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Showing posts with label Liver infection. Show all posts
Showing posts with label Liver infection. Show all posts

Tuesday, 11 November 2014

Hepatitis E

Hepatitis E


Hepatitis E is a waterborne disease caused by the Hepatitis E virus (HEV). Hepatitis E is mainly found in areas with poor sanitation and is typically caused by ingesting fecal matter. This disease is uncommon in the U.S.. However, cases of Hepatitis E have been reported in the Middle East, Asia, Central America, and Africa (CDC).
Hepatitis A and E are normally contracted from eating contaminated food or drinking contaminated water. Hepatitis B, C, and D are contracted through contaminated blood. These forms of hepatitis can be either acute or chronic, although types B and C usually become chronic.

hepatitis e treatment

Although Hepatitis E often causes an acute and self-limiting infection (in that it usually goes away by itself and the patient recovers) with low mortality rates in the western world, it bears a high risk of developing chronic hepatitis in immunocompromised patients with substantial mortality rates. Organ transplant recipients who receive immunosuppressive medication to prevent rejection are thought to be the main population at risk for chronic hepatitis E. Furthermore, in healthy individuals during the duration of the infection (usually several weeks), the disease severely impairs a person’s ability to work, care for family members, and obtain food. Hepatitis E occasionally develops into an acute, severe liver disease, and is fatal in about 2% of all cases. Clinically, it is comparable to hepatitis A, but in pregnant women the disease is more often severe and is associated with a clinical syndrome called fulminant hepatic failure. Pregnant women, especially those in the third trimester, suffer an elevated mortality rate from the disease of around 20%.

Hepatitis E is a viral hepatitis (liver inflammation) caused by infection with a virus called hepatitis E virus (HEV). HEV is a positive-sense single-stranded RNA icosahedral virus with a 7.5 kilobase genome. HEV has a fecal-oral transmission route. It is one of five known hepatitis viruses: A, B, C, D, and E. Infection with this virus was first documented in 1955 during an outbreak in New Delhi, India.A preventative vaccine (HEV 239) is approved for use in China.


History

 The hepatitis E virus causes around 20 million infections a year. These result in around three million acute illnesses and as of 2010, 57,000 deaths annually. It is particularly dangerous for pregnant women, who can develop an acute form of the disease that is lethal in 20 percent of cases. The virus (HEV) is a major cause of illness and of death in the developing world and disproportionate cause of deaths among pregnant women.

hepatitis e treatment

 

The most recent common ancestor of Hepatitis E evolved between 536 and 1344 years ago. It diverged into two clades—an anthropotropic and an enzootic form—which subsequently evolved into genotypes 1 and 2 and genotypes 3 and 4 respectively. The divergence dates for the various genotypes are as follows: Genotypes 1/2 367–656 years ago; Genotypes 3/4 417–679 years ago. For the most recent common ancestor of the various viruses themselves: Genotype 1 between 87 and 199 years ago; Genotype 3 between 265 and 342 years ago; and Genotype 4 between 131 and 266 years ago. The anthropotropic strains (genotype 1 and 2) have evolved more recently than the others suggesting that this virus was originally a zooenosis.
The use of an avian strain confirmed the proposed topology of the genotypes 1–4 and suggested that the genus may have evolved 1.36 million years ago (range 0.23 million years ago to 2.6 million years ago). The use of a rat sequence also confirmed this topology and estimated date of divergence from the swine/human strains was 7.44×104 years ago (range 2.1×104 to 1.4×105 years ago). Since this date is approximately coincident with the advent of agriculture it may be that this virus originally infected rats and subsequently spread to pigs and then to humans. Additional work is required to support or refute this possibility as very few sequences have been isolated from species other than humans and suids.
Genotypes 1, 3 and 4 all increased their effective population sizes in the 20th century. The population size of genotype 1 increased noticeably in the last 30–35 years. Genotypes 3 and 4 population sizes began to increase in the late 19th century up to 1940–1945. Genotype 3 underwent a subsequent increase in population size until the 1960s. Since 1990 both genotypes' population sizes have been reduced back to levels last seen in the 19th century.
The overall mutation rate for the genome has been estimated at ~1.4×10−3 substitutions/site/year.

In 2004, there were two major outbreaks, both of them in sub-Saharan Africa. There was an outbreak in Chad in which, as of September 27, there were 1,442 reported cases and 46 deaths. The second was in Sudan with, as of September 28, 6,861 cases and 87 deaths. Increasingly, hepatitis E is being seen in developed nations, with reports of cases in the UK, US and Japan. The disease is thought to be a zoonosis in that animals are thought to be the source. Both deer and swine have been implicated.
In October 2007, an epidemic of hepatitis E was suspected in Kitgum District of northern Uganda where no previous epidemics had been documented. This outbreak has progressed to become one of the largest hepatitis E outbreaks in the world. By June 2009, the epidemic had caused illness in >10,196 persons and 160 deaths.
In 2011, a minor outbreak was reported in Tangail, a neighborhood of Dhaka, Bangladesh.
In June 2012, an outbreak was reported in city of Ichalkaranji, Maharashtra, India. As of June 14, 2012, 3232 cases were reported and 18 died. and 3 died in Shirol taluka of Kolhapur Maharashtra, India in June 2012. Officials in the Indian state of Maharashtra India suspect that contaminated water from the Panchganga river was responsible for the hepatitis E outbreak in Ichalkaranji.
In July 2012, an outbreak was reported in South Sudanese refugee camps in Maban County near the Sudan border. South Sudan's Ministry of Health reported over 400 cases and 16 fatalities as of September 13, 2012.Progressing further, as of February 2, 2013, 88 have died due to the outbreak. The "Medical charity Medecins Sans Frontieres (MSF) said it had treated almost 4,000 patients."
In April 2014 there was an outbreak in Nepal, Biratnagar Municipality with over 6,000 locals infected and at least 9 dead.
 Hepatitis E

 Signs and symptoms


The incubation period of hepatitis E varies from 3 to 8 weeks. After a short prodromal phase symptoms lasting from days to weeks follow. They may include jaundice, fatigue and nausea. The symptomatic phase coincides with elevated hepatic aminotransferase levels.
Viral RNA becomes detectable in stool and blood serum during incubation period. Serum IgM and IgG antibodies against HEV appear just before onset of clinical symptoms. Recovery leads to virus clearance from the blood, while the virus may persist in stool for much longer. Recovery is also marked by disappearance of IgM antibodies and increase of levels of IgG antibodies.
http://drhanyf75.blogspot.com/
Hepatitis E virus (HEV) particles in the cell culture supernatant of pork liver sausage sample A, collected at 33 dpi. A) Transmission electron micrograph

  



While usually an acute disease, in immunocompromised subjects—particularly in solid organ transplanted patients—hepatitis E may cause a chronic infection. Occasionally this may cause liver fibrosis and cirrhosis.





Hepatitis E
Hepatitis E



Hepatitis E
 

Transmission

Hepatitis E is prevalent in most developing countries, and common in any country with a hot climate. It is widespread in Southeast Asia, northern and central Africa, India, and Central America. It is spread mainly by the fecal-oral route due to fecal contamination of water supplies or food; person-to-person transmission is uncommon.
The incubation period following exposure to the hepatitis E virus ranges from three to eight weeks, with a mean of 40 days. Outbreaks of epidemic hepatitis E most commonly occur after heavy rainfalls and monsoons because of their disruption of water supplies. Major outbreaks have occurred in New Delhi, India (30,000 cases in 1955–1956), Burma (20,000 cases in 1976–1977), Kashmir, India (52,000 cases in 1978), Kanpur, India (79,000 cases in 1991), and China (100,000 cases between 1986 and 1988).
DEFRA said that there was evidence that the increase in hepatitis E in the UK was due to food-borne zoonoses, citing a study that found 10% of pork sausages on sale in the UK contained the virus. Some research suggests that food must reach a temperature of 70°C for 20 minutes to eliminate the risk of infection. An investigation by the Animal Health and Veterinary Laboratories Agency found hepatitis E in 49% of pigs in Scotland.


 Hepatitis E
Domestic animals have been reported as a reservoir for the hepatitis E virus, with some surveys showing infection rates exceeding 95% among domestic pigs. Replicative virus has been found in the small intestine, lymph nodes, colon and liver of experimentally infected pigs. Transmission after consumption of wild boar meat and uncooked deer meat has been reported as well. The rate of transmission to humans by this route and the public health importance of this are, however, still unclear.
A number of other small mammals have been identified as potential reservoirs: the lesser bandicoot rat (Bandicota bengalensis), the black rat (Rattus rattus brunneusculus) and the Asian house shrew (Suncus murinus). A new virus designated rat hepatitis E virus has been isolated.
A rabbit hepatitis E virus has also been described, with a study published in 2014 showing that research rabbits from two different American vendors showed seroprevalences of 40% for Supplier A and 50% for Supplier B when testing for antibodies against hepatitis E virus (HEV). Supplier A was a conventional rabbit farm, and supplier B was a commercial vendor of specific pathogen free (SPF) research rabbits. The study remarks "HEV probably is widespread in research rabbits, but effects on research remain unknown." Laboratory animal care personnel, researchers, and support staff represent a new population at risk for HEV infection, and research facilities should be diligent in measures to prevention of this possibly zoonotic pathogen.
An avian virus has been described that is associated with hepatitis-splenomegaly syndrome in chickens. This virus is genetically and antigenically related to mammalian HEV, and probably represents a new genus in the family.


Treatment

 Apart from supportive care, no specific validated treatment exists for acute hepatis E infection. Although ribavarin is not registered for Hepatitis E treatment, there is off-label experience for treating chronic Hepatitis E with this compound. The use of low doses, 600 to 800 milligrams per day, of ribavirin over a three-month period has been associated with viral clearance in about two-thirds of chronic cases. Other possible treatments include peginterferon or a combination of ribavirin and peginterferon. In general chronic HEV infection is associated with immunosuppressive therapies, but remarkably little is known about how different immunosuppressants affect HEV infection. In one thirds of patients with solid-organ transplantation viral clearance can be achieved by temporal reduction of the level of immunosuppression. Calcineurin inhibitors (like cyclosporin) stimulate and mycophenolic acid inhibit replication of Hepatitis E Virus and this should be considered when physicians select immunosuppressive therapies for patients at risk for Hepatitis E, for instance recipients of organ transplants.


Prevention

Improving sanitation is the most important measure in prevention of hepatitis E; this consists of proper treatment and disposal of human waste, higher standards for public water supplies, improved personal hygiene procedures and sanitary food preparation. Thus, prevention strategies of this disease are similar to those of many others that plague developing nations, and they require large-scale international financing of water supply and water treatment projects.

A vaccine based on recombinant viral proteins was developed in the 1990s and tested in a high-risk population (military personnel of Nepal) in 2001. The vaccine appeared to be effective and safe, but development was stopped for economic reasons, since hepatitis E is rare in developed countries. There is no licensed hepatitis E vaccine for use in the US.
Although other HEV vaccine trials, including trials conducted in populations in southern Asia, have shown candidate vaccines to be effective and well-tolerated, these vaccines have not yet been produced or made available to susceptible populations. The exception is China. After more than a year of scrutiny and inspection by China's State Food and Drug Administration (SFDA), a hepatitis E vaccine developed by Chinese scientists was available at the end of 2012. This vaccine—called HEV 239 and sold as Hecolin by its developer Xiamen Innovax Biotech—was approved for prevention of hepatitis E in 2012 by the Chinese Ministry of Science and Technology, following a phase 3 trial on two groups of 50,000 people each from Jiangsu Province where none of the vaccinated became infected during a 12-month period, compared to 15 in the group given placebo treatment. The first vaccine batches came out of Innovax' factory in late October 2012, and will be sold to Chinese distributors.

References

  1. Zhou X, de Man RA, de Knegt RJ, Metselaar HJ, Peppelenbosch MP, Pan Q.; De Man; De Knegt; Metselaar; Peppelenbosch; Pan (2013). "Epidemiology and management of chronic hepatitis E infection in solid organ transplantation: a comprehensive literature review". Rev Med Virol. 23 (5): 295–304. doi:10.1002/rmv.1751. PMID 23813631.
  2. WHO. "Global Alert and Response (GAR); Hepatitis E". Retrieved 26 January 2012.
  3. Hoofnagle, J. H.; Nelson, K. E.; Purcell, R. H. (2012). "Hepatitis E". New England Journal of Medicine 367 (13): 1237–1244. doi:10.1056/NEJMra1204512. PMID 23013075. edit
  4. Bonnet, D.; Kamar, N.; Izopet, J.; Alric, L. (2012). "L'hépatite virale E : Une maladie émergente". La Revue de Médecine Interne 33 (6): 328–334. doi:10.1016/j.revmed.2012.01.017. PMID 22405325. 
  5. Lu L, Li C, Hagedorn CH; Li; Hagedorn (2006). "Phylogenetic analysis of global hepatitis E virus sequences: genetic diversity, subtypes and zoonosis". Rev Med Virol 16 (1): 5–36. doi:10.1002/rmv.482. PMID 16175650.
  6. Miyahara K, Miyake Y, Yasunaka T et al. (2010). "Acute hepatitis due to hepatitis E virus genotype 1 as an imported infectious disease in Japan". Intern. Med. 49 (23): 2613–6. doi:10.2169/internalmedicine.49.4221. PMID 21139302.
  7. Doward, Jamie (21 September 2013). "Chefs fight for the right to serve their pork pink". The Observer newspaper. Retrieved 22 September 2013.
  8. "Hepatitis E Fact sheet".
  9. Satou K, Nishiura H; Nishiura (2007). "Transmission Dynamics of Hepatitis E Among Swine: Potential Impact upon Human Infection". BMC Vet. Res. 3: 9. doi:10.1186/1746-6148-3-9. PMC 1885244. PMID 17493260.
  10. Li TC, Chijiwa K, Sera N et al. (2005). "Hepatitis E Virus Transmission from Wild Boar Meat". Emerging Infect. Dis. 11 (12): 1958–60. doi:10.3201/eid1112.051041. PMC 3367655. PMID 16485490.
  11. Kuniholm MH & Nelson KE (2008). "Of Organ Meats and Hepatitis E Virus: One Part of a Larger Puzzle Is Solved". J Infect Dis 198 (12): 1727–1728. doi:10.1086/593212. PMID 18983247.
  12. "Wild Rats and Disease".
  13. Johne R, Plenge-Bönig A, Hess M, Ulrich RG, Reetz J, Schielke A; Plenge-Bönig; Hess; Ulrich; Reetz; Schielke (March 2010). "Detection of a novel hepatitis E-like virus in faeces of wild rats using a nested broad-spectrum RT-PCR". J. Gen. Virol. 91 (Pt 3): 750–8. doi:10.1099/vir.0.016584-0. PMID 19889929.
  14. Cheng X, Wang S, Dai X, Shi C, Wen Y, Zhu M, Zhan S, Meng J; Wang; Dai; Shi; Wen; Zhu; Zhan; Meng (2012). "Rabbit as a novel animal model for hepatitis e virus infection and vaccine evaluation". PLoS ONE 7 (12): e51616. doi:10.1371/journal.pone.0051616. PMC 3521758. PMID 23272124




Hepatitis D | hepatitis d symptoms | hepatitis c vaccine | hepatitis d causes,

Hepatitis D

hepatitis D virus (HDV) and classified as Hepatitis delta virus, is a disease caused by a small circular enveloped RNA virus. It is one of five known hepatitis viruses: A, B, C, D, and E. HDV is considered to be a subviral satellite because it can propagate only in the presence of the hepatitis B virus (HBV). Transmission of HDV can occur either via simultaneous infection with HBV (coinfection) or superimposed on chronic hepatitis B or hepatitis B carrier state (superinfection).

Hepatitis D



Hepatitis D, also known as the delta virus, is an infection that causes your liver to swell. It is caused by the hepatitis D virus (HDV) and is uncommon in the United States.
Hepatitis D is one of many forms of hepatitis—other types include hepatitis A, B, C, and E. Unlike the other forms, hepatitis D cannot be contracted on its own. You can only contract hepatitis D if you are already infected with hepatitis B.
There is no cure for hepatitis D and no vaccine to prevent it.

Hepatitis D 



Both superinfection and coinfection with HDV results in more severe complications compared to infection with HBV alone. These complications include a greater likelihood of experiencing liver failure in acute infections and a rapid progression to liver cirrhosis, with an increased chance of developing liver cancer in chronic infections In combination with hepatitis B virus, hepatitis D has the highest mortality rate of all the hepatitis infections, at 20%.

History

  D virus was first reported in the mid-1977 as a nuclear antigen in patients infected with HBV who had severe liver disease. This nuclear antigen was then thought to be a hepatitis B antigen and was called the delta antigen. Subsequent experiments in chimpanzees showed that the hepatitis delta antigen (HDAg) was a structural part of a pathogen that required HBV infection to replicate. The entire genome was cloned and sequenced in 1986. It was subsequently placed in its own genus: Deltavirus.

Hepatitis D

 

Three genotypes (I–III) were originally described. Genotype I has been isolated in Europe, North America, Africa and some Asia. Genotype II has been found in Japan, Taiwan, and Yakutia (Russia). Genotype III has been found exclusively in South America (Peru, Colombia, and Venezuela). Some genomes from Taiwan and the Okinawa islands have been difficult to type but have been placed in genotype 2. However it is now known that there are at least 8 genotypes of this virus (HDV-1 to HDV-8). Phylogenetic studies suggest an African origin for this pathogen.
An analysis of 36 strains of genotype 3 estimated that the most recent common ancestor of these strains originated around 1930. This genotype spread exponentially from early 1950s to the 1970s in South America. The substitution rate was estimated to be 1.07×10−3 substitutions per site per year.
Genotype 8 has also been isolated from South America. This genotype is usually only found in Africa and may have been imported into South America during the slave trade.
Genotypes, with the exception of type 1, appear to be restricted to certain geographical areas: HDV-2 (previously HDV-IIa) is found in Japan, Taiwan and Yakoutia, Russia; HDV-4 (previously HDV-IIb) in Japan and Taiwan; HDV-3 in the Amazonian region; HDV-5, HDV-6, HDV-7 and HDV-8 in Africa


Structure of virus

Hepatitis D

A significant difference between viroids and HDV is that, while viroids produce no proteins, HDV is known to produce one protein, namely HDAg. It comes in two forms; a 27kDa large-HDAg, and a small-HDAg of 24kDa. The N-terminals of the two forms are identical, they differ by 19 more amino acids in the C-terminal of the large HDAg. Both isoforms are produced from the same reading frame which contains an UAG stop codon at codon 196, which normally produces only the small-HDAg. However, editing by cellular enzyme adenosine deaminase-1 changes the stop codon to UCG, allowing the large-HDAg to be produced. Despite having 90% identical sequences, these two proteins play diverging roles during the course of an infection. HDAg-S is produced in the early stages of an infection and enters the nucleus and supports viral replication. HDAg-L, in contrast, is produced during the later stages of an infection, acts as an inhibitor of viral replication, and is required for assembly of viral particles. Thus RNA editing by the cellular enzymes is critical to the virus’ life cycle because it regulates the balance between viral replication and virion assembly.
Hepatitis D

Hepatitis D



Hepatitis D

Hepatitis D

Hepatitis D











Signs and symptoms


The symptoms of hepatitis B and hepatitis D are similar, so it can be difficult to tell which disease is causing your symptoms. Common symptoms include:

  • yellowing of skin and eyes (jaundice)
  • joint pain
  • abdominal pains
  • vomiting
  • loss of appetite                           
    Hepatitis D

  • dark urine
  • fatigue
Hepatitis D can also cause the symptoms of hepatitis B to worsen, or appear in those who have been infected but haven’t yet developed symptoms.
The virus can be acute (short-term) or chronic (long-term). If you have chronic hepatitis D, you are at a higher risk of developing complications from the disease. Long-term or chronic hepatitis D might be present in your body for some time before the symptoms develop.
If you have the chronic form of hepatitis B, you are more likely to develop chronic hepatitis D. 


Transmission

  transmission of hepatitis D are similar to those for hepatitis B. Infection is largely restricted to persons at high risk of hepatitis B infection, particularly injecting drug users and persons receiving clotting factor concentrates. Worldwide more than 15 million people are co-infected. HDV is rare in most developed countries, and is mostly associated with intravenous drug use. However, HDV is much more common in the immediate Mediterranean region, sub-Saharan Africa, the Middle East, and the northern part of South America. In all, about 20 million people may be infected with HDV.

Tests Used to Diagnose Hepatitis D

If you have symptoms of hepatitis D or B, you should see your doctor for a diagnosis. If you have symptoms of the disease without jaundice, your doctor may not suspect hepatitis.
Tell your doctor if you have been around anyone infected with hepatitis or if you’ve traveled to a country where hepatitis B is prevalent. According to the National Institutes of Health (NIH), you are at particularly high risk if you (NIH):
  • use IV drugs
  • are a man who has sex with other men
  • receive many blood transfusions
Your doctor will do a blood test to detect anti-hepatitis D antibodies in your blood. If antibodies are found, it means you have had exposure to the virus.
If your doctor suspects you have liver damage, he or she might also give you a liver function test. This is a blood test that measures the levels of liver enzymes in your blood. Results from this test will show if your liver is stressed or damaged.

Complications of Hepatitis D

Complications of hepatitis D include:

  • scarring of the liver (cirrhosis)
  • liver disease
  • liver cancer
People with long-term hepatitis D are more likely to suffer from these complications.


Treatment and prevention


The vaccine for hepatitis B protects against hepatitis D virus because of the latter's dependence on the presence of hepatitis B virus for it to replicate.
Low quality evidence suggests that interferon alpha can be effective in reducing the severity of the infection and the effect of the disease during the time the drug is given, but the benefit generally stops when the drug is discontinued, indicating that it does not cure the disease. Interferon is effective only in ~20% of cases.


The only known way to prevent hepatitis D is to avoid infection with hepatitis B. There is a vaccine for hepatitis B—which all children should receive. Adults who are at high risk for infection, especially IV drug users, should also be vaccinated.
Hepatitis D


Sources:

 

  • Delta Agent (Hepatitis D). (2010). National Institutes of Health. Retrieved June 26, 2012, from http://www.meddean.luc.edu/lumen/MedEd/orfpath/virhepd.htm
  • Hepatitis D. (2009). Centers for Disease Control and Prevention.Retrieved June 20, 2012, from http://www.cdc.gov/hepatitis/HDV/index.htm
  • Hepatitis D. (n.d.). The Children’s Hospital of Philadelphia.Retrieved June 20, 2012, from http://www.chop.edu/service/viral-hepatitis-clinical-care-program/hepatitis-d.html#diagnosis
  • Hepatitis D. (n.d.). World Health Organization.Retrieved June 20, 2012, from http://www.who.int/csr/disease/hepatitis/whocdscsrncs20011/en/index5.html
  • Viral Hepatitis D. (n.d.). Loyola University Chicago.Retrieved June 20, 2012, from http://www.meddean.luc.edu/lumen/MedEd/orfpath/virhepd.htm
  • Wang, KS; Choo, QL, Weiner, AJ, Ou, JH, Najarian, RC, Thayer, RM, Mullenbach, GT, Denniston, KJ, Gerin, JL, Houghton, M (1986 Oct 9–15). "Structure, sequence and expression of the hepatitis delta (delta) viral genome". Nature 323 (6088): 508–14. doi:10.1038/323508a0. PMID 3762705.
  • Fauquet, CM; Mayo MA; Maniloff J; Desselberger U; Ball LA (2005). "Deltavirus". Eight Report of the International Committee on Taxonomy of Viruses. London: 735–8.
  • Poisson F, Roingeard P, Baillou A, Dubois F, Bonelli F, Calogero RA, Goudeau A; Roingeard; Baillou; Dubois; Bonelli; Calogero; Goudeau (November 1993). "Characterization of RNA-binding domains of hepatitis delta antigen". J. Gen. Virol. 74 (Pt 11): 2473–8. doi:10.1099/0022-1317-74-11-2473. PMID 8245865.
  • Zuccola HJ, Rozzelle JE, Lemon SM, Erickson BW, Hogle JM; Rozzelle; Lemon; Erickson; Hogle (July 1998). "Structural basis of the oligomerization of hepatitis delta antigen". Structure 6 (7): 821–30. doi:10.1016/S0969-2126(98)00084-7. PMID 9687364.
  • Saldanha JA, Thomas HC, Monjardino JP; Thomas; Monjardino (July 1990). "Cloning and sequencing of RNA of hepatitis delta virus isolated from human serum". J. Gen. Virol. 71 (7): 1603–6. doi:10.1099/0022-1317-71-7-1603. PMID 2374010.
  • Elena SF, Dopazo J, Flores R, Diener TO, Moya A; Dopazo; Flores; Diener; Moya (July 1991). "Phylogeny of viroids, viroidlike satellite RNAs, and the viroidlike domain of hepatitis delta virus RNA". Proc. Natl. Acad. Sci. U.S.A. 88 (13): 5631–4. doi:10.1073/pnas.88.13.5631. PMC 51931. PMID 1712103.
  • Sureau, C (2006). "The role of the HBV envelope proteins in the HDV replication cycle". Current topics in microbiology and immunology. Current Topics in Microbiology and Immunology 307: 113–31. doi:10.1007/3-540-29802-9_6. ISBN 978-3-540-29801-4. PMID 16903223.
  • Yan H, Zhong G, Xu G, He W, Jing Z, Gao Z, Huang Y, Qi Y, Peng B, Wang H, Fu L, Song M, Chen P, Gao W, Ren B, Sun Y, Cai T, Feng X, Sui J, Li W; Zhong; Xu; He; Jing; Gao; Huang; Qi; Peng; Wang; Fu; Song; Chen; Gao; Ren; Sun; Cai; Feng; Sui; Li (2012). "Sodium taurocholate cotransporting polypeptide is a functional receptor for human hepatitis B and D virus". ELife 1: e00049. doi:10.7554/eLife.00049. PMC 3485615. PMID 23150796.
  • Engelke, M; Mills, K; Seitz, S; Simon, P; Gripon, P; Schnölzer, M; Urban, S (April 2006). "Characterization of a hepatitis B and hepatitis delta virus receptor binding site". Hepatology (Baltimore, Md.) 43 (4): 750–60. doi:10.1002/hep.21112. PMID 16557545.
  • Schulze, A; Schieck, A; Ni, Y; Mier, W; Urban, S (February 2010). "Fine Mapping of Pre-S Sequence Requirements for Hepatitis B Virus Large Envelope Protein-Mediated Receptor Interaction". Journal of Virology 84 (4): 1989–2000. doi:10.1128/JVI.01902-09. PMC 2812397. PMID 20007265.
  • Xia, YP; Yeh, CT, Ou, JH, Lai, MM (February 1992). "Characterization of nuclear targeting signal of hepatitis delta antigen: nuclear transport as a protein complex". Journal of Virology 66 (2): 914–21. PMC 240792. PMID 1731113.
  • Lehmann E, Brueckner F, Cramer P; Brueckner; Cramer (November 2007). "Molecular basis of RNA-dependent RNA polymerase II activity". Nature 450 (7168): 445–9. doi:10.1038/nature06290. PMID 18004386.
  • Filipovska J, Konarska MM; Konarska (January 2000). "Specific HDV RNA-templated transcription by pol II in vitro". RNA 6 (1): 41–54. doi:10.1017/S1355838200991167. PMC 1369892. PMID 10668797.
  • Greco-Stewart, VS; Schissel, E; Pelchat, M (2009-03-30). "The hepatitis delta virus RNA genome interacts with the human RNA polymerases I and III". Virology 386 (1): 12–5. doi:10.1016/j.virol.2009.02.007. PMID 19246067.


Monday, 10 November 2014

Hepatitis C

 

Hepatitis C

 Hepatitis C

Hepatitis C is an infectious disease affecting primarily the liver, caused by the hepatitis C virus (HCV). The infection is often asymptomatic, but chronic infection can lead to scarring of the liver and ultimately to cirrhosis, which is generally apparent after many years. In some cases, those with cirrhosis will go on to develop liver failure, liver cancer, or life-threatening esophageal and gastric varices.                               



                                                       

                                                                                 



                                      
Hepatitis C
Hep C is a viral infection that causes inflammation and scarring of the liver.  The prognosis of someone with this disease varies greatly. Some people are able to get rid of the disease entirely, some are able to live symptom free for decades and others have many more complications early on. The difference in quality of life can greatly depend on the overall health of the person. Holistic health can support the health of people and the health of their liver for increased quality of life.
- See more at: http://www.herbalremediesadvice.org/hepatitis-c.html#sthash.vwh03V0B.dpuf
Hep C is a viral infection that causes inflammation and scarring of the liver.  The prognosis of someone with this disease varies greatly. Some people are able to get rid of the disease entirely, some are able to live symptom free for decades and others have many more complications early on. The difference in quality of life can greatly depend on the overall health of the person. Holistic health can support the health of people and the health of their liver for increased quality of life.
- See more at: http://www.herbalremediesadvice.org/hepatitis-c.html#sthash.vwh03V0B.dpuf




Hep C is a viral infection that causes inflammation and scarring of the liver.  The prognosis of someone with this disease varies greatly. Some people are able to get rid of the disease entirely, some are able to live symptom free for decades and others have many more complications early on. The difference in quality of life can greatly depend on the overall health of the person. Holistic health can support the health of people and the health of their liver for increased quality of life.
- See more at: http://www.herbalremediesadvice.org/hepatitis-c.html#sthash.vwh03V0B.dpuf
is an infectious disease affecting primarily the liver, caused by the hepatitis C virus (HCV). The infection is often asymptomatic, but chronic infection can lead to scarring of the liver and ultimately to cirrhosis, which is generally apparent after many years. In some cases, those with cirrhosis will go on to develop liver failure, liver cancer, or life-threatening esophageal and gastric varices. 

 Hepatitis C
HCV is spread primarily by blood-to-blood contact associated with intravenous drug use, poorly sterilized medical equipment, and transfusions. An estimated 150–200 million people worldwide are infected with hepatitis C. 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. Hepatitis C infects only humans and chimpanzees.
The virus persists in the liver in about 85% of those infected. This chronic infection can be treated with medication: the standard therapy is a combination of peginterferon and ribavirin, with either boceprevir or telaprevir added in some cases. Overall, 50–80% of people treated are cured. Those who develop cirrhosis or liver cancer may require a liver transplant. Hepatitis C is the leading reason for liver transplantation, though the virus usually recurs after transplantation. No vaccine against hepatitis C is available.
Hepatitis C          

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 Dr. D.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. 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. The discovery led to significant improvements in diagnosis and improved 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 reduced the risk of blood transfusion-associated hepatitis in the U.S. from 30% in 1970 to virtually zero in 2000."
Chiron filed for several patents on the virus and its diagnosis. 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 income. He dropped the suit in 1998 after losing before an appeals court.
Hepatitis C 

It is estimated that 150–200 million people, or ~3% of the world's population, are living with chronic hepatitis C.About 3–4 million people are infected per year, and more than 350,000 people die yearly from hepatitis C-related diseases. 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. Rates have increased substantially in the 20th century due to a combination of intravenous drug abuse and reused but poorly sterilized medical equipment.


Hepatitis C 


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.
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. Rates of new infections have decreased in the Western world since the 1990s due to improved screening of blood before transfusion.
In the United States, about 2% of people have hepatitis C, with the number of new cases per year stabilized at 17,000 since 2007. The number of deaths from hepatitis C has increased to 15,800 in 2008 and by 2007 had overtaken HIV/AIDS as a cause of death in the USA. This mortality rate is expected to increase, as those infected by transfusion before HCV testing become apparent. In Europe the percentage of people with chronic infections has been estimated to be between 0.13 and 3.26%.
The total number of people with this infection is higher in some countries in Africa and Asia. Countries with particularly 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 a now-discontinued mass-treatment campaign for schistosomiasis, using improperly sterilized glass syringes.
 

Transmission / ExposureHepatitis C

Hepatitis C is usually spread when blood from a person infected with the Hepatitis C virus enters the body of someone who is not infected. Today, most people become infected with the Hepatitis C virus by sharing needles or other equipment to inject drugs. Before 1992, when widespread screening of the blood supply began in the United States, Hepatitis C was also commonly spread through blood transfusions and organ transplants.

People can become infected with the Hepatitis C virus during such activities as

  • Sharing needles, syringes, or other equipment to inject drugs
  • Needlestick injuries in health care settings
  • Being born to a mother who has Hepatitis C

Less commonly, a person can also get Hepatitis C virus infection through

  • Sharing personal care items that may have come in contact with another person’s blood, such as razors or toothbrushes
  • Having sexual contact with a person infected with the Hepatitis C virus  
  •  

 HCV in children and pregnancy

Hepatitis C

 

Compared with adults, infection in children is much less well 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. 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%). and prevalence in children (15%).
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. 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. Cesarean sections are not recommended. Breast feeding 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. The presentation in childhood may be asymptomatic or with elevated liver function tests. While infection is commonly asymptomatic both cirrhosis with liver failure and hepatocellular carcinoma may occur in childhood.

Can Hepatitis C be spread through sexual contact?

Yes, but the risk of transmission from sexual contact is believed to be low. The risk increases for those who have multiple sex partners, have a sexually transmitted disease, engage in rough sex, or are infected with HIV. More research is needed to better understand how and when Hepatitis C can be spread through sexual contact.

Can you get Hepatitis C by getting a tattoo or piercing?

A few major research studies have not shown Hepatitis C to be spread through licensed, commercial tattooing facilities. However, transmission of Hepatitis C (and other infectious diseases) is possible when poor infection-control practices are used during tattooing or piercing. Body art is becoming increasingly popular in the United States, and unregulated tattooing and piercing are known to occur in prisons and other informal or unregulated settings. Further research is needed to determine if these types of settings and exposures are responsible for Hepatitis C virus transmission.   




Can Hepatitis C be spread within a household?

Yes, but this does not occur very often. If Hepatitis C virus is spread within a household, it is most likely a result of direct, through-the-skin exposure to the blood of an infected household member.

How should blood spills be cleaned from surfaces to make sure that Hepatitis C virus is gone?

Any blood spills — including dried blood, which can still be infectious — should be cleaned using a dilution of one part household bleach to 10 parts water. Gloves should be worn when cleaning up blood spills.

How long does the Hepatitis C virus survive outside the body?

The Hepatitis C virus can survive outside the body at room temperature, on environmental surfaces, for at least 16 hours but no longer than 4 days.

What are ways Hepatitis C is not spread?

Hepatitis C virus is not spread by sharing eating utensils, breastfeeding, hugging, kissing, holding hands, coughing, or sneezing. It is also not spread through food or water.

Who is at risk for Hepatitis C?

Some people are at increased risk for Hepatitis C, including

  • Current injection drug users (currently the most common way Hepatitis C virus is spread in the United States)
  • Past injection drug users, including those who injected only one time or many years ago
  • Recipients of donated blood, blood products, and organs (once a common means of transmission but now rare in the United States since blood screening became available in 1992)
  • People who received a blood product for clotting problems made before 1987
  • Hemodialysis patients or persons who spent many years on dialysis for kidney failure
  • People who received body piercing or tattoos done with non-sterile instruments
  • People with known exposures to the Hepatitis C virus, such as
    • Health care workers injured by needlesticks
    • Recipients of blood or organs from a donor who tested positive for the Hepatitis C virus
  • HIV-infected persons
  • Children born to mothers infected with the Hepatitis C virus

Hepatitis C
Less common risks include:

  • Having sexual contact with a person who is infected with the Hepatitis C virus
  • Sharing personal care items, such as razors or toothbrushes, that may have come in contact with the blood of an infected person 
  • Hepatitis C

What is the risk of a pregnant woman passing Hepatitis C to her baby?

Hepatitis C is rarely passed from a pregnant woman to her baby. About 4 of every 100 infants born to mothers with Hepatitis C become infected with the virus. However, the risk becomes greater if the mother has both HIV infection and Hepatitis C.

Can a person get Hepatitis C from a mosquito or other insect bite?

Hepatitis C virus has not been shown to be transmitted by mosquitoes or other insects.

Can I donate blood, organs, or semen if I have Hepatitis C?

No, if you ever tested positive for the Hepatitis C virus (or Hepatitis B virus), experts recommend never donating blood, organs, or semen because this can spread the infection to the recipient.
Hepatitis C









Signs and symptoms

acute symptoms

Hepatitis C infection causes acute symptoms in 15% of cases. Symptoms are generally mild and vague, including a decreased appetite, fatigue, nausea, muscle or joint pains, and weight loss and rarely does acute liver failure result. Most cases of acute infection are not associated with jaundice. The infection resolves spontaneously in 10–50% of cases, which occurs more frequently in individuals who are young and female.
Hepatitis C 

Chronic symptoms

About 80% of those exposed to the virus develop a chronic infection. 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. Chronic hepatitis C can be associated with fatigue and mild cognitive problems. Chronic infection after several years may cause cirrhosis or liver cancer. The liver enzymes are normal in 7–53%. Late relapses after apparent cure have been reported, but these can be difficult to distinguish from reinfection.
Hepatitis C 


Fatty changes to the liver occur in about half of those infected and are usually present before cirrhosis develops. Usually (80% of the time) this change affects less than a third of the liver. Worldwide hepatitis C is the cause of 27% of cirrhosis cases and 25% of hepatocellular carcinoma. About 10–30% of those infected develop cirrhosis over 30 years. Cirrhosis is more common in those also infected with hepatitis B, schistosoma, or HIV, in alcoholics and in those of male gender. In those with hepatitis C, excess alcohol increases the risk of developing cirrhosis 100-fold. Those who develop cirrhosis have a 20-fold greater risk of hepatocellular carcinoma. This transformation occurs at a rate of 1–3% per year. Being infected with hepatitis B in additional to hepatitis C increases this risk further.
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. Ascites occurs at some stage in more than half of those who have a chronic infection.

Hepatitis C

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. Hepatitis C is also associated with Sjögren's syndrome (an autoimmune disorder); thrombocytopenia; lichen planus; porphyria cutanea tarda; necrolytic acral erythema; insulin resistance; diabetes mellitus; diabetic nephropathy; autoimmune thyroiditis and B-cell lymphoproliferative disorders. Thrombocytopenia is estimated to occur in 0.16% to 45.4% of people with chronic hepatitis C. 20–30% of people infected have rheumatoid factor — a type of antibody. Possible associations include Hyde's prurigo nodularis and membranoproliferative glomerulonephritis. Cardiomyopathy with associated arrhythmias has also been reported. A variety of central nervous system disorders have been reported. Chronic infection seems to be associated with an increased risk of pancreatic cancer.
Hepatitis C 



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

Several clinical pictures have been associated with this type of infection. 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 haemodialysis or family members of people with occult HCV. The clinical relevance of this form of infection is under investigation. The consequences of occult infection appear to be less severe than with chronic infection but can vary from minimal to hepatocellular carcinoma.
 Hepatitis C



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

Hepatitis C

What are the symptoms of acute Hepatitis C?

Approximately 70%–80% of people with acute Hepatitis C do not have any symptoms. Some people, however, can have mild to severe symptoms soon after being infected, including

  • Fever
  • Fatigue
  • Loss of appetite
  • Nausea
  • Vomiting
  • Abdominal pain
  • Dark urine
  • Clay-colored bowel movements
  • Joint pain
  • Jaundice (yellow color in the skin or eyes)

How soon after exposure to Hepatitis C do symptoms appear?

If symptoms occur, the average time is 6–7 weeks after exposure, but this can range from 2 weeks to 6 months. However, many people infected with the Hepatitis C virus do not develop symptoms.

Can a person spread Hepatitis C without having symptoms?

Yes, even if a person with Hepatitis C has no symptoms, he or she can still spread the virus to others.

Is it possible to have Hepatitis C and not know it?

Yes, many people who are infected with the Hepatitis C virus do not know they are infected because they do not look or feel sick.

What are the symptoms of chronic Hepatitis C?

Most people with chronic Hepatitis C do not have any symptoms. However, if a person has been infected for many years, his or her liver may be damaged. In many cases, there are no symptoms of the disease until liver problems have developed. In persons without symptoms, Hepatitis C is often detected during routine blood tests to measure liver function and liver enzyme (protein produced by the liver) level.

How serious is chronic Hepatitis C?

Chronic Hepatitis C is a serious disease that can result in long-term health problems, including liver damage, liver failure, liver cancer, or even death. It is the leading cause of cirrhosis and liver cancer and the most common reason for liver transplantation in the United States. Approximately 15,000 people die every year from Hepatitis C related liver disease.

What are the long-term effects of Hepatitis C?

Of every 100 people infected with the Hepatitis C virus, about

  • 75–85 people will develop chronic Hepatitis C virus infection; of those,
    • 60–70 people will go on to develop chronic liver disease
    • 5–20 people will go on to develop cirrhosis over a period of 20–30 years
    • 1–5 people will die from cirrhosis or liver cancer

 virus structure

Hepatitis C

Hepatitis C

Hepatitis C

Hepatitis C

Hepatitis C

Hepatitis C





Diagnosis

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). 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. 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. Chronic infections are typically asymptomatic during the first few decades, 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. Diagnosis in the infant is difficult as maternal antibodies may persist for up to 18 months.


Hepatitis C
Hepatitis C testing typically begins with blood testing to detect the presence of antibodies to the HCV, using an enzyme immunoassay. If this test is positive, a confirmatory test is then performed to verify the immunoassay and to determine the viral load. A recombinant immunoblot assay is used to verify the immunoassay and the viral load is determined by a HCV RNA polymerase chain reaction. If there are 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. It takes about 6–8 weeks following infection before the immunoassay will test positive. A number of tests are available as point of care testing which means that results are available within 30 minutes.
Liver enzymes are variable during the initial part of the infection and on average begin to rise at seven weeks after infection. The elevation of liver enzymes does not closely follow disease severity.




Hepatitis C

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



Hepatitis C


It is believed that only 5–50% of those infected in the United States and Canada are aware of their status. Testing is recommended in those at high risk, which includes injection drug users, those who have received blood transfusions before 1992, those who have been in jail, those on long term hemodialysis, and those with tattoos. Screening is also recommended in those with elevated liver enzymes, as this is frequently the only sign of chronic hepatitis. Routine screening is not currently recommended in the United States. In 2012, the U.S. Centers for Disease Control and Prevention (CDC) added a recommendation for a single screening test for those born between 1945 and 1965.



Hepatitis C

Can a person have normal liver enzyme (e.g., ALT) results and still have Hepatitis C?

Yes. It is common for persons with chronic Hepatitis C to have a liver enzyme level that goes up and down, with periodic returns to normal or near normal. Some infected persons have liver enzyme levels that are normal for over a year even though they have chronic liver disease. If the liver enzyme level is normal, persons should have their enzyme level re-checked several times over a 6–12 month period. If the liver enzyme level remains normal, the doctor may check it less frequently, such as once a year.

Who should get tested for Hepatitis C?

Talk to your doctor about being tested for Hepatitis C if any of the following are true:

  • You were born from 1945 through 1965
  • You are a current or former injection drug user, even if you injected only one time or many years ago.
  • You were treated for a blood clotting problem before 1987.
  • You received a blood transfusion or organ transplant before July 1992.
  • You are on long-term hemodialysis treatment.
  • You have abnormal liver tests or liver disease.
  • You work in health care or public safety and were exposed to blood through a needlestick or other sharp object injury.
  • You are infected with HIV.

If you are pregnant, should you be tested for Hepatitis C?

No, getting tested for Hepatitis C is not part of routine prenatal care. However, if a pregnant woman has risk factors for Hepatitis C virus infection, she should speak with her doctor about getting tested.

What blood tests are used to test for Hepatitis C?

  
Several different blood tests are used to test for Hepatitis C. A doctor may order just one or a combination of these tests. Typically, a person will first get a screening test that will show whether he or she has developed antibodies to the Hepatitis C virus. (An antibody is a substance found in the blood that the body produces in response to a virus.) Having a positive antibody test means that a person was exposed to the virus at some time in his or her life. If the antibody test is positive, a doctor will most likely order a second test to confirm whether the virus is still present in the person's bloodstream.
Hepatitis C




Treatment

HCV induces chronic infection in 50–80% of infected persons. Approximately 40–80% of these clear with treatment. In rare cases, infection can clear without treatment. Those with chronic hepatitis C are advised to avoid alcohol and medications toxic to the liver,and to be vaccinated for hepatitis A and hepatitis B. Ultrasound surveillance for hepatocellular carcinoma is recommended in those with accompanying cirrhosis.

In general, treatment is recommended for those with proven HCV infection and signs of liver inflammation. As of 2010, treatments consist of a combination of pegylated interferon alpha and the antiviral drug ribavirin for a period of 24 or 48 weeks, depending on HCV genotype.This produces cure rates of between 70 and 80% for genotype 2 and 3, respectively, and 45 to 70% for other genotypes. When combined with ribavirin, pegylated interferon-alpha-2a may be superior to pegylated interferon-alpha-2b, though the evidence is not strong.
Combining either boceprevir or telaprevir with ribavirin and peginterferon alfa improves antiviral response for hepatitis C genotype 1. Adverse effects with treatment are common, with half of people getting flu like symptoms and a third experiencing emotional problems. Treatment during the first six months is more effective than once hepatitis C has become chronic. If someone develops a new infection and it has not cleared after eight to twelve weeks, 24 weeks of pegylated interferon is recommended. In people with thalassemia, ribavirin appears to be useful but increases the need for transfusions.
Sofosbuvir with ribavirin and interferon appears to be around 90% effective in those with genotype 1, 4, 5, or 6 disease. Sofosbuvir with just ribavirin appears to be 70 to 95% effective in type 2 and 3 disease but has a higher rate of adverse effects. Treatments that contain ledipasvir and sofosbuvir for genotype 1 has success rates of around 93 to 99% but is very expensive. In genotype 6 infection, pegylated interferon and ribavirin is effective in 60 to 90% of cases. There is some tentative data for simeprevir use in type 6 disease as well.


Vaccination

Is there a vaccine that can prevent Hepatitis C?

Not yet. Vaccines are available only for Hepatitis A and Hepatitis B. Research into the development of a vaccine is under way.



Hepatitis C and Employment

Should a person infected with the Hepatitis C virus be restricted from working in certain jobs or settings?

CDC's recommendations for prevention and control of the Hepatitis C virus infection state that people should not be excluded from work, school, play, child care, or other settings because they have Hepatitis C. There is no evidence that people can get Hepatitis C from food handlers, teachers, or other service providers without blood-to-blood contact.



Hepatitis C

Prevention


As of 2011, no vaccine protects against contracting hepatitis C. However, there are a number under development and some have shown encouraging results. 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 intravenous drug users by about 75%.The screening of blood donors is important at a national level, as is adhering to universal precautions within healthcare facilities. In countries where there is an insufficient supply of sterile syringes, medications should be given orally rather than via injection (when possible).



Hepatitis C Diet


Such a diet contains nutrient-rich foods that support the liver as well as overall health. 

Food recommendations:

  • cold water fish high in omega 3’s
  • leafy green vegetables
  • root vegetables such as beets and carrots
  • artichoke hearts
  • grass-fed meats
  • fruits and vegetables high in antioxidants

People should especially avoid: 

  • processed foods
  • vegetables oils
  • trans fats
  • fast food or junk food
  • sugar
  • alcohol



Vitamins for Hepatitis C



The best source of vitamins and minerals is found in a nutrient-rich diet. Sometimes, getting ideal amounts of certain nutrients in the diet can be difficult due to nutrient-deficient soils or improper metabolism in the body. 

The following is an overview of vitamins for hep C. A person may need more or less of these depending on their diet, digestion and personal circumstances. 

  • Vitamin B complex
  • Vitamin C
  • Vitamin D3
  • Magnesium
  • Selenium
  • Essential Fatty Acids, Omega 3’s
  • Probiotics

Hepatitis C




Hepatitis C Diet

Such a diet contains nutrient-rich foods that support the liver as well as overall health.
Food recommendations:
  • cold water fish high in omega 3’s
  • leafy green vegetables
  • root vegetables such as beets and carrots
  • artichoke hearts
  • grass-fed meats
  • fruits and vegetables high in antioxidants
People should especially avoid:
  • processed foods
  • vegetables oils
  • trans fats
  • fast food or junk food
  • sugar
  • alcohol

Vitamins for Hepatitis C

The best source of vitamins and minerals is found in a nutrient-rich diet. Sometimes, getting ideal amounts of certain nutrients in the diet can be difficult due to nutrient-deficient soils or improper metabolism in the body.
The following is an overview of vitamins for hep C. A person may need more or less of these depending on their diet, digestion and personal circumstances.
  • Vitamin B complex
  • Vitamin C
  • Vitamin D3
  • Magnesium
  • Selenium
  • Essential Fatty Acids, Omega 3’s
  • Probiotics
- See more at: http://www.herbalremediesadvice.org/hepatitis-c.html#sthash.vwh03V0B.dpuf

Hepatitis C Diet

Such a diet contains nutrient-rich foods that support the liver as well as overall health.
Food recommendations:
  • cold water fish high in omega 3’s
  • leafy green vegetables
  • root vegetables such as beets and carrots
  • artichoke hearts
  • grass-fed meats
  • fruits and vegetables high in antioxidants
People should especially avoid:
  • processed foods
  • vegetables oils
  • trans fats
  • fast food or junk food
  • sugar
  • alcohol

Vitamins for Hepatitis C

The best source of vitamins and minerals is found in a nutrient-rich diet. Sometimes, getting ideal amounts of certain nutrients in the diet can be difficult due to nutrient-deficient soils or improper metabolism in the body.
The following is an overview of vitamins for hep C. A person may need more or less of these depending on their diet, digestion and personal circumstances.
  • Vitamin B complex
  • Vitamin C
  • Vitamin D3
  • Magnesium
  • Selenium
  • Essential Fatty Acids, Omega 3’s
  • Probiotics
- See more at: http://www.herbalremediesadvice.org/hepatitis-c.html#sthash.vwh03V0B.dpuf

Hepatitis C Diet

Such a diet contains nutrient-rich foods that support the liver as well as overall health.
Food recommendations:
  • cold water fish high in omega 3’s
  • leafy green vegetables
  • root vegetables such as beets and carrots
  • artichoke hearts
  • grass-fed meats
  • fruits and vegetables high in antioxidants
People should especially avoid:
  • processed foods
  • vegetables oils
  • trans fats
  • fast food or junk food
  • sugar
  • alcohol

Vitamins for Hepatitis C

The best source of vitamins and minerals is found in a nutrient-rich diet. Sometimes, getting ideal amounts of certain nutrients in the diet can be difficult due to nutrient-deficient soils or improper metabolism in the body.
The following is an overview of vitamins for hep C. A person may need more or less of these depending on their diet, digestion and personal circumstances.
  • Vitamin B complex
  • Vitamin C
  • Vitamin D3
  • Magnesium
  • Selenium
  • Essential Fatty Acids, Omega 3’s
  • Probiotics
- See more at: http://www.herbalremediesadvice.org/hepatitis-c.html#sthash.vwh03V0B.dpuf

Hepatitis C Diet

Such a diet contains nutrient-rich foods that support the liver as well as overall health.
Food recommendations:
  • cold water fish high in omega 3’s
  • leafy green vegetables
  • root vegetables such as beets and carrots
  • artichoke hearts
  • grass-fed meats
  • fruits and vegetables high in antioxidants
People should especially avoid:
  • processed foods
  • vegetables oils
  • trans fats
  • fast food or junk food
  • sugar
  • alcohol

Vitamins for Hepatitis C

The best source of vitamins and minerals is found in a nutrient-rich diet. Sometimes, getting ideal amounts of certain nutrients in the diet can be difficult due to nutrient-deficient soils or improper metabolism in the body.
The following is an overview of vitamins for hep C. A person may need more or less of these depending on their diet, digestion and personal circumstances.
  • Vitamin B complex
  • Vitamin C
  • Vitamin D3
  • Magnesium
  • Selenium
  • Essential Fatty Acids, Omega 3’s
  • Probiotics
- See more at: http://www.herbalremediesadvice.org/hepatitis-c.html#sthash.vwh03V0B.dpuf

References


  1. Mast EE (2004). "Mother-to-infant hepatitis C virus transmission and breastfeeding". Advances in Experimental Medicine and Biology 554: 211–6. doi:10.1007/978-1-4757-4242-8_18. PMID 15384578.
  2. Shivkumar, S; Peeling, R; Jafari, Y; Joseph, L; Pant Pai, N (2012-10-16). "Accuracy of Rapid and Point-of-Care Screening Tests for Hepatitis C: A Systematic Review and Meta-analysis.". Annals of Internal Medicine 157 (8): 558–66. doi:10.7326/0003-4819-157-8-201210160-00006. PMID 23070489.
  3. Moyer, VA; on behalf of the U.S. Preventive Services Task, Force* (2013-06-25). "Screening for Hepatitis C Virus Infection in Adults: U.S. Preventive Services Task Force Recommendation Statement.". Annals of Internal Medicine 159 (5): 349–57. doi:10.7326/0003-4819-159-5-201309030-00672. PMID 23798026.
  4. Moyer, VA; U.S. Preventive Services Task, Force (2013-09-03). "Screening for hepatitis C virus infection in adults: U.S. Preventive Services Task Force recommendation statement.". Annals of internal medicine 159 (5): 349–57. doi:10.7326/0003-4819-159-5-201309030-00672. PMID 23798026.
  5. Senadhi, V (July 2011). "A paradigm shift in the outpatient approach to liver function tests". Southern Medical Journal 104 (7): 521–5. doi:10.1097/SMJ.0b013e31821e8ff5. PMID 21886053.
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