Hepatitis C

Hepatitis C is an infectious disease caused by the

hepatitis C virus (HCV) that primarily affects the
Hepatitis C
liver;[2] it is a type of viral hepatitis.[7] During the initial
infection people often have mild or no symptoms.[1]
Occasionally a fever, dark urine, abdominal pain, and
yellow tinged skin occurs.[1] The virus persists in the
liver in about 75% to 85% of those initially infected.[1]
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]
Electron micrograph of hepatitis C virus from
HCV is spread primarily by blood-to-blood contact cell culture (scale = 50 nanometers)
associated with injection drug use, poorly sterilized
Specialty Gastroenterology, Infectious
medical equipment, needlestick injuries in healthcare,
disease
and transfusions.[1][3] Using blood screening, the risk
from a transfusion is less than one per two million.[1] It Symptoms Typically none[1]
may also be spread from an infected mother to her baby Complications Liver failure, liver cancer,
during birth.[1] It is not spread by superficial contact.[4] esophageal and gastric
It is one of five known hepatitis viruses: A, B, C, D,
varices[2]
and E.[8]
Duration Long term (80%)[1]
Diagnosis is by blood testing to look for either Causes Hepatitis C virus usually
antibodies to the virus or viral RNA.[1] In the United spread by blood-to-blood
States, screening for HCV infection is recommended in
contact[1][3]
all adults age 18 to 79 years old.[9]
Diagnostic Blood testing for antibodies or
There is no vaccine against hepatitis C.[1][10] method viral RNA[1]
Prevention includes harm reduction efforts among Prevention Sterile needles, testing
people who inject drugs, testing donated blood, and
donated blood[4]
treatment of people with chronic infection.[4][11]
Chronic infection can be cured more than 95% of the Treatment Medications, liver transplant[5]
time with antiviral medications such as sofosbuvir or Medication Antivirals (sofosbuvir,
simeprevir. [6][1][4] Peginterferon and ribavirin were simeprevir, others)[1][4]
earlier generation treatments that had a cure rate of less
Frequency 71 million (2017)[6]
than 50% and greater side effects.[4][12] Getting access
to the newer treatments, however, can be expensive.[4] Deaths 399,000 (2016)[6]
Those who develop cirrhosis or liver cancer may
require a liver transplant.[5] Hepatitis C is the leading reason for liver transplantation, though the virus
usually recurs after transplantation.[5]
An estimated 71 million people (1%) worldwide are infected with hepatitis C as of 2015.[13] 80% of the
health burden is concentrated in low- and middle-income countries,[14] with the highest levels of
prevalence in Africa and Central and East Asia.[4] About 167,000 deaths due to liver cancer and 326,000
deaths due to cirrhosis occurred in 2015 due to hepatitis C.[15] 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.[16]
Hepatitis C infects only humans and chimpanzees.[17]

Contents
Signs and symptoms
Acute infection
Chronic infection
Extrahepatic complications
Occult infection
Play media
Virology
Video summary (script)
Transmission
Drug use
Healthcare exposure
Sexual intercourse
Body modification
Shared personal items
Mother-to-child transmission
Diagnosis
Serology
Biopsy
Screening
Prevention
Treatment
Medications
Surgery
Alternative medicine
Prognosis
Spontaneous resolution
Epidemiology
History
Society and culture
Special populations
Children and pregnancy
Immunosuppressed
Research
Animal models
References
External links
Signs and symptoms

Acute infection

Acute symptoms develop in some 20–30% of those infected.[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][18][19] There is no evidence that acute hepatitis C can
alone cause acute liver failure, though liver injury and elevated liver enzymes may occur.[18][20] 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.[19]

Following the acute phase, the infection may resolve spontaneously in 10–50% of affected people; this
occurs more frequently in young people, and females.[18]

Chronic infection

About 80% of those exposed to the virus develop a chronic infection.[21] This is defined as the presence of
detectable viral replication for at least six months. Most experience minimal or no symptoms during the
initial few decades of the infection.[22] Chronic hepatitis C can be associated with fatigue[23] and mild
cognitive problems.[24] Chronic infection after several years may cause cirrhosis or liver cancer.[5] The
liver enzymes measured from blood samples are normal in 7–53%.[25] (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.[25]

Fatty changes to the liver occur in about half of those infected and are usually present before cirrhosis
develops.[26][27] Usually (80% of the time) this change affects less than a third of the liver.[26] Worldwide
hepatitis C is the cause of 27% of cirrhosis cases and 25% of hepatocellular carcinoma.[28] About 10–30%
of those infected develop cirrhosis over 30 years.[5][19] Cirrhosis is more common in those also infected
with hepatitis B, schistosoma, or HIV, in alcoholics and in those of male sex.[19] In those with hepatitis C,
excess alcohol increases the risk of developing cirrhosis 5-fold.[29] 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][19]
Being infected with hepatitis B in addition to hepatitis C increases this risk further.[30]

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.[31] Ascites occurs at some stage in
more than half of those who have a chronic infection.[32]

Extrahepatic complications

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.[33][34] 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.[35][36] 20–30% of people
infected have rheumatoid factor – a type of antibody.[37] Possible associations include Hyde's prurigo
nodularis[38] and membranoproliferative glomerulonephritis.[23] Cardiomyopathy with associated abnormal
heart rhythms has also been reported.[39] A variety of central nervous system disorders has been
reported.[40] Chronic infection seems to be associated with an increased risk of pancreatic cancer.[10][41]
People may experience other issues in the mouth such as dryness, salivary duct stones, and crusted lesions
around the mouth.[42][43][44]

Occult infection

Persons who have been infected with hepatitis C may appear to clear the virus but remain infected.[45] The
virus is not detectable with conventional testing but can be found with ultra-sensitive tests.[46] 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.[47] A form of infection with persistently moderately
elevated serum liver enzymes but without antibodies to hepatitis C has also been reported.[48] This form is
known as cryptogenic occult infection.

Several clinical pictures have been associated with this type of infection.[49] 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.[50] The
consequences of occult infection appear to be less severe than with chronic infection but can vary from
minimal to hepatocellular carcinoma.[47]

The rate of occult infection in those apparently cured is controversial but appears to be low.[25] 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.[51] How commonly this occurs in children is
unknown.[52]

Virology
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.[23] There are seven major genotypes of HCV,
which are known as genotypes one to seven.[53] 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.[19] 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.[54][55]
In an infected person, about 1012 virus particles are produced each day.[54] In addition to replicating in the
liver the virus can multiply in lymphocytes.[56]

Transmission
Generally, percutaneous contact with contaminated blood is responsible for most infections; however, the
method of transmission is strongly dependent on both a country's geography and economic status.[57]
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;[58] however, many of these are believed to be
accounted for by injection drug use.[18]

Drug use

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 Hepatitis C infection in the United States by source
between 60% and 80% among people who use
injection drugs.[21][59] Twelve countries had rates
greater than 80%.[21] 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.[21] 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 nonsterile equipment.[60][61] Shared intranasal drug use may also be a risk
factor.[62]

Healthcare exposure

Blood transfusion, transfusion of blood products, or organ transplants without HCV screening carry
significant risks of infection.[19] The United States instituted universal screening in 1992[63] and Canada
instituted universal screening in 1990.[64] This decreased the risk from one in 200 units[63] to between one
in 10,000 to one in 10,000,000 per unit of blood.[18][58] 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.[58] Some countries do not screen for hepatitis C due to the cost.[28]

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.[19] The risk is greater if the needle in
question is hollow and the puncture wound is deep.[28] 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.[28]

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.[28] 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 used to have the highest rate of infection in the world back in
2012, and currently one of the lowest in the world in 2021.[65][66]

Sexual intercourse

Sexual transmission of hepatitis C is uncommon.[12] Studies examining the risk of HCV transmission
between heterosexual partners, when one is infected and the other is not, have found very low risks.[12]
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.[12][67] 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.[68]

Body modification

Tattooing is associated with two to threefold increased risk of hepatitis C.[69] This can be due to either
improperly sterilized equipment or contamination of the dyes being used.[69] 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.[69] It is
estimated that nearly half of prison inmates share unsterilized tattooing equipment.[69] It is rare for tattoos in
a licensed facility to be directly associated with HCV infection.[70]

Shared personal items

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.[71][72] Appropriate
caution should be taken regarding any medical condition that results in bleeding, such as cuts and sores.[72]
HCV is not spread through casual contact, such as hugging, kissing, or sharing eating or cooking
utensils,[72] nor is it transmitted through food or water.[73]

Mother-to-child transmission

Mother-to-child transmission of hepatitis C occurs in fewer than 10% of pregnancies.[74] There are no
measures that alter this risk.[74] It is not clear when transmission occurs during pregnancy, but it may occur
both during gestation and at delivery.[58] A long labor is associated with a greater risk of transmission.[28]
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,[75] or if her viral loads are high.[58]

Diagnosis
There are a number of diagnostic tests for
hepatitis C, including HCV antibody enzyme
immunoassay or ELISA, recombinant immunoblot
assay, and quantitative HCV RNA polymerase
chain reaction (PCR).[19] 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.[31]

Diagnosing patients is generally a challenge as

patients with acute illness generally present with
Serologic profile of Hepatitis C infection
mild, non-specific flu-like symptoms,[76] while the
transition from acute to chronic is sub-clinical.[77]
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.[22] Chronic infections are typically asymptomatic during the first few
decades,[22] 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.[28] Diagnosis in the infant is difficult as maternal antibodies may persist for up to 18
months.[52]

Serology

Hepatitis C testing typically begins with blood testing to detect the presence of antibodies to the HCV,
using an enzyme immunoassay.[19] If this test is positive, a confirmatory test is then performed to verify the
immunoassay and to determine the viral load.[19] A recombinant immunoblot assay is used to verify the
immunoassay and the viral load is determined by an HCV RNA polymerase chain reaction.[19] 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.[19] It takes about 6–8 weeks following infection before the immunoassay will test positive.[23] A
number of tests are available as point of care testing which means that results are available within
30 minutes.[78]

Liver enzymes are variable during the initial part of the infection[22] and on average begin to rise at seven
weeks after infection.[23] The elevation of liver enzymes does not closely follow disease severity.[23]

Biopsy

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

It is believed that only 5–50% of those infected in the United States and Canada are aware of their
status.[69] Routine screening for those between the ages of 18 and 79 was recommended by the United
States Preventive Services Task Force in 2020.[9] Previously testing was recommended for those at high
risk, which includes injection drug users, those who have received blood transfusions before 1992,[62]
those who have been in jail, those on long term hemodialysis,[62] and those with tattoos.[69] Screening is
also recommended in those with elevated liver enzymes, as this is frequently the only sign of chronic
hepatitis.[79] As of 2012, the U.S. Centers for Disease Control and Prevention (CDC) recommends a single
screening test for those born between 1945 and 1965.[80][81][82][83] In Canada one time screening is
recommended for those born between 1945 and 1975.[84]

Prevention
As of 2016, no approved vaccine protects against contracting hepatitis C.[85] 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%.[86] The screening of blood
donors is important at a national level, as is adhering to universal precautions within healthcare facilities.[23]
In countries where there is an insufficient supply of sterile syringes, medications should be given orally
rather than via injection (when possible).[28] Recent research also suggests that treating people with active
infection, thereby reducing the potential for transmission, may be an effective preventive measure.[11]
Treatment
Those with chronic hepatitis C are advised to avoid alcohol and medications toxic to the liver.[19] They
should also be vaccinated against hepatitis A and hepatitis B due to the increased risk if also infected.[19]
Use of acetaminophen is generally considered safe at reduced doses.[12] Nonsteroidal anti-inflammatory
drugs (NSAIDs) are not recommended in those with advanced liver disease due to an increased risk of
bleeding.[12] Ultrasound surveillance for hepatocellular carcinoma is recommended in those with
accompanying cirrhosis.[19] Coffee consumption has been associated with a slower rate of liver scarring in
those infected with HCV.[12]

Medications

Approximately 90% of chronic cases clear with treatment.[4]

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

No prior treatment
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): 12 weeks of elbasvir/grazoprevir,
glecaprevir/pibrentasvir, 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): 12 weeks of elbasvir/grazoprevir,
glecaprevir/pibrentasvir, 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): 12 weeks of sofosbuvir/velpatasvir or
glecaprevir/pibrentasvir. 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): 12 weeks of glecaprevir/pibrentasvir,
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): A 12-week regimen of sofosbuvir/velpatasvir,
glecaprevir/pibrentasavir, 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): If no cirrhosis is present, then
8 weeks of glecaprevir/pibrentasvir is recommended. If cirrhosis is present, then a 12-week
course of glecaprevir/pibrentasvir, sofosbuvir/velpatasvir, or ledipasvir/sofosbuvir is
warranted.[100]

Chronic infection can be cured in more than 90% of people with medications.[101] Getting access to these
treatments however can be expensive.[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.[19] This produces cure rates of between 70 and 80% for
genotype 2 and 3, respectively, and 45 to 70% for genotypes 1 and 4.[103] Adverse effects with these
treatments were common, with half of people getting flu-like symptoms and a third experiencing emotional
problems.[19] Treatment during the first six months is more effective than once hepatitis C has become
chronic.[31] In those with chronic hepatitis B, treatment for hepatitis C results in reactivation of hepatitis B
in about 25%.[104]

Surgery

Cirrhosis due to hepatitis C is a common reason for liver transplantation[31] 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 unclear evidence regarding if antiviral medication
was useful if the graft became reinfected.[108]

Alternative medicine

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 in hepatitis C, and no evidence exists that alternative therapies have any effect on the virus at
all.[109][110][111]

Prognosis
 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 the
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]
Disability-adjusted life year for hepatitis C in
2004 per 100,000 inhabitants Prior to 2012 sustained response occurs in about 40–
no data 35–40 50% in people with HCV genotype 1 given 48 weeks
<10 40–45 of treatment.[5] A sustained response is seen in 70–80%
10–15 45–50 of people with HCV genotypes 2 and 3 with 24 weeks
15–20 50–75 of treatment.[5] A sustained response occurs about 65%
20–25 75–100 in those with genotype 4 after 48 weeks of treatment.
25–30 >100 Finally for genotype 6, a 48 weeks treatment with
30–35
pegylated interferon and ribavirin results in a higher rate
in sustained responses than for genotype 1 (86% vs.
52%). Further studies are needed for a 24 weeks
treatment and at lower dosages.[114]

Spontaneous resolution

About 15–45% of those infected spontaneously clear the virus within 6 months, with the rest going on the
develop chronic infection.[4] Spontaneous resolution following acute infection appears more common in
females, and younger persons, and appears to also be influenced by genetic factors.[18] Chronic infection
may also resolve spontaneously months or years after the acute phase, though this is unusual.[18]

Epidemiology
WHO estimated that 71 million (1%) people
globally are living with chronic hepatitis C in
its 2017 Global Hepatitis Report.[13] About
1.75 million people are infected per year, and
about 400,000 people die yearly from
hepatitis C-related diseases.[4] During 2010 it
is estimated that 16,000 people died from
acute infections while 196,000 deaths
occurred from liver cancer secondary to the
infection.[115] Rates have increased
substantially in the 20th century due to a
combination of intravenous drug abuse and Percentage of people infected with hepatitis C in 2015
reused but poorly sterilized medical
equipment.[28]

Rates are high (>3.5% population infected) in Central and East Asia, North Africa and the Middle East,
they are intermediate (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
they are low (<1.5%) in Asia-Pacific, Tropical Latin America and North America.[116]
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.[117] Rates of
new infections have decreased in the Western world since the 1990s due to improved screening of blood
before transfusion.[31]

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.[65] It was believed that the high prevalence in Egypt was
linked to a discontinued mass-treatment campaign for schistosomiasis, using improperly sterilized glass
syringes.[28]

In the United States, about 2% of people have chronic hepatitis C.[19] 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 England about 160,000 people are chronically infected.[124] Between 2006 and 2011 28,000, about 3%,
received treatment.[124] About half of people using a needle exchange in London in 2017/8 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 medication have been available to eradication the disease in 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
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. In April 1989, the discovery of HCV was
published in two articles in the journal Science.[131][132] The discovery led to significant improvements in
diagnosis and improved antiviral treatment.[10][130] In 2000, Alter and Houghton were honored with the
Lasker Award for Clinical Medical Research for
"pioneering work leading to the discovery of the
virus that causes hepatitis C and the development
of screening methods that reduced the risk of
blood transfusion-associated hepatitis in the U.S.
from 30% in 1970 to virtually zero in 2000."[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 coinventor, and receive damages and royalty Nobel Prize in Physiology or Medicine 2020: Seminal
income. He dropped the suit in 1998 after losing experiments by HJ Alter, M Houghton and CM Rice
before an appeals court.[135] leading to the discovery of HCV as the causative agent
of non-A, non-B hepatitis.
On October 5, 2020, Houghton and Alter,
together with Charles M. Rice, were awarded the
Nobel Prize in Physiology or Medicine for their work.[136][137]

Society and culture

World Hepatitis Day, held on July 28, is coordinated by the World Hepatitis Alliance.[138] 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[139] with the cost of a liver transplant as of
2011 costing approximately US$200,000.[140] In Canada the cost of a course of antiviral treatment is as
high as 30,000 CAD in 2003,[141] while the United States costs are between 9,200 and 17,600 in 1998
USD.[139] 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.[142] In the English National
Health Service treatment rates for hepatitis C are higher among wealthier groups per 2010–2012 data.[124]
Spanish anaesthetist Juan Maeso infected 275 patients between 1988 and 1997 as he used the same needles
to give both himself and the patients opioids.[143] For this he was jailed.[144]

Special populations

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.[145] 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%)[146][147] and prevalence in children (15%).[148]

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.[147] 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.[149] 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.[150] The presentation in childhood may be asymptomatic or with
elevated liver function tests.[151] While infection is commonly asymptomatic both cirrhosis with liver
failure and hepatocellular carcinoma may occur in childhood.

Immunosuppressed

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.[152] 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.[153]

Research
As of 2011, there are about one hundred medications in development for hepatitis C.[140] These include
vaccines to treat hepatitis, immunomodulators, and cyclophilin inhibitors, among others.[154] These
potential new treatments have come about due to a better understanding of the hepatitis C virus.[155] There
are a number of vaccines under development and some have shown encouraging results.[85]

The combination of sofosbuvir and velpatasvir in one trial (reported in 2015) resulted in cure rates of
99%.[156] More studies are needed to investigate the role of the preventive antiviral medication against
HCV recurrence after transplantation.[157]

Animal models

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.[158]

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 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.[158] Alternatively, generating inbred mice with susceptibility to
HCV would simplify the process of studying mouse models.

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External links
Hepatitis C (https://curlie.org/Health/Conditions_and_Diseases/Digestive_Disorders/Liver/H
epatitis/Hepatitis_C) at Curlie
"Recommendations for Testing, Managing, and Treating Hepatitis C" (http://www.hcvguidelin
es.org/). www.hcvguidelines.org. IDSA/AASLD. Retrieved 28 July 2017.
"Hepatitis C" (https://medlineplus.gov/hepatitisc.html). MedlinePlus. U.S. National Library of
Medicine.
Classification ICD-10: B17.1 (htt D
ps://icd.who.int/bro
wse10/2019/en#/B
17.1), B18.2 (http
s://icd.who.int/brow
se10/2019/en#/B1
8.2) · ICD-9-CM:
070.70 (http://www.
icd9data.com/getIC
D9Code.ashx?icd9
=070.70),070.4 (htt
p://www.icd9data.c
om/getICD9Code.a
shx?icd9=070.4),
070.5 (http://www.ic
d9data.com/getICD
 9Code.ashx?icd9=
070.5) · OMIM:
609532 (https://omi
m.org/entry/60953
2) · MeSH:
D006526 (https://w
ww.nlm.nih.gov/cgi/
mesh/2015/MB_cg
i?field=uid&term=D
006526) ·
DiseasesDB: 5783
(http://www.disease
sdatabase.com/dd
b5783.htm) ·
SNOMED CT:
186643004 (http://s
nomed.info/id/1866
43004)
External MedlinePlus:
resources 000284 (https://ww
w.nlm.nih.gov/medli
neplus/ency/article/
000284.htm) ·
eMedicine:
med/993 (https://e
medicine.medscap
e.com/med/993-ov
erview) ped/979 (ht
tp://www.emedicin
e.com/ped/topic97
9.htm#) · Patient
UK: Hepatitis C (htt
ps://patient.info/doc
tor/hepatitis-c-pro)

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