Hepatitis C overview: Difference between revisions
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*[[HIV]] infection | *[[HIV]] infection | ||
*[[Tattoo]] or [[piercing]] with infected needle sticks | *[[Tattoo]] or [[piercing]] with infected needle sticks | ||
==Screening== | |||
Persons living in regions highly prevalent with HCV and who have engaged in high risk should be screened. Screening by [[serological testing]], confirmed by [[nucleic acid amplification]] (NAT) for [[HCV RNA]] is required. Additionally, screening for other [[bloodborne infections]], such as [[HBV]] and [[HIV]], is required once diagnosis is made. The frequency of testing in these patients is unclear and should be individualized according to frequency of exposure to risk. | |||
==Treatment== | ==Treatment== | ||
Revision as of 14:18, 28 July 2014
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Hepatitis C |
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Diagnosis |
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Treatment |
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Hepatitis C overview On the Web |
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American Roentgen Ray Society Images of Hepatitis C overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-In-Chief: Yazan Daaboul; Serge Korjian
Overview
Hepatitis C virus (HCV) is a single-stranded RNA virus that causes liver injury. Initially discovered in 1989, HCV was found to be a bloodborne infection that tends to persist into a chronic state in the majority of cases. Although the exact pathogenesis and life cycle of HCV are poorly understood, it has been demonstrated that impaired innate and adaptive immunity to acute HCV may contribute to the development of chronic infection. While the transfusion of blood and blood products along with injectable therapy were considered the most common risk factors for HCV in the past, the use of injectable illicit drugs is currently the most important risk factor. In the absence of treatment, chronic HCV leads to liver cirrhosis several years after the initial infection, a course complicated by decompensated liver failure or hepatocellular carcinoma. Other extra-hepatic manifestations are also common. Specific patient populations should be screened for HCV first using HCV serological testing, or rarely directly by measuring HCV RNA in patients who have had previous HCV exposure, treatment-induced clearance, or immunosuppression. The diagnosis is made when anti-HCV and HCV RNA both demonstrate positive results. Measures to slow the progression of liver disease, such as vaccines against other diseases and awareness against the use of alcohol or drugs that injure the liver should be taken following diagnosis. Classically, interferon (IFN) therapy was used to treat HCV, followed by the use of ribavirin. More recently, protease inhibitors emerged as effective drugs of choice for HCV infection.
Historical Perspective
The discovery of hepatitis C virus was made based on early findings of patients with signs and symptoms of viral hepatitis lacking positive serologies for hepatitis A or B. These patients were originally described in 1974-5 to have "non-A, non-B viral hepatitis" (NANBH). It was not until 1989 that hepatitis C virus (HCV) was truly discovered when Qui-Lim Choo and colleagues successfully isolated the first cDNA clone 5-1-1 derived from NANBH genome. The first interferon-alpha (INF-a) to treat HCV was developed in 1986 and approved in 1991. Approximately 10-15 years later, the global effort to reduce the burden of HCV was launched; worldwide campaigns were led by the World Health Organization (WHO) and Centers for Disease Control and Prevention (CDC).
Pathophysiology
Hepatitis C virus (HCV) is a member of the genus Hepacivirus that belongs to the Flaviviridae family. It is an enveloped, single-stranded RNA virus that measures approximately 60 nm in diameter. The virus enters the cell using E1 and E2 envelope proteins. HCV RNA acts as template for the production of new proteins by translational, co-translational, and post-translational processes. These mechanisms lead to the synthesis of 10 proteins, 3 of which are structural and 7 of which are non-structural. In isolated acute HCV infection, the host immune system causes secretion of interferon-alpha and activation of natural killer cells, along with proper activation of adaptive immune cells. Chronic HCV is characterized by the impairment of these mechanisms. Eventually, chronic HCV infection leads to local inflammation and fibrogenesis causing hepatic injury and cirrhosis. Hepatocellular carcinoma, a known complication of chronic HCV infection, arises in cases of cirrhosis; the role of oncogenic proteins of HCV in the pathogenesis of hepatocellular carcinoma is yet to be elucidated.
Epidemiology and Demographics
HCV is a worldwide prevalent infection whose incidence rate is difficult to estimate due to its asymptomatic course early in the disease and lack of statistical figures in most countries. While the disease appears to be declining, several countries still suffer from a highly prevalence disease burden. Egypt is the country with the highest prevalence of HCV, HCV-associated cirrhosis, and hepatocellular carcinoma, and the prevalence tends to increase with age, suggesting ongoing new cases of HCV. Approximately one-fourth of all cases of cirrhosis and hepatocellular carcinoma are attributed to HCV worldwide. HCV infects males and females equally.
Risk Factors
The most important mode of HCV transmission is percutaneous blood exposure. Intravenous drug use is currently considered the most important risk factor for HCV infection. Populations at highest risk of HCV infection are those who have received blood and blood products, especially before 1992, and those who have received unsafe therapeutic injections, especially in Hemophilia patients before 1987.
Other less important risk factors are[1]:
- Hemodialysis
- Solid organ transplantation from infected donors
- Occupational exposure to blood, such as contaminated needle sticks
- Birth to infected mother in cases of detectable maternal HCV PCR at delivery
- Sexual intercourse with infected partner
- Sexual intercourse with multiple partners
- HIV infection
- Tattoo or piercing with infected needle sticks
Screening
Persons living in regions highly prevalent with HCV and who have engaged in high risk should be screened. Screening by serological testing, confirmed by nucleic acid amplification (NAT) for HCV RNA is required. Additionally, screening for other bloodborne infections, such as HBV and HIV, is required once diagnosis is made. The frequency of testing in these patients is unclear and should be individualized according to frequency of exposure to risk.
Treatment
The treatment of hepatitis C has changed dramatically over the past decade. Whereas relatively new protease inhibitors telaprevir and boceprevir were added to the regular regimen of IFN and ribavirin in 2011 to treat patients with genotype 1 HCV, newer oral agents sofosbuvir and simeprevir have demonstrated greater efficacy in viral clearance along with a better safety profile. New guidelines from the AASLD and the IDSA have recommended the use of these oral agents (particularly sofosbuvir) as first line agents in the treatment of chronic HCV in both relapsers and treatment-naive patients.
References
- ↑ Alter MJ (2007). "Epidemiology of hepatitis C virus infection". World J Gastroenterol. 13 (17): 2436–41. PMID 17552026.