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32 Cards in this Set
- Front
- Back
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Hepatitis B virus Replication
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Reverse transcription of pregenomic RNA using protein (minus strand) and oligoribonucleotide (plus strand) primers
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Hepatitis B virus Disease
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Immune mediate (virus in the absence of an immune response is non-cytopathic)
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Hepatitis B Virus Infection
by Age at Infection |
As we grow older chronic infections decrease but symptoms of infection increase
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Hepatitis B Virus Infection Signs and Symptoms
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Symptom
there may be none loss of appetite, malaise, nausea, vomiting, abdominal pain, arthralgias, myalgias Signs there may be none jaundice, fever, dark urine |
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Progression to Chronic Hepatitis B Virus Infection
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IgM anti HBc first increases then falls but total anti Hbc stays high while the antigen is also high
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Acute Hepatitis B Virus Infection with Recovery
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HBsAg increases and IgM anti Bc also increases as well as total anti HBc. IgM decreases and total anti Hbc remains high as HBsAg decreases.
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How do you get hepatitis B?
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It is passed by contact with the blood or other body fluids of someone who has the virus.
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Hepatitis Virus B in
1) blood serum, wound exudates 2)semen, vaginal fluid, saliva 3) urine, feces, sweat, tears, breast milk |
1) high
2) moderate 3)low |
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Hepatitis B Virus
Modes of Transmission |
Sexual
Parenteral Perinata |
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Risk factors associated with hepatitis
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Multiple sex partners>injection drug use>sexual contact with person with the virus>gays
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The hepatitis B virus takes about
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2 months to show up in your blood. It may stay in your blood for months or years.
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Will I ever get rid of the virus?
Acute Hepatitis B. |
9 out of every 10 adults will get rid of the virus from their bodies after a few months. We say they have acute hepatitis B.
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Will I ever get rid of the virus?
Chronic Hepatitis B. |
1 out of every 10 adults will never get rid of the virus from their bodies. We say they have chronic hepatitis B. They are called carriers.
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Will I die from hepatitis B?
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Most people do not die from it. There are cases where hepatitis B can cause liver damage (cirrhosis [sir-O-sis]) that does not go away.
Hepatitis B can also cause liver cancer, which may lead to death. Good medical care can make your risk less for these. |
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About 1/3 of chronic HBV infections in the United States start in
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perinatal and early childhood
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Except flu and pneumococcal infections, HBV
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kills more people/year than any other vaccine-preventable disease (VPD) (>5,000 HBV deaths/year)
HBV causes hepatocellular carcinoma that kills about 1,000 Americans annually |
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look for
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hep B replication cycle and infection
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HBV leads to liver cancer
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epidemiologic correlation in many populations
risk for HCC is 12-300 times greater in HBsAg+ persons HBV DNA is incorporated into DNA of hepatoma cells |
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Baby shots for hep B if mother has hep B
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At birth: Hep B vaccine + H-BIG
1-2 months: Hep B vacc 6 months: Hep B vacc |
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Up to 9 out of 10 babies born to infected mothers will end up
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being carriers for the rest of their lives, if they do not get the shots.
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Babies who end up as carriers have a
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1 out of 4 chance of dying from liver problems.
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19 out of 20 babies who get the shots will be
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be protected for life!
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Treatments for chronic HBV
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interferon alfa-2b (IntronA), recombinant administered subcutaneously (also licensed for use in children
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Characteristics of Hepatitis D virus
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Obligatory co-infection with HBV
Viriod-like agent: d Ag nucleocapsid within the HBsAg envelope Replication: Rolling circle utilizing host RNA polymerase II (and also possibly pol I) and d ribozymes – genomic and antigenomic RNAs Tropism: Liver (due to HBsAg envelope) Disease: Usually more extreme than HBV alone |
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HDV is a defective single‑stranded RNA virus that requires
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the helper function of HBV to replicate. HDV requires HBV for synthesis of envelope protein composed of HBsAg, which is used to encapsulate the HDV genome.
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Hepatitis D Coinfection with HBV
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severe acute disease
low risk of chronic infection |
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Hepatitis D Superinfection on top of chronic HBV
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usually develop chronic HDV infection
high risk of severe chronic liver disease |
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HBV – HDV Coinfection
Typical Serological Course |
In most persons with HBV‑HDV coinfection, both IgM antibody to HDV (anti‑HDV) and IgG anti‑HDV are detectable during the course of infection. However, in about 15% of patients the only evidence of HDV infection may be the detection of either IgM anti‑HDV alone during the early acute period of illness or IgG anti‑HDV alone during convalescence. Anti‑HDV generally declines to subdetectable levels after the infection resolves and there is no serologic marker that persists to indicate that the patient was ever infected with HDV. Hepatitis Delta antigen (HDAg) can be detected in serum in only about 25% of patients with HBV‑HDV coinfection. When HDAg is detectable it generally disappears as HBsAg disappears and most patients do not develop chronic infection. Tests for IgG anti‑HDV are commercially available in the United States. Tests for IgM anti‑HDV, HDAg and HDV RNA by PCR are only available in research laboratories.
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In patients with chronic HBV infection who are superinfected with HDV several characteristic serologic features generally occur, including:
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the titer of HBsAg declines at the time HDAg appears in the serum,
HDAg and HDV RNA remain detectable in the serum because chronic HDV infection generally occurs in most patients with HDV superinfection, unlike the case with coinfection, high titers of both IgM and IgG anti‑HDV are detectable, which persist indefinitely |
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Hepatitis D Virus
Modes of Transmission |
Percutanous exposures
injecting drug use Permucosal exposures sex contact |
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Hepatitis D - Prevention
HBV-HDV Coinfection |
Pre or postexposure prophylaxis to prevent HBV infection (HBIG and/or Hepatitis B vaccine)
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Hepatitis D - Prevention
HBV-HDV Superinfection |
Education to reduce risk behaviors among persons with chronic HBV infection
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