Hepatitis C is an infectious disease caused by hepatitis C virus (HCV) that primarily affects the liver. During initial infection people often have mild or no symptoms. Sometimes fever, dark urine, stomach pain, and yellow-colored skin occur. This virus survives in the liver of about 75% to 85% of those initially infected. Early chronic infections usually have no symptoms. However, over the years, it often causes liver disease and sometimes cirrhosis. In some cases, those with cirrhosis will develop complications such as liver failure, liver cancer, or dilated blood vessels in the esophagus and stomach.
HCV is spread primarily by blood-to-blood contact associated with intravenous drug use, non-sterilized medical equipment, needle injury in health care, and transfusion. Using blood screening, the risk of transfusion is less than one-half-a-million. It can also spread from an infected mother to her baby during birth. It does not spread through superficial contact. This is one of five known hepatitis viruses: A, B, C, D, and E. The diagnosis is done by blood testing to look for antibodies against viruses or RNA. Testing is recommended for all people at risk.
There is no vaccine against hepatitis C. Prevention includes harm reduction efforts among people taking intravenous drugs and donated blood tests. Chronic infection can be cured about 95% of the time with antiviral drugs such as sofosbuvir or simeprevir. Peginterferon and ribavirin are the treatment of previous generations that have a cure rate of less than 50% and greater side effects. Gain access to newer treatments but can be expensive. Those who develop cirrhosis or liver cancer may require liver transplantation. Hepatitis C is the main reason for liver transplant, although viruses usually recur after transplantation.
It is estimated that 143 million people (2%) worldwide are infected with hepatitis C by 2015. In 2013 about 11 million new cases occurred. This is most common in Africa and Central and East Asia. Approximately 167,000 deaths from liver cancer and 326,000 deaths due to cirrhosis occur in 2015 due to hepatitis C. The presence of hepatitis C - initially only identified as a non-A type of non-B hepatitis - was recommended in the 1970s and proven in 1989. Hepatitis C only infecting humans and chimpanzees.
Video Hepatitis C
Signs and symptoms
Acute infection
Infection Hepatitis C causes acute symptoms in 15% of cases. Symptoms are generally mild and unclear, including decreased appetite, fatigue, nausea, muscle or joint pain, and weight loss and uncommon acute liver failure. Most cases of acute infection are not associated with jaundice. Infection resolves spontaneously in 10-50% of cases, which occurs more frequently in young individuals and women.
Chronic infection
About 80% of those exposed to the virus develop chronic infections. This is defined as the presence of detected viral replication for at least six months. Most have minimal or no symptoms during the initial decades of infection. Chronic hepatitis C can be associated with fatigue and mild cognitive problems. Chronic infection after a few years can cause cirrhosis or liver cancer. Normal liver enzymes in 7-53%. Relapse late after healing has clearly been reported, but this can be difficult to distinguish from re-infection.
Fatty changes in the liver occur in about half of those infected and are usually present before cirrhosis develops. Usually (80% of the time) these changes affect less than a third of the liver. Hepatitis C worldwide is the cause of 27% of cases of cirrhosis and 25% of hepatocellular cancer. About 10-30% of those infected develop cirrhosis for 30 years. Cirrhosis is more common in those who are also infected with hepatitis B, schistosoma, or HIV, in alcoholics and in men. In those with hepatitis C, excess alcohol increases the risk of developing 100-fold cirrhosis. Those who developed cirrhosis had a 20-fold greater risk of hepatocellular carcinoma. This transformation occurs at a rate of 1-3% per year. Hepatitis B infection other than hepatitis C increases this risk further.
Cirrhosis of the liver can cause portal hypertension, ascites (accumulation of fluid in the abdomen), easy bruising or bleeding, varicose veins (especially in the stomach and esophagus), jaundice, and cognitive impairment syndrome known as hepatic encephalopathy. Ascites occur at some stage in more than half of those with chronic infection.
Extrahepatic complications
The most common problem due to hepatitis C but not involving the liver is mixed cryoglobulinemia (usually type II) - inflammation of small and medium blood vessels. Hepatitis C is also associated with autoimmune disorders SjÃÆ'¶gren syndrome, low platelet count, lichen planus, cutanea tarda porphyry, necrolytic erythema, insulin resistance, diabetes mellitus, diabetic nephropathy, autoimmune thyroiditis, and lymphoproliferative disorders cell-B. 20-30% of infected people have a rheumatoid factor - a type of antibody. Associations that may include Hyde prurigo nodularis and membranoproliferative glomerulonephritis. Cardiomyopathy with associated abnormal heart rhythms has also been reported. Various central nervous system disorders have been reported. Chronic infection appears to be associated with an increased risk of pancreatic cancer.
Invisible infection
People who have been infected with hepatitis C may appear to clear the virus but remain infected. The virus is not detected by conventional testing but can be found with ultra-sensitive tests. The original detection method was to show the viral genome in liver biopsy, but newer methods included antibody tests for viral core proteins and virus genome detection after first concentrating virus particles with ultracentrifugation. A form of infection with moderate elevated serum liver enzymes but no antibodies to hepatitis C has also been reported. This form is known as a cryptogenic occult infection.
Some clinical images have been linked to this type of infection. It can be found in people with anti-hepatitis-C antibody but with normal serum levels of liver enzymes; in antibody-negative individuals with elevated liver enzymes caused by unknown causes; in healthy populations without evidence of liver disease; and in groups at risk for HCV infection including those undergoing hemodialysis or family members of people with occult HCV. The clinical relevance of this form of infection is under investigation. The consequences of a hidden infection appear to be less severe than with chronic infection but may vary from minimal to hepatocellular carcinoma.
The degree of occult infection in those who seem to be cured is controversial but appears to be low. 40% of those with hepatitis but with negative hepatitis C serology and absence of detectable serum genomes in serum have hepatitis C virus in the liver on biopsy. How common this happens to children is unknown.
Maps Hepatitis C
Virology
Hepatitis C virus (HCV) is a small, enclosed, single-stranded, and positive RNA virus. It is a member of the genus Hepacivirus in the family Flaviviridae . There are seven major genotypes of HCV, known as genotype 1-7. The genotype is divided into several subtypes with the number of subtypes dependent 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 other genotype. Genotype 1 is also the most common in South America and Europe.
The half-life of viral particles in serum is about 3 hours and may be as short as 45 minutes. In an infected person, about 10 12 virus particles are produced daily. In addition to replicate in the liver, the virus can multiply in lymphocytes.
Transmission
The main route of transmission in developed countries is the use of intravenous drugs (IDUs), while in developing countries the main methods are blood transfusions and unsafe medical procedures. The cause of transmission remains unknown in 20% of cases; However, many of these are believed to be taken into account by IDUs.
Drug use
Intravenous drug use (IDU) is a major risk factor for hepatitis C in many parts of the world. Of the 77 countries reviewed, 25 (including the United States) were found to have a prevalence of hepatitis C in intravenous drug users between 60% and 80%. Twelve countries have rates of more than 80%. It is believed that ten million injecting 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 total. The occurrence of hepatitis C among prisoners in the United States is 10 to 20 times of the events observed in the general population; this has been linked to high-risk behavior in prisons such as IDUs and tattoos with nonsterile equipment. The use of shared intranasal drugs can also be a risk factor.
Healthcare Exposure
Blood transfusions, blood product transfusions, or organ transplants without HCV screening carry significant risk of infection. The United States conducted universal screening in 1992 and Canada performed universal screening in 1990. It reduced the risk from one in 200 units to between one in 10,000 to one in 10,000,000 per unit of blood. This low risk persists because there is a period of about 11-70 days between potential blood donors getting hepatitis C and a positive blood test depends on the method. Some countries do not filter hepatitis C because of the cost.
Those who have had a hypodermic needle injury from a person who is HCV positive have about 1.8% chance then contract the disease itself. The risk is greater if the needle is hollow and stab wound inside. There is a risk of exposure to the mucosa to the blood, but this risk is low, and there is no risk if blood exposure occurs on the skin intact.
Hospital equipment has also been documented as a hepatitis C transmission method, including reuse of needles and syringes; multi-drug bottles; infusion bag; and improperly sterilized surgical equipment, among others. Limitations in the implementation and enforcement of rigorous standard precautions in public and private dental and medical facilities are known to be a major cause of HCV spread in Egypt, the country with the highest infection rates in the world.
Sexual intercourse
Sexual transmission of hepatitis C is rare. Studies that examine the risk of HCV transmission between heterosexual couples, when one is infected and others do not, have found a very low risk. Sexual practices that involve higher levels of trauma in anogenital mucosa, such as rectal penetrating sex, or those that occur when there are concurrent sexually transmitted infections, including HIV or genital ulceration, present a greater risk. The US Department of Veterans Affairs recommends the use of condoms to prevent the transmission of hepatitis C to those who have multiple partners, but not in relationships involving only one partner.
Body modification
Tattoos are associated with a two to three times increased risk of hepatitis C . This may be caused by non-sterilized equipment or contamination of the dye used. Tattoos or piercings performed well before the mid-1980s, "underground," or non-professionals of particular concern, because sterile techniques in such settings may be lacking. The risk also appears to be larger for larger tattoos. It is estimated that almost half of the inmates share an unsterilized tattoo equipment. Rarely for tattoos in licensed facilities to be directly linked to HCV infection.
Personal care items such as razors, toothbrushes, and manicuring or pedicuring equipment can be contaminated with blood. Sharing such items has the potential to cause exposure to HCV. Appropriate attention should be taken regarding any medical conditions that cause bleeding, such as injuries and injuries. HCV does not spread through ordinary contact, such as hugging, kissing, or sharing a meal or cooking utensil. Nor is it transmitted through food or water.
Mother-to-child transmission
Transmission of mother-to-baby hepatitis C occurs in less than 10% of pregnancies. There is no action to change this risk. It is not clear when transmission occurs during pregnancy, but can occur during pregnancy and during labor. Prolonged labor is associated with a greater risk of transmission. There is no evidence that breastfeeding spreads HCV; However, to be careful, infected mothers are advised to avoid breastfeeding if their nipples are cracked and bleeding, or if their viral load is high.
Diagnosis
There are a number of diagnostic tests for hepatitis C , including antibody enzymes HCV or ELISA antibodies, recombinant immunoblot assays, and chain reaction of quantitative HCV RNA polymerase (PCR). HCV RNA can be detected by PCR usually one to two weeks after infection, while antibodies can be substantially longer formed and thus detectable.
Chronic hepatitis C is defined as an infection with a hepatitis C virus that persists for more than six months based on the presence of RNA. Chronic infection is usually asymptomatic for the first few decades, and is thus most commonly found after investigation of elevated liver enzyme levels or during routine screening of high-risk individuals. The test can not distinguish between acute and chronic infections. Diagnosis in infants is difficult because maternal antibodies can last up to 18 months.
Serology
Testing Hepatitis C usually begins with a blood test to detect the presence of antibodies against HCV, using the immunoassay enzyme. If the test is positive, a confirmatory test is then performed to verify the immunoassay and to determine the viral load. The recombinant immunoblot test is used to verify the immunoassay and viral load determined by the HCV RNA polymerase chain reaction. If there is no RNA and a positive immunoblot, it means that the person tested has an earlier infection but cleans it with treatment or spontaneously; if the immunoblot is negative, that means the immunoassay is wrong. It takes about 6-8 weeks after infection before immunoassay will be tested positive. A number of tests are available as testing point of care which means the results are available in 30 minutes.
Liver enzymes vary during the early part of the infection and the average begins to increase at seven weeks after infection. Increased liver enzymes do not closely follow the severity of the disease.
Biopsy
Liver biopsy is used to determine the extent of liver damage; However, there is a risk of this procedure. Typical changes seen are lymphocytes in the parenchyma, lymphoid follicles in the portal triad, and changes in the bile ducts. There are a number of blood tests available that try to determine the degree of liver fibrosis and reduce the need for biopsy.
Screening
It is believed that only 5-50% of those infected in the United States and Canada are aware of their status. Tests are recommended for those at high risk, including injecting drug users, those who have received blood transfusions before 1992, those who have been imprisoned, those who underwent long-term hemodialysis, and those with tattoos. Screening is also recommended in those who have high liver enzymes, as this is the only sign of chronic hepatitis. Routine screening is currently not recommended in the United States. In 2012, the US Centers for Disease Control and Prevention (CDC) added recommendations for a screening test for those born between 1945 and 1965. In Canada, one screening is recommended for those born between 1945 and 1975.
Prevention
By 2016, no approved vaccine protects against contracting hepatitis C . The combination of harm reduction strategies, such as the provision of new needles and syringes and the treatment of substance use, lowers the risk of hepatitis C to intravenous drug users by about 75%. Blood screening is important at the national level, such as following universal precautions in health facilities. In countries where supply of sterile needles is insufficient, drugs should be given orally rather than by injection (if possible).
Treatment
HCV induces chronic infection in 80% of infected people. Approximately 95% is clear with treatment. In rare cases, the infection can be cured without treatment. Those who are chronically hepatitis C are advised to avoid toxic drugs in the liver and alcohol. They should be vaccinated against hepatitis A and hepatitis B. The use of acetaminophen is generally considered safe at reduced doses. Non-steroidal anti-inflammatory drugs (NSAIDs) are not recommended in those with advanced liver disease due to an increased risk of bleeding. Ultrasound surveillance for hepatocellular carcinoma is recommended in those with accompanying cirrhosis. Coffee consumption has been associated with a slower rate of liver scarring in those who are infected with HCV.
Drugs
Treatment with antiviral drugs is recommended in all people with proven chronic hepatitis C who are not at high risk of dying from other causes. People with the highest risk of complications should be treated first, with the risk of complications based on the level of scarring of the liver. The recommended initial treatment depends on the type of hepatitis C virus, if the person has received previous hepatitis C treatment, and whether a person has cirrhosis or not.
No previous 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 copies viral per milliliter of blood) or 12 weeks of elbasvir/grazoprevir, ledipasvir/sofosbuvir, or sofosbuvir/velpatasvir. Sofosbuvir with daclatasvir or simeprevir can also be used.
- HCV genotype 1a (with compensatory cirrhosis): 12 weeks elbasvir/grazoprevir, glecaprevir/pibrentasvir, ledipasvir/sofosbuvir, or sofosbuvir/velpatasvir. Alternative treatment regimens of elbasvir/grazoprevir with weight-based ribavirin for 16 weeks can be used if HCV is found to have an antiviral resistance mutation against the NS5A protease inhibitor.
- HCV genotype 1b (no cirrhosis): 8 weeks of glecaprevir/pibrentasvir or ledipasvir/sofosbuvir (with the above mentioned limit) or 12 weeks elbasvir/grazoprevir, ledipasvir/sofosbuvir, or sofosbuvir/velpatasvir. Alternative regimens include 12 weeks of ombitasvir/paritaprevir/ritonavir with dacabuvir or 12 weeks of sofosbuvir with daclatasvir or simeprevir.
- HCV genotype 1b (with compensated cirrhosis): 12 weeks elbasvir/grazoprevir, glecaprevir/pibrentasvir, ledipasvir/sofosbuvir, or sofosbuvir/velpatasvir. The 12-week paritaprevir/ritonavir/ombitasvir program with dacabuvir can also be used.
- HCV genotype 2 (no cirrhosis): 8 weeks of glecaprevir/pibrentasvir or 12 weeks of sofosbuvir/velpatasvir. Alternatively, 12 weeks of sofosbuvir/daclatasvir may be used.
- HCV genotype 2 (with compensatory cirrhosis): 12 weeks of sofosbuvir/velpatasvir or glecaprevir/pibrentasvir. Alternative sofosbuvir/daclatasvir regimens may be used for 16-24 weeks.
- HCV genotype 3 (no cirrhosis): 8 weeks of glecaprevir/pibrentasvir or 12 weeks of sofosbuvir/velpatasvir or sofosbuvir and daclatasvir.
- HCV genotype 3 (with compensatory cirrhosis): 12 weeks of glecaprevir/pibrentasvir, sofosbuvir/velpatasvir, or if there is a specific antiviral mutation, 12 weeks of sofosbuvir/velpatasvir/voxilaprevir (when there are certain antiviral mutations), or 24 weeks of sofosbuvir and daclatasvir.
- HCV genotype 4 (no cirrhosis): 8 weeks glecaprevir/pibrentasvir or 12 weeks of sofosbuvir/velpatasvir, elbasvir/grazoprevir, or ledipasvir/sofosbuvir. 12 weeks of ombitasvir/paritaprevir/ritonavir regimen is also acceptable in combination with ribavirin by weight.
- HCV genotype 4 (with compensatory cirrhosis): A 12 weeks' weekly sofosbuvir/velpatasvir regimen, glecaprevir/pibrentasavir, elbasvir/grazoprevir, or ledipasvir/sofosbuvir is recommended. 12 weeks of ombitasvir/paritaprevir/ritonavir with weight-based ribavirin is an acceptable alternative.
- HCV genotype 5 or 6 (with or without compensatory cirrhosis): If there is no cirrhosis, then 8 weeks of glareprevir/pibrentasvir is recommended. If cirrhosis is present, then 12 weeks of glecaprevir/pibrentasvir, sofosbuvir/velpatasvir, or ledipasvir/sofosbuvir are justified.
Chronic infection can be cured about 95% of the time with recommended treatment by 2017. Getting access to this treatment can be expensive. The combination of sofosbuvir, velpatasvir, and voxilaprevir can be used in those who have previously been treated with sofosbuvir or other drugs that inhibit NS5A and do not recover.
Prior to 2011, treatment consisted of a combination of pegylated interferon alpha and ribavirin for a period of 24 or 48 weeks, depending on the HCV genotype. This results in a cure rate of between 70 and 80% for genotypes 2 and 3, respectively, and 45 to 70% for genotypes 1 and 4. Adverse effects with this treatment are common, with half of people experiencing flu-like symptoms and one-third experiencing emotional problems. Treatment for the first six months is more effective than once hepatitis C becomes chronic. In those with chronic hepatitis B, treatment for hepatitis C results in reactivation of hepatitis B in about 25%.
Surgery
Cirrhosis due to hepatitis C is a common reason for liver transplant although the virus usually (80-90% of cases) recurs thereafter. Transplant infections cause 10-30% of people develop cirrhosis within five years. Treatment with pegylated interferon and post-transplant ribavirin reduced the risk of recurrence by up to 70%.
Alternative medicine
Some alternative therapies are claimed by their supporters to help for hepatitis C including milk thistle, ginseng, and colloidal silver. However, no alternative therapy has been shown to improve outcomes in hepatitis C , and there is no evidence that alternative therapies have any effect on the virus at all.
Prognosis
The response to treatment was measured by sustained viral response (SVR), defined as the absence of detectable RNA from hepatitis C virus in blood serum for at least 24 weeks after discontinuation, and rapid virologic response (RVR) defined as level undetectable achieved within four weeks of treatment. Successful treatment reduces the future risk of hepatocellular carcinoma by 75%.
Prior to 2012 ongoing responses occurred in about 40-50% in people with HCV genotype 1 who were given 48 weeks of treatment. Continuous responses are seen in 70-80% of people with HCV genotype 2 and 3 with 24 weeks of treatment. The ongoing response occurs about 65% in those with genotype 4 after 48 weeks of treatment. Evidence for treatment in genotype 6 is still uncommon and what evidence supports treatment for 48 weeks at the same dose used for genotype 1 disease.
Epidemiology
It is estimated that 143 million people (2%) of people worldwide live with chronic hepatitis C . About 3-4 million people are infected annually, and more than 350,000 people die each year from hepatitis C-related diseases. During 2010 it is estimated that 16,000 people died from acute infections while 196,000 deaths result from liver cancer due to infection. Prices have risen substantially in the 20th century due to a combination of intravenous drug abuse and reuse but less sterilized medical equipment.
High prices (& gt; 3.5% of the infected population) in Central and Eastern Asia, North Africa and the Middle East, they are medium (1.5% -3.5%) in South and Southeast Asia, sub-Saharan Africa, Andean , Central and South America, Latin America, the Caribbean, Oceania, Australasia and Central Europe, East and West; and they are low (& lt; 1.5%) in Asia-Pacific, Tropical Latin America and North America.
Among those who are chronically infected, the risk of cirrhosis after 20 years varies between studies but is estimated to be ~ 10-15% for men and ~ 1-5% for women. The reason for this difference is unknown. After cirrhosis is formed, the rate of development of hepatocellular carcinoma is ~ 1-4% per year. The rate of new infections has declined in the Western world since the 1990s due to increased blood screening prior to transfusion.
In the United States, about 2% of people have chronic hepatitis C . By 2014, an estimated 30,500 new acute hepatitis C cases occur (0.7 per 100,000 population), an increase from 2010-2012. The number of deaths due to hepatitis C has increased to 15,800 in 2008 after taking over HIV/AIDS as the cause of death in the United States in 2007. By 2014 it is the largest cause of infectious deaths in the United States. The mortality rate is expected to increase, as those infected by transfusions prior to the HCV test become clear. In Europe the percentage of people with chronic infection is estimated to be between 0.13 and 3.26%.
In the UK about 160,000 people are chronically infected. Between 2006 and 2011 28,000 about 3%, received treatment.
The total number of people with this infection is higher in some countries in Africa and Asia. Countries with very high rates of infection include Egypt (22%), Pakistan (4.8%) and China (3.2%). It is believed that the high prevalence in Egypt is linked to the now-discontinued mass-drug campaign for schistosomiasis, using improperly sterile glass spray.
History
In the mid-1970s, Harvey J. Alter, Head of the Infectious Disease Section at the Transfusion Medicine Department at the National Institutes of Health, and his team of researchers demonstrates how most cases of post-transfusion hepatitis are not due to hepatitis A or B virus. Despite this discovery, an international research effort to identify the virus, originally 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, in collaboration with Daniel W. Bradley at the Centers for Disease Control and Prevention, used a new molecular cloning approach to identify unknown organisms and develop diagnostic tests. In 1988, Alter confirmed the virus by verifying its presence in the NANBH specimen panel. In April 1989, the invention of HCV was published in two articles in the journal Science. These findings led to significant improvements in the diagnosis and improvement of antiviral treatment. In 2000, Drs. 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 reduce the risk of blood transfusion-related hepatitis in the US from 30% in 1970 to almost zero by 2000."
Chiron filed several patents on the virus and diagnosis. A patent application compromised by the CDC was dropped in 1990 after Chiron paid $ 1.9 million for the CDC and $ 337,500 to Bradley. In 1994, Bradley sued Chiron, attempting to revoke patent rights, including himself as a coin exchange, and received royalty damages and revenues. He dropped his lawsuit in 1998 after losing before a court of appeal.
Society and culture
World Hepatitis Day, held on July 28, is coordinated by the World Hepatitis Alliance. The economic cost of hepatitis C is significant both for individuals and communities. In the United States the average lifetime cost of the illness is estimated at 33,407 USD in 2003 with the cost of liver transplant in 2011 at a cost of about 200,000 USD. In Canada the cost of antiviral treatment was as high as 30,000 CAD in 2003, while the cost of the United States was between 9,200 and 17,600 in 1998 USD. In many areas of the world, people can not afford to pay for antiviral treatment because they have no insurance or insurance that they have will not pay for antivirus. At the UK National Health Service's treatment level for hepatitis C is higher among the rich group per 2010-2012 data. Spanish anesthesiologist Juan Maeso infected 275 patients between 1988 and 1997 when he used the same needle to provide opioids to patients and patients. For this he was imprisoned.
Custom population
Children and pregnancy
Compared with adults, infections in children are much less well understood. Worldwide the prevalence of hepatitis C virus infection in pregnant women and children has been estimated at 1-8% and 0.05-5%, respectively. The vertical transmission rate is estimated at 3-5% and there is a high level of spontaneous cleansing (25-50%) in children. Higher rates have been reported for both vertical transmissions (18%, 6-36% and 41%). and prevalence in children (15%).
In developed countries, transmission around the time of birth is now a major cause of HCV infection. In the absence of virus in the mother's blood transmission seems rare. Factors associated with increased rates of infection include ruptured membranes more than 6 hours before delivery and procedures to expose the baby to maternal blood. Cesareans are not recommended. Breastfeeding is considered safe if the nipple is not damaged. Infection around the time of birth in one child does not increase the risk of subsequent pregnancy. All genotypes appear to have the same transmission risk.
HCV infection is common in children who were previously suspected of having non-B, non-B, and cryptogenic hepatitis. Presentation in childhood may be asymptomatic or with a high liver function test. While the infection is generally asymptomatic, cirrhosis with liver failure and hepatocellular carcinoma can occur in childhood.
Immunosuppressed
The rate of hepatitis C in people who are immunosuppressed is higher than the normal population. This is especially true of those with human immunodeficiency virus infection, organ transplant recipients and those with hypogammaglobulinemia. The infection in these people is associated with rapid development of extraordinary into cirrhosis.
Research
As of 2011, there are about a hundred drugs under development for hepatitis C. These include vaccines to treat hepatitis, immunomodulators, and cyclophilin inhibitors, among others. This potential new treatment occurs because of a better understanding of hepatitis C virus. There are a number of vaccines under development and some have shown encouraging results.
The combination of sofosbuvir and velpatasvir in one trial (reportedly in 2015) resulted in a 99% cure rate.
Animal model
One barrier to finding treatment for hepatitis C is the lack of appropriate animal models. Despite its moderate success, current research highlights the need for pre-clinical testing in mammalian systems such as mice, especially for vaccine development in poorer communities. Currently, chimpanzees remain a living system available for study, but their use has ethical issues and regulatory restrictions. While scientists have used human cell culture systems such as hepatocytes, questions have been asked about their accuracy in reflecting the body's response to infection.
One aspect of hepatitis research is to reproduce infections in mammalian models. The strategy is to introduce the liver tissue from humans to mice, a technique known as xenotransplantation. This is done by producing chimeric mice, and exposing mouse HCV infection. This engineering process is known to create humane rats, and provides an opportunity to study hepatitis C in the design of 3D liver architecture and evaluate antiviral compounds. Alternatively, producing rats raised with susceptibility to HCV will simplify the process of studying mouse models.
References
External links
- Hepatitis C in Curlie (based on DMOZ)
- "Recommendations for Testing, Managing, and Treating Hepatitis C". www.hcvguidelines.org . IDSA/AASLD . Retrieved July 28 2017 .
- Media related to Hepatitis C in Wikimedia Commons
- Drug portals
- Virus Portal
Source of the article : Wikipedia
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