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Fecal-Oral Transmission & NAKED

Virus Family Pathogenesis Sx Dx Tx Notes
HAV Picorna Incub: 2wk-40wk
Enteric mucosa--1' viremia--liver--bile duct--feces
**Liver: lymphoid cell infiltrate, necroses of
parenchymal cells, prolif of Kupffer cells**
Jaundice
Fatigue
Abdominal pain
Loss of appetite
N & D
IgM against HAV Passive immunization w/Ig
Inactivated •
Virosomes (VLP) •
HAV Vaccine
T mediated: HLA I restricted
Acute
One serotype
Natural host: Human
Severity corr w/lvl of necrosis
HEV Hepe Incub: 2wk-40wk (young-mid aged adult)
Mexico, Central Am, Asia, NE Africa •
Recent travel to high HEV areas
Similar to HAV HEV Ab Acute
20% mortality in Pregnant women
One serotype
Blood borne or Sexual contact •
Parenteral Transmission & ENVELOPED
Virus Family Pathogenesis Sx Dx Tx Notes
HCV Flavi
(RNA+)
Incub: 6-7wks
HLA-I restricted Tc
responsible for most
liver damage
Acute: mild & vague
NO jaundice
Chronic: Cirrhosis, Liver
failure, Hepatocellular
carcinoma
Used only to
monitor liver dmg
-
Liver enzyme NOT
consistent for Dx
Index of suspicion
HCAb immunoblot, ELISA,
RNA assay
vRNA via RT-PCR
Treat EARLY!!!
PEG-IFNα + ribavirin
Most common chronic blood borne infection
aka. Post transfusion hepatitis
At least 9 genotypes; 1 being most common
21% of all acute hep; 70% chronic
Leading cause of liver transplant
Infection comes from: tattoos, piercing,
shared razor blades, shared toothbrush,
manicures, snuffed cocaine
HGV Flavi
(RNA+)
Blood borne
Transplant recipients
Vertical, Sexual, shared
contam items
**No obvious imm resp
to HGV**
Almost none RT-PCR None Infections are PERSISTENT
Using HBsAg/cAg/eAg & Abs to determine
stage of HBV infection
HBV Hepadna
(partial
dsDNA)
N, F, Joint Pn, Jaundice,
Hx with IV drugs Recombinvax HB
Engerix-B
HBV vaccines:
Tx:
PEG-IFNα + Lamivudine
Acute: mile or severe
5% chronic
HDV Delta
(ssRNA-) Simultaneous •
Coinfect w/HBV
HBV 1st •
HDV later •
Superinfect w/HBV
Exacerbates HBV inf HBV vaccine will also
protect against HDV
Virus-like
Interact with JAK-STAT & cellular translation pathways •
Blocks IFN signaling (can't tell rest of body that it's infected) •
Loss of tumor suppressor kinase PKR-->carcinogenesis •
NS5A protein 1.
Blocks innate imm pathway that recognizes viral infection •
CD80/86 to activate T-cells 
IL-6 & IL-12 are proinflammatory 
RANTES: induce migration T/B cells 
IFN & ISG normal fxn: □
NO IFN or IFN stimulated genes (ISG) activated 
NO activation of NFkB or IRF3 •
NS3/4a protease 2.
HCV remain chronic mainly with two proteins:
Increase errors made by polymerase to generate mutations in vital
genes of virus

Ribavirin
TT to TC change in gene that encodes IFN-λ3 protein •
SNP (single nucleotide polymorphism) has been ID for HCV •
Biomarkers for HCV infection
HCV
Evade immune sys •
Persistence of virus •
Clades=Nucleotide sequences of same genotype in diff countries had
substantial sequence diversity
Env prot has hypervariable regions--multiple HCV variants (Quasi-species)
Latency up to 20yrs
20% coinfect w/HGV
Virion=Dane particle •
With same surf mlc as Dane ○
Bind to Ab so Dane can escape ○
Decoy=subviral particle •
Partial duplex genome (complete DNA- & incomplete DNA+) •
HBsAg=envelop •
HBcAg=core/capsid •
HBeAg=secreted; indicate actively infectious state •
HBV
HBcAg & HBeAg
Two AUGs (stop codon) in core ORF
Sent to ER, cleaved to
HBcAg and HBeAg in serum

Capsid ◊
-------------------HBcAg
--------------------------HBeAg
--------------------------------mRNA
-------------pre-C
Superhelical covalenly closed ○
Virion DNA+ is finished by RT (DNA/RNA-dep DNA
Pol)

DNA- is transcribed into pgRNA (mRNA) by Pol II •
pgRNA is transcribed to DNA- by RT •
DNA+ is translated by Pol II •
Assembly occurs before DNA+ finishes •
Replication of HBV
HBsAg has 3 forms:
PreS2 has sequence for receptor binding •
Dane have L forms •
Thus, can't bind & not infectious ○
Subvirals do not have L forms •
Small "a" determinanet
Medium a+PreS1
Large a+PreS1+PreS2
Has HBsAg (pseudotype) ○
HBV vaccine also protect against HDV ○
Use HBV env as own •
RNA- recogn by Host RNA Pol II •
Rolling circle replication •
Cleaves individual genome copies from a single long RNA precursor ○
RNA catalysis (Ribozyme) •
Change RNA sequence after it has been made ○
UGA (stop)-->UGG(Trp) ○
Only the larger delta Ag can interact with HBV env prot 
Change replication to chronic form □
Low lvl of delta Ag in cells forever □
Inhibits virus replication 
Larger HDV Ag ○
RNA editing •
HDV
Hepatitis Virus
Tuesday, September 03, 2013
10:00 AM
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