10.13 Viral Hepatitis A, C, and E – Flashcards
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| T/F Hepatitis can be caused by protozoa. |
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| true |
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| What is the genome of hep A? |
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| +ssRNA |
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| What is the genome of hep C? |
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| +ssRNA |
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| What is the genome of hep D? |
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| -ssRNA |
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| What is the genome of hep E? |
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| +ssRNA |
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| What is the genome of hep G? |
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| +ssRNA |
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| Which viral hepatitises do we have a vaccine for? |
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| hep A, hep B hep E is forthcoming |
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| What viral family is hep A apart of? What is the structure of its virion? |
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| picornavirus; icosahedral, non-enveloped |
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| How many serotypes of hep A are there? |
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| 1 |
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| T/F Hep A is shed in the feces before symptoms. |
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| true |
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| What is the incubation of HAV? |
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| "short" 15-45 days (3 weeks) |
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| What are the symptoms of HAV? |
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| prodrome: fever, nausea, anorexia, pain in RUQ, dark urine, clay-colored stool icteric: jaundice, pruritis, hepatomegally |
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| T/F Many people infected with HAV do not become icteric. |
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| true |
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| What percent of HAV infections result in fulminant liver failure? |
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| .1% |
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| How do you diagnose hep A? |
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| IgM anti-HAV |
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| How does HAV cause disease? |
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| viral replicaiton in the liver leads to lymphoid cell infiltration, necrosis of parenchymal cells, proliferation of kupffer cells, biliary stasis and CTL damage to hepatocytes |
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| T/F Chronic infections due to HAV can occur. |
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| true but they are extremely rare |
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| What abnormal laboratory finding coincides exactly with the symptoms of HAV? |
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| increased ALT |
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| What's teh infection: disease ratio for HAV in adults? children? |
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| A 1:1 C 20:1 |
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| How long does the patient have IgM and IgG anti-HAV? |
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| IgM anti-HAV for 3-6 months; IgG anti-HAV for lifetime |
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| Besides the traditional hep a, b, c, etc. what other viruses cause hepatitis? |
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| CMV, EBV, coxsackievirus, etc. |
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| In a patient presenting with symptoms of hep a, what else should also be in your differential? |
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| other viral hepatitis, other infecitons (toxoplasmosis and others), drugs, alcohol, gallbladder disease, pancreatitis, autoimmune liver disease |
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| What two tests should you order on a person presenting with symptoms of hep A? |
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| hepatitis serologies and ultrasound |
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| What are the risk factors for HAV? |
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| personal contact, poor hygeine, overcrowding, day care, nursing homes, contaminated food (shellfish, vegetables, milk, water), illicit drug use, international travel, MSM |
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| How much has the incidence of HAV declined from 1995 to 2007? |
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| 92% |
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| What percent of adults of US and world have serological evidence of HAV infection? |
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| <50% of US >90% of world |
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| How do you treat hep A? |
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| supportive= anti-itch meds, anti-emetics, rest, adequate nutrition isolate pt if uncontrolled diarrhea |
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| How do you prevent hepatitis A? |
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| prophylaxis (improve hygiene or vaccinate) post exposure: passive immunity with Ig (.02 ml/kg IM) |
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| What type of vaccine is the HAV vaccine? |
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| inactivated whole virus vaccine (cell culture-adapted virus, inactivated wtih formalin) |
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| What are the commercial names for the hep A vaccine? |
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| Havrix (glaxosmithkline) and vaqta (merck) |
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| How many doses of the HAV vaccine are there? |
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| 2 doses 6-12 months apart |
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| What is twinrix? |
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| a vaccine for hep a and b |
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| Who should get the HAV vaccine? |
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| in1996 the CDC recommended only the at risk population but in 2006 it was recommended as part of routine vaccination of all children |
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| How do you administer HAV Ig? Is it effective? |
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| administer .02 mL/kg within 2 weeks and it is 80-90% effective |
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| What can you offer a person exposed to HAV to help prevent them getting the diseaes? |
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| single dose of hep A or Ig asap (give Ig for persons aged >40 years or those with underlying medical condition) |
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| What did hep c used to be called? |
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| non-A, non-B |
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| Describe the three genes that make the large precursor polyproten of hep C? |
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| C= nucleocapsid, core protein; conserved E= envelope (E1 and E2), hypervariable NS= nonstructural proteins |
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| T/F Envelope proteins and transmembrane proteins are both structural proteins of hep C. |
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| FALSE! envelope glycoproteins are structure; transmembrane proteins are nonstructural (both are part of hep c) |
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| T/F Hep C does not grow well in tissue culture. |
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| true |
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| ANtigenic variation for hep C is predominant in what protein? |
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| envelope glycoprotein E2 |
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| How is hep C able to establish such a chronic infeciton? |
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| exists as a quasispecies which enables immune escape |
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| How many genotypes of hep C are there? |
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| 6 |
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| What are the most common strains of hep C in the world? in the US? |
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| 1a and 1b in the world 1a in the US |
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| What is the most common chronic bloodborne infection in the US? |
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| HCV infection; approximately 3.2 million persons are chronically infected in the US |
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| What is the trend of HCV incidence in the US? |
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| declined after peak in 1992, since 2003, rates have plateaued |
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| What is the most common risk factor for HCV? |
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| injection drug-use |
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| How is HCV transmitted? |
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| percutaneous exposure to infectious blood |
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| Wheredoes HCV replicate? |
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| initally in monocytes, B and T cells then spread to liver where they replicate in hepatocytes with a high rate of infection |
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| What percent of hepatocytes are infected by HCV and how many virions are produced per day? |
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| 10% of hepatocytes 1x10^12 virions per day |
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| What percent of people with HCV clear the virus and don't develop chornic infection? |
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| 15-25% |
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| What percent of people experience HAV like symptoms 4-12 weeks after infection with HCV? |
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| 20-30% |
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| Infection with HCV results in a chronic carrier state in up to ___% of adults. |
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| 85% |
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| HCV infection is often diagnosed as a result of... |
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| routine examinations that reveal elevated ALT or when they are screened for blood donation |
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| T/F Chronic HCV diseaes is always severe. |
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| false, can range from mild to severe |
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| What is the average duration of time from infection with HCV to development of chronic hepatitis? |
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| 10-18 years |
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| What are the late sequalae of chronic hepatitis? |
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| cirrhosis and HCC |
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| What percent of those chronically infected with hep C go on to cirrhosis? |
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| 20% |
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| What percent of those with chronic HCV go on to develop HCC? |
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| 5% |
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| What percent of those chronically infected with HCV go on to experience fulminant liver failure? |
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| .1% |
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| What causes disease in HCV infection? |
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| mainly immune mediated cytokine storm (TH1, CTL, gamma interferon, perforins, apoptosis via NK cells, immune complex formation) |
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| How do certain viral proteins of HCV directly inhibit the immune response? |
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| inhibit interferon; HCV core binds to TNF receptor |
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| What is the leading cause of liver transplants? |
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| hep C |
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| What can affect the progression of hep C? |
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| genetics, immune status, behavioral factors, severeity increased with smoking and alcohol abuse and other co-infections |
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| How many deaths per year are due to hep C? |
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| 8,000-10,000 |
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| What are the different tests you can use to check for hep c infection and the pros and cons of each? |
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| hep c antigens are not detectable in the blood so we screen for antibodies. Antibodies are not found for 1-3 weeks after clinical onset and are absent in some patients. You can measure Ab to multiple hep C antigens by ELISA or other immunoassay PCR for viral RNA may be more sensitive |
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| What are the three tests used to test for hep C infection? |
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| check for anti-HCV antibodies via EIA/ELISA HCV recombinant immunoblot assay (HCV RIBA) nucleic acid test (NAT) for HCV RNA |
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| What is the treatment for Hep C? |
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| peglyated interferon alpha plus ribavirin for 24-48 weeks |
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| Pegylated interferon alpha plus ribavirin leads to rapid improvements in ALT levels are disappearance of detectable HCV RNA in up to ___% of patients. |
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| 70% |
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| A response to HCV treatment is considered "sustained" if... |
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| HCV RNA remains undetectable for 6 months or more after stopping therapy |
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| What is the new treatment for HCV/ |
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| telaprevir (Incivek) from vertex beceprevir (victrelis) from merck |
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| What is the cure rate when a protease inhibitor is added to conventional hep C treatment? |
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| 80% cure rate |
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| Which hep virus has no family? |
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| hep E, similar to calici and rubella viruses |
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| What is the genus of hep E? |
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| hepeviridae |
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| What is the genome and structure of hep E? |
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| +ssRNA nonenveloped, icosahedral |
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| How many genotypes/serotypes of hep E are there? |
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| 4 genotypes but only 1 serotype |
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| Is hep E zoonotic? |
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| man is the natural host but antibodies to HEV like viruses have been detected in primates and other animals. May be found in pigs and associated with eating undercooked pig liver. Also in boars, deer, and camels |
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| What is the major cause of acute hepatitis worldwide? |
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| HEV, most cases are in developing countries with poor sanitation |
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| T/F Hep E is frequently subclnical. |
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| true |
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| What percent of hep E results in fulminant liver failure? |
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| 1-3% (more common in pregnant women 15-25%) |
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| Which people who get hep E are most likely to have symptoms? |
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| adolescents and young adults (aged 15-44 yoa) and pregnant women In developed countries, symptoms are more common among older people (>45 yoa) particularly men |
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| Which population usually has mild or no symptoms when infected with hep E? |
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| children |
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| How long is the incubation period of hep E/ |
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| 40 days |
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| What causes the disease in hep E? |
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| immune response to virus and antigen/antibody complexes |
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| What are the risk factors for hep E/ |
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| poor sanitation person to person is uncommon and there is no evidence of sexual transmission or tranmission by transfusion |
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| Hwo do you prevent hep E? |
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| avoid drinking water of unknown purity, uncooked shellfish, and uncooked fruit/vegetables not peeled or prepared by traveler. passive immunization= high titer IgG (monoclonal antibodies in monkeys) working on vaccine: virus like particles made in insect cells or bacteria |
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| How do you diagnose hep E? |
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| should test with IgM but it's not available. Can get IgG in the US but its not routine. antigen test and PCR-feces test are in development |
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| What type of virus is hepatitis G? (family, genome) |
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| flavivirus; + ssRNA |
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| How common is hepatitis G infection? |
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| 2% of blood donors are positive; 35% of HIV patients are positive |
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| How do you transmit HGV? |
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| blood borne, maybe sexually, vertically |
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| Where does hep G replicate? |
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| lymphocytes, not hepatocytes (not shown to cause acute or chronic hepatitis) |
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| How do you diagnose HGV? |
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| HGV RNA |
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| Being coinfected with HGV can possibly benefit patients infected with... |
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| HIV |
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| What percent of viral hepatitis is caused by either HAV, HBV, or HCV? |
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| >95% |
