 35546205.
18. ^ a b c d Kanwal F, Bacon BR (2011). "Does Treatment Alter the Natural History of Chronic HCV?". In Schiffman ML (ed.). Chronic Hepatitis C Virus Advances in Treatment, Promise for the Future. Springer Verlag. pp. 103–04. ISBN 978-1-4614-1191-8.
19. ^ a b c d e f g Ray SC, Thomas DL (2009). "Chapter 154: Hepatitis C". In Mandell GL, Bennett, Dolin R (eds.). Mandell, Douglas, and Bennett's principles and practice of infectious diseases (7th ed.). Philadelphia, PA: Churchill Livingstone. ISBN 978-0-443-06839-3.
20. ^ Forton DM, Allsop JM, Cox IJ, Hamilton G, Wesnes K, Thomas HC, Taylor-Robinson SD (October 2005). "A review of cognitive impairment and cerebral metabolite abnormalities in patients with hepatitis C infection". AIDS. 19 (Suppl 3): S53-63. doi:10.1097/01.aids.0000192071.72948.77. PMID 16251829.
21. ^ a b c Nicot F (2004). "Chapter 19. Liver biopsy in modern medicine.". Occult hepatitis C virus infection: Where are we now?. BoD – Books on Demand. ISBN 978-953-307-883-0.
22. ^ a b El-Zayadi AR (July 2008). "Hepatic steatosis: a benign disease or a silent killer". World Journal of Gastroenterology. 14 (26): 4120–6. doi:10.3748/wjg.14.4120. PMC 2725370. PMID 18636654.
23. ^ Paradis V, Bedossa P (December 2008). "Definition and natural history of metabolic steatosis: histology and cellular aspects". Diabetes & Metabolism. 34 (6 Pt 2): 638–42. doi:10.1016/S1262-3636(08)74598-1. PMID 19195624.
24. ^ a b c d e f g h i j Alter MJ (May 2007). "Epidemiology of hepatitis C virus infection". World Journal of Gastroenterology. 13 (17): 2436–41. doi:10.3748/wjg.v13.i17.2436 (inactive 2024-11-14). PMC 4146761. PMID 17552026.{{cite journal}}: CS1 maint: DOI inactive as of November 2024 (link)
25. ^ Mueller S, Millonig G, Seitz HK (July 2009). "Alcoholic liver disease and hepatitis C: a frequently underestimated combination". World Journal of Gastroenterology. 15 (28): 3462–71. doi:10.3748/wjg.15.3462. PMC 2715970. PMID 19630099.
26. ^ Fattovich G, Stroffolini T, Zagni I, Donato F (November 2004). "Hepatocellular carcinoma in cirrhosis: incidence and risk factors". Gastroenterology. 127 (5 Suppl 1): S35-50. doi:10.1053/j.gastro.2004.09.014. PMID 15508101.
27. ^ a b c d e Ozaras R, Tahan V (April 2009). "Acute hepatitis C: prevention and treatment". Expert Review of Anti-Infective Therapy. 7 (3): 351–61. doi:10.1586/eri.09.8. PMID 19344247. S2CID 25574917.
28. ^ Zaltron S, Spinetti A, Biasi L, Baiguera C, Castelli F (2012). "Chronic HCV infection: epidemiological and clinical relevance". BMC Infectious Diseases. 12 (Suppl 2): S2. doi:10.1186/1471-2334-12-S2-S2. PMC 3495628. PMID 23173556.
29. ^ Dammacco F, Sansonno D (September 2013). "Therapy for hepatitis C virus-related cryoglobulinemic vasculitis". The New England Journal of Medicine. 369 (11): 1035–45. doi:10.1056/NEJMra1208642. PMID 24024840. S2CID 205116488.
30. ^ Iannuzzella F, Vaglio A, Garini G (May 2010). "Management of hepatitis C virus-related mixed cryoglobulinemia". The American Journal of Medicine. 123 (5): 400–8. doi:10.1016/j.amjmed.2009.09.038. PMID 20399313.
31. ^ Zignego AL, Ferri C, Pileri SA, Caini P, Bianchi FB (January 2007). "Extrahepatic manifestations of Hepatitis C Virus infection: a general overview and guidelines for a clinical approach". Digestive and Liver Disease. 39 (1): 2–17. doi:10.1016/j.dld.2006.06.008. PMID 16884964.
32. ^ Ko HM, Hernandez-Prera JC, Zhu H, Dikman SH, Sidhu HK, Ward SC, Thung SN (2012). "Morphologic features of extrahepatic manifestations of hepatitis C virus infection". Clinical & Developmental Immunology. 2012: 740138. doi:10.1155/2012/740138. PMC 3420144. PMID 22919404.
33. ^ Dammacco F, Sansonno D, Piccoli C, Racanelli V, D'Amore FP, Lauletta G (2000). "The lymphoid system in hepatitis C virus infection: autoimmunity, mixed cryoglobulinemia, and Overt B-cell malignancy". Seminars in Liver Disease. 20 (2): 143–57. doi:10.1055/s-2000-9613. PMID 10946420. S2CID 260318352.
34. ^ Lee MR, Shumack S (November 2005). "Prurigo nodularis: a review". The Australasian Journal of Dermatology. 46 (4): 211–18, quiz 219–20. doi:10.1111/j.1440-0960.2005.00187.x. PMID 16197418. S2CID 30087432.
35. ^ Matsumori A (2006). "Role of hepatitis C virus in cardiomyopathies.". Ernst Schering Research Foundation Workshop. Vol. 55. pp. 99–120. doi:10.1007/3-540-30822-9_7. ISBN 978-3-540-23971-0. PMID 16329660.
36. ^ Moretti R, Giuffrè M, Merli N, Caruso P, Di Bella S, Tiribelli C, Crocè LS (November 2021). "Hepatitis C Virus-Related Central and Peripheral Nervous System Disorders". Brain Sciences. 11 (12): 1569. doi:10.3390/brainsci11121569. PMC 8699483. PMID 34942871.
37. ^ Monaco S, Ferrari S, Gajofatto A, Zanusso G, Mariotto S (2012). "HCV-related nervous system disorders". Clinical & Developmental Immunology. 2012: 236148. doi:10.1155/2012/236148. PMC 3414089. PMID 22899946.
38. ^ Xu JH, Fu JJ, Wang XL, Zhu JY, Ye XH, Chen SD (July 2013). "Hepatitis B or C viral infection and risk of pancreatic cancer: a meta-analysis of observational studies". World Journal of Gastroenterology. 19 (26): 4234–41. doi:10.3748/wjg.v19.i26.4234. PMC 3710428. PMID 23864789.
39. ^ Lodi G, Porter SR, Scully C (July 1998). "Hepatitis C virus infection: Review and implications for the dentist". Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics. 86 (1): 8–22. CiteSeerX 10.1.1.852.7880. doi:10.1016/S1079-2104(98)90143-3. PMID 9690239.
40. ^ Carrozzo M, Gandolfo S (2003-03-01). "Oral diseases possibly associated with hepatitis C virus". Critical Reviews in Oral Biology and Medicine. 14 (2): 115–27. doi:10.1177/154411130301400205. PMID 12764074.
41. ^ Little JW, Falace DA, Miller C, Rhodus NL (2013). Dental Management of the Medically Compromised Patient. p. 151. ISBN 978-0323080286.
42. ^ Sugden PB, Cameron B, Bull R, White PA, Lloyd AR (September 2012). "Occult infection with hepatitis C virus: friend or foe?". Immunology and Cell Biology. 90 (8): 763–73. doi:10.1038/icb.2012.20. PMID 22546735. S2CID 23845868.
43. ^ Carreño V (November 2006). "Occult hepatitis C virus infection: a new form of hepatitis C". World Journal of Gastroenterology. 12 (43): 6922–5. doi:10.3748/wjg.12.6922. PMC 4087333. PMID 17109511.
44. ^ a b Carreño García V, Nebreda JB, Aguilar IC, Quiroga Estévez JA (March 2011). "[Occult hepatitis C virus infection]". Enfermedades Infecciosas y Microbiologia Clinica. 29 (Suppl 3): 14–9. doi:10.1016/S0213-005X(11)70022-2. PMID 21458706.
45. ^ Pham TN, Coffin CS, Michalak TI (April 2010). "Occult hepatitis C virus infection: what does it mean?". Liver International. 30 (4): 502–11. doi:10.1111/j.1478-3231.2009.02193.x. PMID 20070513. S2CID 205651069.
46. ^ Carreño V, Bartolomé J, Castillo I, Quiroga JA (June 2012). "New perspectives in occult hepatitis C virus infection". World Journal of Gastroenterology. 18 (23): 2887–94. doi:10.3748/wjg.v18.i23.2887. PMC 3380315. PMID 22736911.
47. ^ Carreño V, Bartolomé J, Castillo I, Quiroga JA (May–June 2008). "Occult hepatitis B virus and hepatitis C virus infections". Reviews in Medical Virology. 18 (3): 139–57. doi:10.1002/rmv.569. PMID 18265423. S2CID 12331754.
48. ^ Scott JD, Gretch DR (February 2007). "Molecular diagnostics of hepatitis C virus infection: a systematic review". JAMA. 297 (7): 724–732. doi:10.1001/jama.297.7.724. PMID 17312292.
49. ^ a b Robinson JL (July 2008). "Vertical transmission of the hepatitis C virus: Current knowledge and issues". Paediatrics & Child Health. 13 (6): 529–541. doi:10.1093/pch/13.6.529. PMC 2532905. PMID 19436425.
50. ^ Nakano T, Lau GM, Lau GM, Sugiyama M, Mizokami M (February 2012). "An updated analysis of hepatitis C virus genotypes and subtypes based on the complete coding region". Liver International. 32 (2): 339–45. doi:10.1111/j.1478-3231.2011.02684.x. PMID 22142261. S2CID 23271017.
51. ^ a b Lerat H, Hollinger FB (January 2004). "Hepatitis C virus (HCV) occult infection or occult HCV RNA detection?". The Journal of Infectious Diseases. 189 (1): 3–6. doi:10.1086/380203. PMID 14702146.
52. ^ Pockros P (2011). Novel and Combination Therapies for Hepatitis C Virus, An Issue of Clinics in Liver Disease. Elsevier Health Sciences. p. 47. ISBN 978-1-4557-7198-1. Archived from the original on 2016-05-21.
53. ^ Zignego AL, Giannini C, Gragnani L, Piluso A, Fognani E (August 2012). "Hepatitis C virus infection in the immunocompromised host: a complex scenario with variable clinical impact". Journal of Translational Medicine. 10 (1): 158. doi:10.1186/1479-5876-10-158. PMC 3441205. PMID 22863056.
54. ^ Hagan LM, Schinazi RF (February 2013). "Best strategies for global HCV eradication". Liver International. 33 (s1): 68–79. doi:10.1111/liv.12063. PMC 4110680. PMID 23286849.
55. ^ a b c d e Pondé RA (February 2011). "Hidden hazards of HCV transmission". Medical Microbiology and Immunology. 200 (1): 7–11. doi:10.1007/s00430-010-0159-9. PMID 20461405. S2CID 664199.
56. ^ a b c d e f Jafari S, Copes R, Baharlou S, Etminan M, Buxton J (November 2010). "Tattooing and the risk of transmission of hepatitis C: a systematic review and meta-analysis". International Journal of Infectious Diseases. 14 (11): e928-40. doi:10.1016/j.ijid.2010.03.019. PMID 20678951.
57. ^ "Hepatitis C" (PDF). Centers for Disease Control and Prevention (CDC). Archived (PDF) from the original on 5 January 2012. Retrieved 2 January 2012.
58. ^ Laureen Veevers (1 October 2006). "'Shared banknote' health warning to cocaine users". The Observer. Retrieved 2008-07-26.
59. ^ a b Xia X, Luo J, Bai J, Yu R (October 2008). "Epidemiology of hepatitis C virus infection among injection drug users in China: systematic review and meta-analysis". Public Health. 122 (10): 990–1003. doi:10.1016/j.puhe.2008.01.014. PMID 18486955.
60. ^ a b c Nelson PK, Mathers BM, Cowie B, Hagan H, Des Jarlais D, Horyniak D, Degenhardt L (August 2011). "Global epidemiology of hepatitis B and hepatitis C in people who inject drugs: results of systematic reviews". Lancet. 378 (9791): 571–83. doi:10.1016/S0140-6736(11)61097-0. PMC 3285467. PMID 21802134.
61. ^ Imperial JC (June 2010). "Chronic hepatitis C in the state prison system: insights into the problems and possible solutions". Expert Review of Gastroenterology & Hepatology. 4 (3): 355–64. doi:10.1586/egh.10.26. PMID 20528122. S2CID 7931472.
62. ^ Vescio MF, Longo B, Babudieri S, Starnini G, Carbonara S, Rezza G, Monarca R (April 2008). "Correlates of hepatitis C virus seropositivity in prison inmates: a meta-analysis". Journal of Epidemiology and Community Health. 62 (4): 305–13. doi:10.1136/jech.2006.051599. PMID 18339822. S2CID 206989111.
63. ^ a b c Moyer VA (September 2013). "Screening for hepatitis C virus infection in adults: U.S. Preventive Services Task Force recommendation statement". Annals of Internal Medicine. 159 (5): 349–57. doi:10.7326/0003-4819-159-5-201309030-00672. PMID 23798026. S2CID 8563203.
64. ^ Cramer L (1 September 2011). "Fomites, fomites, fomites!". Microblogology. Archived from the original on 23 September 2020. Retrieved 8 March 2019.
65. ^ Lock G, Dirscherl M, Obermeier F, Gelbmann CM, Hellerbrand C, Knöll A, et al. (September 2006). "Hepatitis C - contamination of toothbrushes: myth or reality?". Journal of Viral Hepatitis. 13 (9): 571–3. doi:10.1111/j.1365-2893.2006.00735.x. PMID 16907842. S2CID 24264376.
66. ^ a b c "Hepatitis C FAQs for Health Professionals". Centers for Disease Control and Prevention (CDC). Archived from the original on 4 January 2012. Retrieved 2 January 2012.
67. ^ Wong T, Lee SS (February 2006). "Hepatitis C: a review for primary care physicians". CMAJ. 174 (5): 649–59. doi:10.1503/cmaj.1030034. PMC 1389829. PMID 16505462.
68. ^ a b Marx J (2010). Rosen's emergency medicine: concepts and clinical practice (7th ed.). Philadelphia, PA: Mosby/Elsevier. p. 1154. ISBN 978-0-323-05472-0.
69. ^ Day RA, Paul P, Williams B (2009). Brunner & Suddarth's textbook of Canadian medical-surgical nursing (Canadian 2nd ed.). Philadelphia, PA: Lippincott Williams & Wilkins. p. 1237. ISBN 978-0-7817-9989-8. Archived from the original on 2016-04-25.
70. ^ "Egypt becomes the first country to achieve WHO validation on the path to elimination of hepatitis C".
71. ^ a b Lam NC, Gotsch PB, Langan RC (November 2010). "Caring for pregnant women and newborns with hepatitis B or C" (PDF). American Family Physician. 82 (10): 1225–9. PMID 21121533. Archived (PDF) from the original on 2013-05-21.
72. ^ Mast EE (2004). "Mother-to-Infant Hepatitis C Virus Transmission and Breastfeeding". Protecting Infants through Human Milk. Advances in Experimental Medicine and Biology. Vol. 554. pp. 211–16. doi:10.1007/978-1-4757-4242-8_18. ISBN 978-1-4419-3461-1. PMID 15384578.
73. ^ Tohme RA, Holmberg SD (October 2010). "Is sexual contact a major mode of hepatitis C virus transmission?". Hepatology. 52 (4): 1497–505. doi:10.1002/hep.23808. PMID 20635398. S2CID 5592006.
74. ^ "Hepatitis C Group Education Class". United States Department of Veteran Affairs. Archived from the original on 2011-11-09. Retrieved 2011-11-20.
75. ^ Westbrook RH, Dusheiko G (November 2014). "Natural history of hepatitis C". Journal of Hepatology. 61 (1 Suppl): S58-68. doi:10.1016/j.jhep.2014.07.012. PMID 25443346.
76. ^ Patel K, Muir AJ, McHutchison JG (April 2006). "Diagnosis and treatment of chronic hepatitis C infection". BMJ. 332 (7548): 1013–7. doi:10.1136/bmj.332.7548.1013. PMC 1450048. PMID 16644828.
77. ^ Shivkumar S, Peeling R, Jafari Y, Joseph L, Pant Pai N (October 2012). "Accuracy of rapid and point-of-care screening tests for hepatitis C: a systematic review and meta-analysis". Annals of Internal Medicine. 157 (8): 558–66. doi:10.7326/0003-4819-157-8-201210160-00006. PMID 23070489. S2CID 5650682.
78. ^ Senadhi V (July 2011). "A paradigm shift in the outpatient approach to liver function tests". Southern Medical Journal. 104 (7): 521–5. doi:10.1097/SMJ.0b013e31821e8ff5. PMID 21886053. S2CID 26462106.
79. ^ Smith BD, Morgan RL, Beckett GA, Falck-Ytter Y, Holtzman D, Teo CG, et al. (August 2012). "Recommendations for the identification of chronic hepatitis C virus infection among persons born during 1945-1965" (PDF). MMWR. Recommendations and Reports. 61 (RR-4): 1–32. PMID 22895429.
80. ^ "Testing Recommendations for Hepatitis C Virus Infection – HCV – Division of Viral Hepatitis". U.S. Centers for Disease Control and Prevention (CDC). 12 June 2019. Retrieved 11 January 2020.
81. ^ "People Born 1945–1965 (Baby Boomers) – Populations and Settings – Division of Viral Hepatitis". U.S. Centers for Disease Control and Prevention (CDC). 26 July 2019. Archived from the original on 22 October 2019. Retrieved 11 January 2020.
82. ^ "Final Update Summary: Hepatitis C: Screening". US Preventive Services Task Force. Retrieved 11 January 2020.
83. ^ Shah H, Bilodeau M, Burak KW, Cooper C, Klein M, Ramji A, et al. (June 2018). "The management of chronic hepatitis C: 2018 guideline update from the Canadian Association for the Study of the Liver". CMAJ. 190 (22): E677–E687. doi:10.1503/cmaj.170453. PMC 5988519. PMID 29866893.
84. ^ CDC (2021-06-14). "Hepatitis C | CDC". Centers for Disease Control and Prevention. Retrieved 2023-03-27.
85. ^ Hagan H, Pouget ER, Des Jarlais DC (July 2011). "A systematic review and meta-analysis of interventions to prevent hepatitis C virus infection in people who inject drugs". The Journal of Infectious Diseases. 204 (1): 74–83. doi:10.1093/infdis/jir196. PMC 3105033. PMID 21628661.
86. ^ "Biden Administration, Others Working Towards Eliminating Hepatitis C". 13 March 2023.
87. ^ a b AASLD/IDSA HCV Guidance Panel (September 2015). "Hepatitis C guidance: AASLD-IDSA recommendations for testing, managing, and treating adults infected with hepatitis C virus". Hepatology. 62 (3): 932–54. doi:10.1002/hep.27950. PMID 26111063.
88. ^ a b "HCV Guidance: Recommendations for Testing, Managing, and Treating Hepatitis C" (PDF). 12 April 2017. Archived from the original (PDF) on 2017-07-10. Retrieved 28 July 2017.
89. ^ Jakobsen JC, Nielsen EE, Feinberg J, Katakam KK, Fobian K, Hauser G, et al. (September 2017). "Direct-acting antivirals for chronic hepatitis C". The Cochrane Database of Systematic Reviews. 2017 (9): CD012143. doi:10.1002/14651858.CD012143.pub3. PMC 6484376. PMID 28922704.
90. ^ "Treatment: Naive Genotype 1a Without Cirrhosis". HCV Guidance: Recommendations for Testing, Managing, and Treating Hepatitis C. American Association for the Study of Liver Diseases. Retrieved 26 April 2017 – via www.hcvguidelines.org.
91. ^ "Treatment: Naive Genotype 1a With Compensated Cirrhosis". HCV Guidance: Recommendations for Testing, Managing, and Treating Hepatitis C. American Association for the Study of Liver Diseases. Retrieved 26 April 2017 – via www.hcvguidelines.org.
92. ^ "Treatment: Naive Genotype 1b Without Cirrhosis". HCV Guidance: Recommendations for Testing, Managing, and Treating Hepatitis C. American Association for the Study of Liver Diseases. Retrieved 26 April 2017 – via www.hcvguidelines.org.
93. ^ "Treatment: Naive Genotype 1b With Compensated Cirrhosis". HCV Guidance: Recommendations for Testing, Managing, and Treating Hepatitis C. American Association for the Study of Liver Diseases. Retrieved 26 April 2017 – via www.hcvguidelines.org.
94. ^ "Treatment; Naive Genotype 2 Without Cirrhosis". HCV Guidance: Recommendations for Testing, Managing, and Treating Hepatitis C. American Association for the Study of Liver Diseases. Retrieved 26 April 2017 – via www.hcvguidelines.org.
95. ^ "Treatment – Naive Genotype 2 With Compensated Cirrhosis". HCV Guidance: Recommendations for Testing, Managing, and Treating Hepatitis C. American Association for the Study of Liver Diseases. Retrieved 26 April 2017 – via www.hcvguidelines.org.
96. ^ "Treatment: Naive Genotype 3 Without Cirrhosis". HCV Guidance: Recommendations for Testing, Managing, and Treating Hepatitis C. American Association for the Study of Liver Diseases. Retrieved 26 April 2017 – via www.hcvguidelines.org.
97. ^ "Treatment: Naive Genotype 3 With Compensated Cirrhosis". HCV Guidance: Recommendations for Testing, Managing, and Treating Hepatitis C. American Association for the Study of Liver Diseases. Retrieved 26 April 2017 – via www.hcvguidelines.org.
98. ^ "Treatment: Naive Genotype 4 Without Cirrhosis". HCV Guidance: Recommendations for Testing, Managing, and Treating Hepatitis C. American Association for the Study of Liver Diseases. Retrieved 26 April 2017 – via www.hcvguidelines.org.
99. ^ "Treatment: Naive Genotype 4 With Compensated Cirrhosis". HCV Guidance: Recommendations for Testing, Managing, and Treating Hepatitis C. American Association for the Study of Liver Diseases. Retrieved 26 April 2017 – via www.hcvguidelines.org.
100. ^ "Treatment: Naive Genotype 5 or 6". HCV Guidance: Recommendations for Testing, Managing, and Treating Hepatitis C. American Association for the Study of Liver Diseases. Retrieved 26 April 2017 – via www.hcvguidelines.org.
101. ^ "Hepatitis C Questions and Answers for Health Professionals". www.cdc.gov. 2 July 2019. Retrieved 23 July 2019.
102. ^ "FDA approves Vosevi for Hepatitis C". U.S. Food and Drug Administration (FDA) (Press release). 18 July 2017. Archived from the original on 23 July 2017. Retrieved 27 July 2017.
103. ^ Liang TJ, Ghany MG (May 2013). "Current and future therapies for hepatitis C virus infection". The New England Journal of Medicine. 368 (20): 1907–17. doi:10.1056/NEJMra1213651. PMC 3893124. PMID 23675659.
104. ^ Mücke MM, Backus LI, Mücke VT, Coppola N, Preda CM, Yeh ML, et al. (March 2018). "Hepatitis B virus reactivation during direct-acting antiviral therapy for hepatitis C: a systematic review and meta-analysis". The Lancet. Gastroenterology & Hepatology. 3 (3): 172–180. doi:10.1016/S2468-1253(18)30002-5. PMID 29371017.
105. ^ Sanders M (2011). Mosby's Paramedic Textbook. Jones & Bartlett Publishers. p. 839. ISBN 978-0-323-07275-5. Archived from the original on 2016-05-11.
106. ^ Ciria R, Pleguezuelo M, Khorsandi SE, Davila D, Suddle A, Vilca-Melendez H, et al. (May 2013). "Strategies to reduce hepatitis C virus recurrence after liver transplantation". World Journal of Hepatology. 5 (5): 237–50. doi:10.4254/wjh.v5.i5.237. PMC 3664282. PMID 23717735.
107. ^ Coilly A, Roche B, Samuel D (February 2013). "Current management and perspectives for HCV recurrence after liver transplantation". Liver International. 33 (Suppl 1): 56–62. doi:10.1111/liv.12062. PMID 23286847. S2CID 23601091.
108. ^ Gurusamy KS, Tsochatzis E, Toon CD, Xirouchakis E, Burroughs AK, Davidson BR (December 2013). "Antiviral interventions for liver transplant patients with recurrent graft infection due to hepatitis C virus". The Cochrane Database of Systematic Reviews. 2014 (12): CD006803. doi:10.1002/14651858.CD006803.pub4. PMC 8930021. PMID 24307460.
109. ^ a b Hepatitis C and CAM: What the Science Says Archived 2011-03-20 at the Wayback Machine. National Center for Complementary and Alternative Medicine (NCCAM). March 2011. (Retrieved 7 March 2011)
110. ^ Liu J, Manheimer E, Tsutani K, Gluud C (March 2003). "Medicinal herbs for hepatitis C virus infection: a Cochrane hepatobiliary systematic review of randomized trials". The American Journal of Gastroenterology. 98 (3): 538–44. doi:10.1111/j.1572-0241.2003.07298.x. PMID 12650784. S2CID 20014583.
111. ^ Rambaldi A, Jacobs BP, Gluud C (October 2007). "Milk thistle for alcoholic and/or hepatitis B or C virus liver diseases". The Cochrane Database of Systematic Reviews. 2009 (4): CD003620. doi:10.1002/14651858.CD003620.pub3. PMC 8724782. PMID 17943794.
112. ^ Helms RA, Quan DJ, eds. (2006). Textbook of Therapeutics: Drug and Disease Management (8th ed.). Philadelphia, PA [u.a.]: Lippincott Williams & Wilkins. p. 1340. ISBN 978-0-7817-5734-8. Archived from the original on 5 December 2015. Retrieved 7 November 2014.
113. ^ Morgan RL, Baack B, Smith BD, Yartel A, Pitasi M, Falck-Ytter Y (March 2013). "Eradication of hepatitis C virus infection and the development of hepatocellular carcinoma: a meta-analysis of observational studies". Annals of Internal Medicine. 158 (5 Pt 1): 329–37. doi:10.7326/0003-4819-158-5-201303050-00005. PMID 23460056. S2CID 15553488.
114. ^ Fung J, Lai CL, Hung I, Young J, Cheng C, Wong D, Yuen MF (September 2008). "Chronic hepatitis C virus genotype 6 infection: response to pegylated interferon and ribavirin". The Journal of Infectious Diseases. 198 (6): 808–12. doi:10.1086/591252. PMID 18657036.
115. ^ Mohd Hanafiah K, Groeger J, Flaxman AD, Wiersma ST (April 2013). "Global epidemiology of hepatitis C virus infection: new estimates of age-specific antibody to HCV seroprevalence". Hepatology. 57 (4): 1333–42. doi:10.1002/hep.26141. PMID 23172780. S2CID 16265266.
116. ^ Yu ML, Chuang WL (March 2009). "Treatment of chronic hepatitis C in Asia: when East meets West". Journal of Gastroenterology and Hepatology. 24 (3): 336–45. doi:10.1111/j.1440-1746.2009.05789.x. PMID 19335784. S2CID 27333980.
117. ^ "Hepatitis C prevalence in Egypt drops from 7% to 2% thanks to Sisi's initiative". EgyptToday. 2021-02-06. Retrieved 2021-03-06.
118. ^ "Surveillance for Viral Hepatitis – United States, 2014". CDC. May 17, 2016. Archived from the original on 2016-08-08. Retrieved 2016-08-04.
119. ^ "Table 4.5. Number and rate* of deaths with hepatitis C listed as a cause of death†, by demographic characteristic and year — United States, 2004–2008". Viral Hepatitis Statistics & Surveillance. Atlanta, GA: Centers for Disease Control and Prevention. June 7, 2012. Archived from the original on 9 March 2014. Retrieved 28 July 2013.
120. ^ Bakalar N (27 February 2012). "Hepatitis C Deaths Creep Past AIDS, Study Finds". New York Times. Archived from the original on 30 June 2017. Retrieved 28 July 2013.
121. ^ "Hepatitis C Kills More Americans than Any Other Infectious Disease". Centers for Disease Control and Prevention. May 4, 2016. Archived from the original on 9 August 2016. Retrieved 3 August 2016.
122. ^ Blatt LM, Tong M (2004). Colacino JM, Heinz BA (eds.). Hepatitis prevention and treatment. Basel: Birkhäuser. p. 32. ISBN 978-3-7643-5956-0. Archived from the original on 2016-06-24.
123. ^ Blachier M, Leleu H, Peck-Radosavljevic M, Valla DC, Roudot-Thoraval F (March 2013). "The burden of liver disease in Europe: a review of available epidemiological data". Journal of Hepatology. 58 (3): 593–608. doi:10.1016/j.jhep.2012.12.005. PMID 23419824.
124. ^ "Hepatitis C". NHS UK. 27 October 2021.
125. ^ Burns C (17 May 2018). "More than half of patients using needle exchange pilot tested positive for Hepatitis C". The Pharmaceutical Journal.
126. ^ "Legal action firm among winners for largest medicines procurement". Health Service Journal. 30 April 2019. Retrieved 9 June 2019.
127. ^ Holmberg S (2011-05-12). Brunette GW, Kozarsky PE, Magill AJ, Shlim DR, Whatley AD (eds.). CDC Health Information for International Travel 2012. New York: Oxford University Press. p. 231. ISBN 978-0-19-976901-8.
128. ^ "Hepatitis C". World Health Organization (WHO). June 2011. Archived from the original on 2011-07-12. Retrieved 2011-07-13.
129. ^ a b c d e f Lombardi A, Mondelli MU (March 2019). "Hepatitis C: Is eradication possible?". Liver International. 39 (3): 416–426. doi:10.1111/liv.14011. hdl:2434/870308. PMID 30472772.
130. ^ Boyer JL (2001). Liver cirrhosis and its development: proceedings of the Falk Symposium 115. Springer. pp. 344. ISBN 978-0-7923-8760-2.
131. ^ Barnum A (May 12, 1992). "US Biotech is Thriving in Japan: Chiron got its start by using blood test on Emperor Hirohito" (PDF). San Francisco Chronicle.[permanent dead link‍]
132. ^ Choo QL, Kuo G, Weiner AJ, Overby LR, Bradley DW, Houghton M (April 1989). "Isolation of a cDNA clone derived from a blood-borne non-A, non-B viral hepatitis genome" (PDF). Science. 244 (4902): 359–62. Bibcode:1989Sci...244..359C. CiteSeerX 10.1.1.469.3592. doi:10.1126/science.2523562. PMID 2523562.
133. ^ Kuo G, Choo QL, Alter HJ, Gitnick GL, Redeker AG, Purcell RH, et al. (April 1989). "An assay for circulating antibodies to a major etiologic virus of human non-A, non-B hepatitis". Science. 244 (4902): 362–4. Bibcode:1989Sci...244..362K. doi:10.1126/science.2496467. PMID 2496467.
134. ^ EP patent 0318216, Houghton M, Choo QL, Kuo G, "NANBV diagnostics", issued 1989-05-31, assigned to Chiron 
135. ^ Wilken (20 February 1998). "United States Court of Appeals for the Federal Circuit". United States Court of Appeals for the Federal Circuit. Archived from the original on 19 November 2009.
136. ^ "Hepatitis C Investigative guidelines" (PDF). Oregon Health Authority. January 2020.
137. ^ Barnum A (May 12, 1992). "US Biotech is Thriving in Japan: Chiron got its start by using blood test on Emperor Hirohito" (PDF). San Francisco Chronicle. Archived from the original (PDF) on August 11, 2022. Retrieved July 24, 2022.
138. ^ O'Harrow R (September 12, 2000). "Grass Roots seeded by Drugmaker". Washington Post.
139. ^ Wakita T, Pietschmann T, Kato T, Date T, Miyamoto M, Zhao Z, et al. (July 2005). "Production of infectious hepatitis C virus in tissue culture from a cloned viral genome". Nature Medicine. 11 (7): 791–796. doi:10.1038/nm1268. PMC 2918402. PMID 15951748.
140. ^ Jakobsen JC, Nielsen EE, Feinberg J, Katakam KK, Fobian K, Hauser G, et al. (September 2017). "Direct-acting antivirals for chronic hepatitis C". The Cochrane Database of Systematic Reviews. 2017 (9): CD012143. doi:10.1002/14651858.CD012143.pub3. PMC 6484376. PMID 28922704.
141. ^ Koretz RL, Lin KW, Ioannidis JP, Lenzer J (January 2015). "Is widespread screening for hepatitis C justified?". BMJ. 350: g7809. doi:10.1136/bmj.g7809. PMID 25587052. S2CID 36816304.
142. ^ McNeil D (December 15, 2015). "Curing Hepatitis C, in an Experiment the Size of Egypt". The New York Times.
143. ^ Gallagher J (2020-10-05). "Hepatitis C discovery wins the Nobel Prize". BBC News. Retrieved 2020-10-05.
144. ^ Ledford H (19 October 2020). "The unsung heroes of the Nobel-winning hepatitis C discovery". Nature. 586 (7830): 485. Bibcode:2020Natur.586..485L. doi:10.1038/d41586-020-02932-y. PMID 33082542. S2CID 224822368. Retrieved 20 October 2020.
145. ^ Eurosurveillance editorial team (July 2011). "World Hepatitis Day 2011" (PDF). Euro Surveillance. 16 (30). PMID 21813077. Archived (PDF) from the original on 2011-11-25.
146. ^ a b Wong JB (2006). "Hepatitis C: cost of illness and considerations for the economic evaluation of antiviral therapies". PharmacoEconomics. 24 (7): 661–72. doi:10.2165/00019053-200624070-00005. PMID 16802842. S2CID 6713508.
147. ^ a b El Khoury AC, Klimack WK, Wallace C, Razavi H (March 2012). "Economic burden of hepatitis C-associated diseases in the United States". Journal of Viral Hepatitis. 19 (3): 153–60. doi:10.1111/j.1365-2893.2011.01563.x. PMID 22329369. S2CID 27409621.
148. ^ "Hepatitis C Prevention, Support and Research ProgramHealth Canada". Public Health Agency of Canada. Nov 2003. Archived from the original on 22 March 2011. Retrieved 10 January 2012.
149. ^ Thomas H, Lemon S, Zuckerman A, eds. (2008). Viral Hepatitis (3rd ed.). Oxford: John Wiley & Sons. p. 532. ISBN 978-1-4051-4388-2. Archived from the original on 2016-06-17.
150. ^ Blackledge C (19 March 2015). "Commissioning supplement: Health inequalities tell a tale of data neglect". Health Service Journal. Archived from the original on 28 July 2015.
151. ^ "Spanish Anesthetist Infected Patients". The Washington Post. Associated Press. 15 May 2007. Archived from the original on 22 August 2016.
152. ^ "Spanish Hep C anaesthetist jailed". BBC. 15 May 2007. Archived from the original on 23 October 2007.
153. ^ Arshad M, El-Kamary SS, Jhaveri R (April 2011). "Hepatitis C virus infection during pregnancy and the newborn period--are they opportunities for treatment?". Journal of Viral Hepatitis. 18 (4): 229–36. doi:10.1111/j.1365-2893.2010.01413.x. PMID 21392169. S2CID 35515919.
154. ^ Hunt CM, Carson KL, Sharara AI (May 1997). "Hepatitis C in pregnancy". Obstetrics and Gynecology. 89 (5 Pt 2): 883–90. doi:10.1016/S0029-7844(97)81434-2. PMID 9166361. S2CID 23182340.
155. ^ a b Thomas SL, Newell ML, Peckham CS, Ades AE, Hall AJ (February 1998). "A review of hepatitis C virus (HCV) vertical transmission: risks of transmission to infants born to mothers with and without HCV viraemia or human immunodeficiency virus infection". International Journal of Epidemiology. 27 (1): 108–17. doi:10.1093/ije/27.1.108. PMID 9563703.
156. ^ Fischler B (June 2007). "Hepatitis C virus infection". Seminars in Fetal & Neonatal Medicine. 12 (3): 168–73. CiteSeerX 10.1.1.852.7880. doi:10.1016/j.siny.2007.01.008. PMID 17320495.
157. ^ Indolfi G, Resti M (May 2009). "Perinatal transmission of hepatitis C virus infection". Journal of Medical Virology. 81 (5): 836–43. doi:10.1002/jmv.21437. PMID 19319981. S2CID 21207996.
158. ^ González-Peralta RP (November 1997). "Hepatitis C virus infection in pediatric patients". Clinics in Liver Disease. 1 (3): 691–705, ix. doi:10.1016/s1089-3261(05)70329-9. PMID 15560066.
159. ^ Suskind DL, Rosenthal P (February 2004). "Chronic viral hepatitis". Adolescent Medicine Clinics. 15 (1): 145–58, x–xi. doi:10.1016/j.admecli.2003.11.001. PMID 15272262.
160. ^ Einav S, Koziel MJ (June 2002). "Immunopathogenesis of hepatitis C virus in the immunosuppressed host". Transplant Infectious Disease. 4 (2): 85–92. doi:10.1034/j.1399-3062.2002.t01-2-02001.x. PMID 12220245. S2CID 27843061.
161. ^ Iorio A, Marchesini E, Awad T, Gluud LL (January 2010). "Antiviral treatment for chronic hepatitis C in patients with human immunodeficiency virus". The Cochrane Database of Systematic Reviews (1): CD004888. doi:10.1002/14651858.CD004888.pub2. PMID 20091566.
162. ^ Ahn J, Flamm SL (August 2011). "Hepatitis C therapy: other players in the game". Clinics in Liver Disease. 15 (3): 641–56. doi:10.1016/j.cld.2011.05.008. PMID 21867942.
163. ^ Vermehren J, Sarrazin C (February 2011). "New HCV therapies on the horizon". Clinical Microbiology and Infection. 17 (2): 122–34. doi:10.1111/j.1469-0691.2010.03430.x. PMID 21087349.
164. ^ Abdelwahab KS, Ahmed Said ZN (January 2016). "Status of hepatitis C virus vaccination: Recent update". World Journal of Gastroenterology. 22 (2): 862–73. doi:10.3748/wjg.v22.i2.862. PMC 4716084. PMID 26811632.
165. ^ Feld JJ, Jacobson IM, Hézode C, Asselah T, Ruane PJ, Gruener N, et al. (December 2015). "Sofosbuvir and Velpatasvir for HCV Genotype 1, 2, 4, 5, and 6 Infection". The New England Journal of Medicine. 373 (27): 2599–607. doi:10.1056/NEJMoa1512610. hdl:10722/226358. PMID 26571066.
166. ^ Gurusamy KS, Tsochatzis E, Toon CD, Davidson BR, Burroughs AK (December 2013). "Antiviral prophylaxis for the prevention of chronic hepatitis C virus in patients undergoing liver transplantation". The Cochrane Database of Systematic Reviews. 2013 (12): CD006573. doi:10.1002/14651858.CD006573.pub3. PMC 6599865. PMID 24297303.
167. ^ a b Sandmann L, Ploss A (January 2013). "Barriers of hepatitis C virus interspecies transmission". Virology. 435 (1): 70–80. doi:10.1016/j.virol.2012.09.044. PMC 3523278. PMID 23217617.

External links

[edit] Wikimedia Commons has media related to Hepatitis C. Listen to this article (2 minutes)

This audio file was created from a revision of this article dated 26 July 2014 (2014-07-26), and does not reflect subsequent edits.(Audio help · More spoken articles)

• "Recommendations for Testing, Managing, and Treating Hepatitis C". IDSA/AASLD. Retrieved 28 July 2017 – via www.hcvguidelines.org.
• "Hepatitis C". MedlinePlus. U.S. National Library of Medicine.

Classification	D ICD-10: B17.1, B18.2 ICD-9-CM: 070.70,070.4, 070.5 OMIM: 609532 MeSH: D006526 DiseasesDB: 5783 SNOMED CT: 186643004
External resources	MedlinePlus: 000284 eMedicine: med/993 ped/979 Patient UK: Hepatitis C

Portals:

• Medicine
• Viruses

v t e Infectious diseases – viral systemic diseases
Oncovirus	DNA virus HBV Hepatocellular carcinoma HPV Cervical cancer Anal cancer Penile cancer Vulvar cancer Vaginal cancer Oropharyngeal cancer KSHV Kaposi's sarcoma EBV Nasopharyngeal carcinoma Burkitt's lymphoma Hodgkin lymphoma Follicular dendritic cell sarcoma Extranodal NK/T-cell lymphoma, nasal type MCPyV Merkel-cell carcinoma RNA virus HCV Hepatocellular carcinoma Splenic marginal zone lymphoma HTLV-I Adult T-cell leukemia/lymphoma
Immune disorders	HIV AIDS
Central nervous system	Encephalitis/meningitis DNA virus Human polyomavirus 2 Progressive multifocal leukoencephalopathy RNA virus MeV Subacute sclerosing panencephalitis LCV Lymphocytic choriomeningitis Arbovirus encephalitis Orthomyxoviridae (probable) Encephalitis lethargica RV Rabies Chandipura vesiculovirus Herpesviral meningitis Ramsay Hunt syndrome type 2 Myelitis Poliovirus Poliomyelitis Post-polio syndrome HTLV-I Tropical spastic paraparesis Eye Cytomegalovirus Cytomegalovirus retinitis HSV Herpes of the eye
Cardiovascular	CBV Pericarditis Myocarditis
Respiratory system/acute viralnasopharyngitis/viral pneumonia	DNA virus Epstein–Barr virus EBV infection/Infectious mononucleosis Cytomegalovirus RNA virus IV: Human coronavirus 229E/NL63/HKU1/OC43 Common cold MERS coronavirus Middle East respiratory syndrome SARS coronavirus Severe acute respiratory syndrome SARS-CoV-2 COVID-19 V, Orthomyxoviridae: Influenza virus A/B/C/D Influenza/Avian influenza V, Paramyxoviridae: Human parainfluenza viruses Parainfluenza Human orthopneumovirus hMPV
Human digestive system	Pharynx/Esophagus MuV Mumps Cytomegalovirus Cytomegalovirus esophagitis Gastroenteritis/diarrhea DNA virus Adenovirus Adenovirus infection RNA virus Rotavirus (Gastroenteritis) Norovirus Astrovirus Coronavirus Hepatitis DNA virus HBV (B) RNA virus CBV HAV (A) HCV (C) HDV (D) HEV (E) Pancreatitis CBV
Urogenital	BK virus MuV Mumps

v t e Diseases of the human digestive system
Upper GI tract	Esophagus Esophagitis Candidal Eosinophilic Herpetiform Rupture Boerhaave syndrome Mallory–Weiss syndrome Zenker's diverticulum Barrett's esophagus Esophageal motility disorder Nutcracker esophagus Achalasia Esophagogastric junction outflow obstruction Diffuse esophageal spasm Gastroesophageal reflux disease (GERD) Laryngopharyngeal reflux (LPR) Esophageal stricture Inlet patch Megaesophagus Esophageal intramural pseudodiverticulosis Acute esophageal necrosis Stomach Gastritis Atrophic Ménétrier's disease Gastroenteritis Peptic (gastric) ulcer Cushing ulcer Dieulafoy's lesion Dyspepsia Functional dyspepsia Pyloric stenosis Achlorhydria Gastroparesis Gastroptosis Portal hypertensive gastropathy Gastric antral vascular ectasia Gastric dumping syndrome Gastric volvulus Buried bumper syndrome Gastrinoma Zollinger–Ellison syndrome
Lower GI tract Enteropathy	Small intestine (Duodenum/Jejunum/Ileum) Enteritis Duodenitis Jejunitis Ileitis Peptic (duodenal) ulcer Curling's ulcer Malabsorption: Coeliac Tropical sprue Blind loop syndrome Small intestinal bacterial overgrowth Whipple's Short bowel syndrome Steatorrhea Milroy disease Bile acid malabsorption Large intestine (Appendix/Colon) Appendicitis Colitis Pseudomembranous Ulcerative Ischemic Microscopic Collagenous Lymphocytic Dysentery Functional colonic disease IBS Intestinal pseudoobstruction / Ogilvie syndrome Megacolon / Toxic megacolon Diverticulitis/Diverticulosis/SCAD Large and/or small Enterocolitis Necrotizing Gastroenterocolitis IBD Crohn's disease Vascular: Abdominal angina Mesenteric ischemia Angiodysplasia Bowel obstruction: Ileus Intussusception Volvulus Fecal impaction Constipation Functional Diarrhea Infectious Intestinal adhesions Rectum Proctitis Radiation proctitis Proctalgia fugax Rectal prolapse Anismus Solitary rectal ulcer syndrome Rectal stricture Anal canal Anal fissure/Anal fistula Anal abscess Hemorrhoid Anal dysplasia Pruritus ani Anal stricture
GI bleeding	Blood in stool Upper Hematemesis Melena Lower Hematochezia
Accessory	Liver Hepatitis Viral hepatitis Autoimmune hepatitis Alcoholic hepatitis Cirrhosis PBC Fatty liver MASLD Vascular Budd–Chiari syndrome Hepatic veno-occlusive disease Portal hypertension Nutmeg liver Alcoholic liver disease Liver failure Hepatic encephalopathy Acute liver failure Liver abscess Pyogenic Amoebic Hepatorenal syndrome Peliosis hepatis Metabolic disorders Wilson's disease Hemochromatosis Gallbladder Cholecystitis Gallstone / Cholelithiasis Cholesterolosis Adenomyomatosis Postcholecystectomy syndrome Porcelain gallbladder Bile duct/ Other biliary tree Cholangitis Primary sclerosing cholangitis Secondary sclerosing cholangitis Ascending Cholestasis/Mirizzi's syndrome Biliary fistula Haemobilia Common bile duct Choledocholithiasis Biliary dyskinesia Sphincter of Oddi dysfunction Pancreatic Pancreatitis Acute Chronic Hereditary Pancreatic abscess Pancreatic pseudocyst Exocrine pancreatic insufficiency Pancreatic fistula
Other	Hernia Diaphragmatic Congenital Hiatus Inguinal Indirect Direct Umbilical Femoral Obturator Spigelian Lumbar Petit's Grynfeltt–Lesshaft Undefined location Incisional Internal hernia Richter's Peritoneal Peritonitis Spontaneous bacterial peritonitis Hemoperitoneum Pneumoperitoneum

Authority control databases: National	Germany United States France BnF data Japan Czech Republic Israel