Hepatitis A,D,E,G Infections Flashcards
Hepatitis A
Known as “infectious hepatitis”
27 nm
(+) ssRNA virus
- naked icosahedral capsid that is quasi-enveloped
Interacts with HAVCR-1 receptors on liver cells and T-cells to activate
is NOT cytolytic
HAV pathogenesis
Replicates initially in the enterocyte mucosa and them goes to the liver via viremia transmission
Causes necrosis of liver parnechymal cells and proliferation of kupffer cells
Can be tested in stool samples
is limited by IFN, but NK cells and CD-8 Tcells are required to kill it
cant produce chronic finections and cant produce hepatocarcinomas
HAV symptoms
Incubates for 15-45 days
Symptoms: (lasts up to two months)
- flu-like symptoms
- intense fever (104F/40C)
- fatigue
- nausea/vomiting
- right upper quad pain
- pale stool
- jaundice (70-80%)
- increased ALT levels
- hepatosplenomegaly
disease is mild in children, often asymptomatic
rare chance (1%) of fulminant hepatitis (hepatic necrosis that is irreversible) which has an 80% mortality rate
How does antibody levels change with respect to time of exposure to hepatitis A?
IgM anti HAV (acute)
- begins production at 15 days
- peaks at 2.5-2 months and gradually decreases overtime
IgG anti HAV (chronic)
- begins production at 1 month
- peaks at 6 months and never decreases (immunity)
Diagnosis of HAV
ELISA
- shows anti HAV IgM or IgG
RT-PCR/qPCR
- shows viral particles
Use stool and blood samples to detect virus
- note that feces will not have any particles if no symptoms are present
Epidemiology of HAV
Most common in Asia/Africa/Middle East
- 90% of these patients are seropositive
- is less common in US and 1st world due to HAV vaccine in 1995
Transmission is via:
- fecal-oral
- sexual contact
- IV drug use
- NOT BLOOD TRANSFUSION
Prevention of HAV
Increased hygiene
Vaccination
- 2 doses, 6-12 months apart
- HAVRIX/VAQTA/TQINRIX are all fair vaccines
Also can give prophylactic IgG if traveling to endemic regions
Hepatitis D
Called “delta agent”
Circular virus
(-)ssRNA virus
- icosahedral capsid and enveloped
cant replicate itself since it doesnt produce RNA polymerase. Because of this it is considered a “complementation infection” since it only becomes bad if hepatitis B is present
Can be confection (get both HDV and HBV at the same time) or superinfection (already has chronic HBV and now has acute HDV on top of it
Epidemiology of HDV
Coexists in 5% of hepatitis B infected persons globally
- most common in Asia/Africa/Mongolia
often shows up in HIV/HBV coinfected patients (need to be wary of these folk)
*HEPCLUDEX = HDV Durga to help combat infection *
Pathogenesis of HDV
Only infects hepatocytes and is almost identical in steps to infection as HBV (since it needs HBV surface antigen in order to penetrate hepatocytes)
Surface HBV antigen = sodium taurocholate cotransporting polypeptide receptor
- *has very high levels of cytosine and guanine which causes it to form a rod-like structure in its genome**
- genome codes for HDV antigens (however needs to be transcribed by host RNA poly 1 and 2 (ONLY KNOWN RNA VIRUS TO DO THIS)
Host poly 2 = generates the HDV antigen itself
Host poly 1= rolling cycle replication which produces antigenomic copies to replicate its own genome over and over again
Pathogenesis of HDV
Varies (usually depends on how much HBV has damaged the liver)
Extensive liver damage = anti-HDV IgM is present
- causes HDV viremia and elevated ALT/AST
Mild liver damage = anti-HDV IgG is present
- less elevation
Requires TH1/CD4/CD8 (innate immunity) to fight more than adaptive
HDV symptoms and transmission
Transmitted:
- blood
- perinatal (pretty rare though)
Symptoms:
- elevated ALTs (shows a biphasic pattern)
- fulminant hepatitis (way more common in HBV/HDV superinfections
- symptoms of HBV just exaggerated
- liver cirrhosis
- hepatosplenomegaly
acute infection is usually self-limiting after 160 days, chronic infection = fulminant hepatitis or stronger HBV infections that dont go away
What mortalities are increased in HDV/HBV coinfections?
Liver Cirrhosis (80% get it within 5 years)
Hepatocellular carcinoma (3x more likely)
HIV (questionable, but has been shown to have increased rates of developing HIV once exposed (titer levels increase faster))
What happens if a patient is infected with HBV/HCV/HDV all at the same time?
HBV and HDV replicate, but HCV doesnt
Diagnosis and treatment of HDV
diagnosis: ELISA and PCR
- looks for Anti-HDV antibodies and HDV-RNA respectively
Treatment: high doses of PEG IFN-a for 48 weeks
- liver transplant if fulminant hepatitis occurs
