Bohomolets Microbiology Lecture #16
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By Ms. Kostiuk from Microbiology department
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Bohomolets Microbiology Lecture #16
- 2. Changes in liver in patients with hepatitis Cirrhosis Hepatocellular carcinoma Local destruction in hepatocytes Norm Fibrose
- 4. Spreading of viral hepatitis
- 5. Incidence graphs for hepatitis
- 6. Obligate hepatotropic viruses ss – single-stranded ds – double-stranded l- linear c – circular Nonenveloped ssc DNA Cirkoviridae SENV Nonenveloped ssc DNA Parvoviridae TTV Enveloped ssl RNA + Flaviviridae HGV Nonenveloped ssl RNA + Caliciviridae HEV Enveloped ssc RNA - Deltavirus HDV Enveloped ssl RNA + Flaviviridae HCV Enveloped частково длц DNA Hepadnaviridae HBV Nonenveloped ssl RNA + Picornaviridae HAV Structure Genome Family Virus
- 7. Geographic distribution of Hepatitis A virus infection
- 9. Structure of HAV 5’ end of RNA has a protein that serves as a primer for transcription by RNA polymerase
- 10. Hepatitis A rate, by age and gender (United States, 1990) Transmission – fecal-oral route.
- 11. Hepatitis A rate, by age and gender (United States, 2001)
- 12. Events in hepatitis A virus infection
- 13. Concentration of Hepatitis A virus in various body fluids
- 16. Geographic distribution of Hepatitis B virus infection High Intermediate Low
- 17. Electron micrograph of Hepatitis B viruses
- 19. Some members of hepadnaviridae family infect certain rodents and ducks (but not HBV)
- 21. Electron micrograph of different types of HBV
- 22. Structure of HBV particles
- 23. HBV antigens HBsAg - hepatitis B surface antigen HBcAg – hepatitis B core antigen HBeAg –hepatitis B e antigen
- 24. Nucleic acid of HBV
- 25. Events during reproduction of HBV (1) Adherence with viral HBsAg
- 26. Events during reproduction of HBV (2) Some of the formed double-stranded closed-circular DNA integrates into the hepatocyte DNA (provirus)
- 27. Events during reproduction of HBV (3) HBs
- 31. The clinical features of hepatitis B
- 32. Man with jaundice caused by HBV
- 33. Hepatocellular carcinoma (hepatoma) associated with HBV-infection
- 35. Window period
- 37. Serologic test results in four stages of HBV infection Positive Positive Positive Positive HBcAb Negative Positive Negative Negative HBsAb Positive Negative Negative Positive HBsAg Chronic carries state Complete recovery Window phase Acute disease Test
- 39. Geographic distribution of HDV infection
- 41. Structure of HDV HDV uses the surface antigen of HBV (HBsAg) as a coat
- 46. Geographic distribution of HCV infection
- 48. Structure of hepatitis C virus
- 55. Geographic distribution of HEV infection
- 57. Clinical features of hepatitis viruses No None No ? Fecal-oral HEV No Ab to delta Ag. RNA Yes With coin-fection, same as HBV Parenteral HDV No HCV Ab. RNA Yes 5-9 weeks Parenteral HCV Yes HBsAg, HBsAb, IgM HBcAb. DNA Yes 10-15 weeks Parenteral HBV Yes IgM HAV. RNA No 3-5 weeks Fecal-oral HAV Vaccine Laboratory diagnosis ( immunoassay, PCR ) Chronic carriers Incuba-tion period Mode of transmission Virus
Notas del editor
- When certain viruses infect the liver, they cause hepatitis, an inflammatory disease marked by necrosis of hepatocytes and a mononuclear response that swells and disrupts the liver architecture.
- Many viruses cause hepatitis. Of these, 5 are commonly described as “hepatitis viruses”: HAV; HBV; non-A, non-B viruses, of which HCV is the most common; HDV – delta agent; and HEV.
- Viral hepatitis is a cause of considerable morbidity and mortality in the human population, both from acute infection and chronic sequel which include, in the case of hepatitis B, C and D, chronic active hepatitis and cirrhosis.
- The picture show us the most damaged by virus Hepatitis A regions.
- HAV is also known as enterovirus 72.
- Humans are the reservoir for HAV. HAV is transmitted by the fecal-oral route. Therefore children are the most frequently infected group. Common-source outbreaks arise from fecally contaminated water or food such as oysters grown in polluted water and eaten raw.
- As for pathogenesis, the virus probably replicates in the gastrointestinal tract and spreads to the liver via the blood. Hepatocytes are infected. But the mechanism by which cell damage occurs is unclear. HAV infection of cultured cells produces no cytopathic effect. It is likely that attack by cytotoxic T-cells causes the damage to the hepatocytes. The infection is cleared, the damage is repaired, and no chronic infection ensues.
- Decrease of cases of hepatitis A after beginning of vaccination program is evidence anti-hepatitis A vaccine effectiveness
- HAV is also known as enterovirus 72.
- Spherical and filamentous particles don’t contain DNA, they consist only of HBsAg
- HBsAg is responsible for the ability of the virus to infect its hosts
- mRNA not only functions in protein synthesis but also is the template for the minus strand of the progeny DNA (during 9-th event)
- Many HBV infections are asymptomatic and are detected only by the presence of antibody to HBsAg. After entering the blood, the viruses infects hepatocytes, causing necrosis and inflammation. Immune attack against viral antigens on infected hepatocytes is mediated by cytotoxic T cells. The pathogenesis of hepatitis B is probably the result of this cell-mediated immune injury, because HBV does not cause a cytopathic effect. Ag-Ab complexes cause some of the early symptoms, eg, arthralgias, other. Unlike hepatitis A patients, about 10% of patients with hepatitis B become chronic carriers of HBV. A chronic carrier is someone who has HBsAg persisting in their blood for at least 6 months. HBV DNA exists primarily as an episome in the cytoplasm of persistantly infected cells; a small number of copies of HBV DNA are integrated into cell chromosome.
- When viruses infect the liver, they cause necrosis of hepatocytes. The pathologic change interferes with the liver’s excretion of bile pigments such as bilirubin into the intestine. When bilirubin, a greenish-yellow pigment, accumulates in the blood and tissues, it causes jaundice, a yellow tinge in the skin and eyes.
- Hepatocellular carcinoma which is one of the ten most common cancers worldwide, is closely associated with hepatitis B, and at least in some regions of the world with hepatitis C virus. A high rate of hepatocellular carcinoma occurs in chronic carriers. Lifelong immuniti is mediated by humoral antibody against HBsAg.
- Testing procedure fall into 2 categories: detection of different viral Ag and antiviral Ab
- There is a period of several weeks when HBsAg has disappeared but HBsAb is not yet detectable. This is the “window phase”.
- Delta hepatitis virus has a worldwide distribution, with relatively high frequency in Italy, the Middle East, Africa and South America.
- Because HDV can replicate only in cells also infected with HBV, Hepatitis delta can occur only in a person infected with HBV. A person cal either be infected with both HDV and HBV at the same time, be “coinfected” Or be previously infected with HBV and then “superinfected” with HDV. Hepatitis in patient coinfected with HDV and HBV is more severe that in those infected with HBV alone. There is some evidence that delta virus is cytopathic for hepatocytes.
- Hepatitis in chronic carriers of HBV who become superinfected with HDV is much more severe, and the incidence of fulminant, life-threatening hepatitis, chronic hepatitis, and liver failure is significantly higher.
- Testing procedure fall into 2 categories: detection of different viral Ag and antiviral Ab
- Incubation period is 8 weeks. HCV infects hepatocytes primarily, but there is no evidence for a virus-induced cytopathic effect on the liver cells. HCV infection strobgly predisposes to hepatocellular carcinoma. Antibodies against HCV are made, but perhaps as many as half of patients are chronically infected and continue to produce virus for at least a year. Chronic active hapatitis and cirrhosis occur in approximately 10% of these patients.