B5.027 - Hepatitis Viruses Flashcards
describe HAV
picornoviridae HAV aka enterovirus 72 small (27nm) non enveloped ssRNA (+) replication exclusively in cytoplasm
HAV typical serologic course
1-2 months after exposure - fecal HAV, ALT rises total anti HAV develops after 2-4 months, stays for life IgM starts after 1 month, drops around 4
is there a vaccine for HAV?
yes, greatly reduced incidence after 1995
incubation period, jaundice by age group, complications/clinical sequelae of HAV
avg 30 days 6-14 yo - 40-50% >14 yo - 70-80% fulminant hepatitis cholestatic hepatitis relapsing hepatitis no clinical sequelae
HAV vaccine
inactivated vaccine adsorbed onto aluminum hydroxide 94-100% effective
what types of enveloped proteins does HBV have
small, medium and large
what role does the large protein have
has receptor binding site
what proteins does HBV need to make it infectious
small and large proteins
why does HBV need small particles
to ensure release of proteins from cell
possible mechanisms of HBV induced liver carcinogenesis
- integration of HBV DNA into host DNA leading to genome instability and mutations 2. DNA damage from chronic infection 3. X protein acts as transcription activator 4. persistent liver damage resulting in hepatocyte proliferation
treatment of HBV in order of use
- tenofovir 2. entecavir 3. telbivudine 4. adefovir 5. lamivudine 6. Pegylated IFN 7. IFN alpha
first line treatment of HBV
tenofovir entecavir
describe labs for HBV
HBsAg - surface angigen, marker of infectivity when found in serum anti-HBsAg - antibody to HBsAg, marker of immunity anti-HBcAg - marker of past or current infection
what is IgM anti-HBc
antibody indicating recent infection with HBV
IgG anti HBc
IgG is a subclass of anti HBc indicates older infection with HBV
what is HBeAg
Hepatitis B e antigen can only be present if HBsAg is positive. Indicates active infection
what is anti HBe
antibody to e antigen may be present in infected or immune person
susceptible to HBV infection
HBsAg neg
Anti HBc pos
Anti HBs pos
immune to natural infection
HBsAg neg
Anti HBc neg
AntiHBs pos
immune due to vaccine
HBsAg pos
AntiHBc pos
IgM antiHBc pos
anti HBs neg
acutely infected
HBsAg pos
anti HBc pos
IgM antiHBc neg
anti HBs neg
chronically infected
HBsAg neg
IgM anti HBc pos
anti HBs neg
- resolved HBV infection
- may be susceptible with a false positive anti HBc
- may have low level chronic infection
- may be resolving an acute infection
describe the two types of HDV infection
coinfection with HBV
Superinfection (ad different times)
outcomes of coinfection
3-4% fulminate hepatitis –> death
90% - acute severe disease –> recovery
5% - crhonic –> cirrhosis
superinfection outcomes
5% - fulminate hepatitis –> death
10-15% acute severe disease –> recovery
80% - chronic hepatitis –> cirrhosis
HCV
incubation period, acute illness, case fatality rate from acute infx
6-7 wks
mild <20%
low
current treatment of HCV
ledipasvir and sofosbuvir
describe the developement of HCV associated HCC
viral entry and replication
inflammation, cellular growth signals, resistance to apoptosis, oxidative stress, metabolic disorders
fibrogenesis, hypoxia, genetic instability, LPS translocation from intestinal microbiota
incidence of HCC in different hepatitis
HBV - 60%
HCV - 25%
neither - 12%
both - 3%
host of the four types of HEV
1 - humans and pigs
2 - humans
3 - humans and animals
route of admin of 4 types of HEV
1, 2 - fecal oral, vertical
3, 4 - zootonic usually swine, environmental and blood transfusion
geographical distribution of the 4 types of HEV
1 - mainly asia
2 - MX and west africa
3 - worldwide
4 - china, east asia, central europe, america
seasonality of types of HEV
1,2, - flooding/monsoon season
3,4 - no
clinical presentation of HEV types
1,2 - acute self limited hepatitis
3,4 - may lead to chronocity in immunosuppressed (3)
prognosis/chronic infection of HEV types
1 - high mortality in pregnancy
2 - fulminant hepatitis not noted, no chronic
3, 4 - higher overall mortality relative to 1, and in older adutls, yes chronic
