DNA VIRUSES

HAPPYy Viruses:
ENVELO
NAKED
H- Herpes PED

H- Hepadna DOUBLE- SINGLE- DOUBLE-

stranded stranded stranded
A- Adeno
ICOSAHED ICOSAHED
P- Papova ICOSAHED COMPLE RAL RAL
ADEN
RAL X
PARV O
P- Parvo ----linear*
HERPES PO O PAPOV
P- Pox HEPADN X A ---circular*
A

Specific Pathogenic Viruses: 3. Papova viridae

1. Hepadna viridae a. Human papilloma virus
a. Hepatitis B virus b. BK polyoma virus
b. Herpes viridae c. JC polyoma virus
2. Herpes simplex virus 1 and 2 4. Parvo viridae
a. Varicella-zoster virus a. Erythema infectiosum
b. Cytomegalo virus b. Transient aplastic anemia crisis
c. Epstein-barr virus 5. Pox viridae
d. Human herpes 6 (roseola) a. Smallpox
b. Vaccinia
c. Molluscum contagiosum
 HEPATITIS B: caused by Hepadnavirus
- Incubation period: 1-6 months (4-24weeks)
- Etiology:
HBV is a double-stranded icosahedral DNA virus, enveloped, non-cytopathic, hepatotrophic, and highly
infectious DNA virus that belongs in the hepadnaviruses family
HBsAg—surface antigen--the most abundant of which is the S protein. The development of cellular and humoral
immunity to HBsAg is protective.
HbcAg--partially double-stranded circular DNA. HBcAg-derived peptides induce a crucial host cellular immune
response against HBV—not protective.
HBeAg serves as a marker for active replication and highly infectious state.
X protein (HBx) may play a role in development of hepatocellular carcinoma.
DNA polymerase serves a reverse-transcriptase function for the synthesis of both negative and positive strands
of HBV DNA.

- Epidemiology:
 Globally, 2 billion people have been infected by HBV, of whom 400 million have chronic HBV. The incidence
of acute infection and prevalence of the chronic carrier state vary across the world, and there are areas of
high, intermediate, and low endemicity. Nearly half of all infections are in the highly endemic areas of
Southeast Asia (excluding Japan), China, and Africa.
 Genotypes B and C are found in Asia and the US. Genotype B is associated with earlier age of HBeAg
seroconversion, less active hepatic necro-inflammation, more sustained remission after HBeAg
seroconversion, a slower rate of progression to cirrhosis, and a lower rate of hepatocellular carcinoma,
compared with genotype C.

- Mode of transmission:
 Perinatal (from mother to baby at birth) – vertical transmission
 Early childhood infections (inapparent infection through close interpersonal contact with infected household
contacts)
 Unsafe injection practices
 Blood transfusions
 Sexual contact
 - Signs and Symptoms:
 Anorexia, N/V, fatigue, malaise, arthralgia, myalgias, headache, photophobia, pharyngitis, JAUNDICE,
enlarged and tender liver (RUQ pain).

- Pathogenesis: Pathophysio (refer to next page)

- Diagnosis:
Table 298-3 Commonly Encountered Serologic Patterns of Hepatitis B Infection

HBsAg Anti-HBs Anti-HBc HBeAg Anti-HBe Interpretation

+ – IgM + – Acute hepatitis B, high infectivity
+ – IgG + – Chronic hepatitis B, high infectivity
+ – IgG – + 1. Late acute or chronic hepatitis B, low infectivity

2. HBeAg-negative ("precore- mutant") hepatitis B (chronic or, rarely, acute)

+ + + +/– +/– 1. HBsAg of one subtype and heterotypic anti-HBs (common)

2. Process of seroconversion from HBsAg to anti-HBs (rare)

– – IgM +/– +/– 1. Acute hepatitis B

2. Anti-HBc "window"
– – IgG – +/– 1. Low-level hepatitis B carrier

2. Hepatitis B in remote past

– + IgG – +/– Recovery from hepatitis B
– + – – – 1. Immunization with HBsAg (after vaccination)

2. Hepatitis B in the remote past (?)

3. False-positive

- Treatment:
 Interferon alpha – suppress HBV DNA level prevent progression  Adefovir
 Lumivudine – NRTI, suppress HBV DNA level to cirrhosis.  Interferon + Rivabirin
- Prophylaxis and vaccination
 Hep B vaccine (0.5ml) –3 doses + booster -- vaccination
 HBIg (0.06ml/kg) IM + Hep.B vaccine(w/in the week) – direct percutaneous or transmucosal exposure
 HBIg (0.5ml) IM thigh + Hep. B vaccine(w/in 12hours of life) –vertical transmission
 HBIg (0.06ml’kg) IM + Hep. B vaccine(w/in 14days) – sexual transmission