Hepatitis C
Hepatitis C | |
---|---|
liver transplant[5] | |
Medication | Antivirals (sofosbuvir, simeprevir, others)[1][4] |
Frequency | 58 million (2019)[4] |
Deaths | 290,000 (2019)[4] |
Hepatitis C is an
HCV is spread primarily by blood-to-blood contact associated with
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.
Signs and symptoms
Acute infection
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
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]
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
The most common problem due to hepatitis C but not involving the liver is mixed
Occult infection
Persons who have been infected with hepatitis C may appear to clear the virus but remain infected. 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
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
Drug use
Healthcare exposure
Those who have experienced a
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.[63]
For more, see HONOReform (Hepatitis Outbreaks National Organization for Reform).
Sexual intercourse
Sexual transmission of hepatitis C is uncommon.
Body modification
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.[68][69] Appropriate caution should be taken regarding any medical condition that results in bleeding, such as cuts and sores.[69] HCV is not spread through casual contact, such as hugging, kissing, or sharing eating or cooking utensils,[69] nor is it transmitted through food or water.[70]
Mother-to-child transmission
Diagnosis
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,[73] while the transition from acute to chronic is sub-clinical.[74] 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
Hepatitis C testing typically begins with
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
Screening
It is believed that only 5–50% of those infected in the United States and Canada are aware of their status.[66] 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,[60] those who have been incarcerated, those on long-term hemodialysis,[60] and those with tattoos.[66] Screening is also recommended for those with elevated liver enzymes, as this is frequently the only sign of chronic hepatitis.[76] 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.[77][78][79][80] In Canada, a one-time screening is recommended for those born between 1945 and 1975.[81]
Prevention
As of 2022, no approved
Hepatitis C vaccine phase 1 clinical trials are set to begin in the summer of 2023.[84]
Treatment
Those with chronic hepatitis C are advised to avoid
Medications
More than 95% of chronic cases clear with treatment.
No prior treatment
- HCV genotype 1a (no cirrhosis): 8 weeks of 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.[88] Sofosbuvir with either daclatasvir or simeprevir may also be used.[86]
- 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.[89]
- 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.[90]
- 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.[91]
- 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.[92]
- 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.[93]
- HCV genotype 3 (no cirrhosis): 8 weeks of glecaprevir/pibrentasvir or 12 weeks of sofosbuvir/velpatasvir or sofosbuvir and daclatasvir.[94]
- 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.[95]
- 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.[96]
- 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.[97]
- 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.[98]
More than 95% of people with chronic infection can be cured when treated with medications;[99] 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.[100]
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.[101] 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.[102]
Surgery
Cirrhosis due to hepatitis C is a common reason for
Alternative medicine
Several
Prognosis
no data <10 10–15 15–20 20–25 25–30 30–35 | 35–40 40–45 45–50 50–75 75–100 >100 |
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,[110] 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%.[111]
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.[112]
Spontaneous resolution
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
This section needs to be updated.(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.[113]
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.[114] 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.[115] 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.[116] The number of deaths from hepatitis C has increased to 15,800 in 2008[117] having overtaken HIV/AIDS as a cause of death in the US in 2007.[118] In 2014, it was the single greatest cause of infectious death in the United States.[119] This mortality rate is expected to increase, as those infected by transfusion before HCV testing become apparent.[120] In Europe, the percentage of people with chronic infections has been estimated to be between 0.13 and 3.26%.[121]
In the United Kingdom, about 118,000 people were chronically infected in 2019.
The total number of people with this infection is higher in some countries in Africa and Asia.[125] Countries with particularly high rates of infection include Pakistan (4.8%) and China (3.2%).[126]
Since 2014, extremely effective treatments have been available to eradicate the disease within 8–12 weeks in most people.[127] 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.[127] These numbers differ by country and improved in 2016, with some countries achieving higher cure rates than new infection rates (mostly high income countries).[127] By 2018, twelve countries are on track to achieve HCV elimination.[127] While antiviral agents will curb new infections, it is less clear whether they impact overall deaths and morbidity.[127] 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).[127]
History
In the mid-1970s,
At the time, Chiron was in talks with the Japanese health ministry to sell a biotech version of the hepatitis B vaccine. Simultaneously,
In April 1989, the "discovery" of HCV was published in two articles in the journal Science.[130][131] Chiron filed for several patents on the virus and its diagnosis.[132] 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.[133]
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.
Hepatitis C was finally "discovered" in 2005 when a Japanese team was able to propagate a molecular clone in a cell culture called Huh7.[137] 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.[138][139]
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).[140]
On October 5, 2020, Houghton and Alter, together with Charles M. Rice, were awarded the Nobel Prize in Physiology or Medicine for their work.[141][142]
Society and culture
This section needs to be updated.(July 2020) |
World Hepatitis Day, held on July 28, is coordinated by the World Hepatitis Alliance.[143] 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[144] with the cost of a liver transplant as of 2011[update] costing approximately US$200,000.[145] In Canada, the cost of a course of antiviral treatment is as high as 30,000 CAD in 2003,[146] while the United States costs are between 9,200 and US$17,600 in 1998.[144] 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.[147] In the English National Health Service treatment rates for hepatitis C were higher among less deprived groups in 2010–2012.[148]
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.[149][150]
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.[151] 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%)[152][153] and prevalence in children (15%).[154]
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.[153] 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.[155] 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.[156] The presentation in childhood may be asymptomatic or with elevated liver function tests.[157] 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
Research
As of 2011[update], there are about one hundred medications in development for hepatitis C.
The combination of sofosbuvir and velpatasvir in one trial (reported in 2015) resulted in cure rates of 99%.[163] More studies are needed to investigate the role of the preventive antiviral medication against HCV recurrence after transplantation.[164]
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
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.[165] Alternatively, generating inbred mice with susceptibility to HCV would simplify the process of studying mouse models.
See also
- PSI-6130, an experimental drug treatment
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External links
- Hepatitis C at Curlie
- "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.