HBV Infectionmain Aspects: N. Shavgulidze, MD

HBV INFECTIONMAIN
ASPECTS
N. SHAVGULIDZE, MD
Hepatitis B is a viral infection that attacks the liver
and can cause both acute and chronic disease.
 Hepatitis B is a potentially life-threatening liver
infection caused by the hepatitis B virus (HBV). It is a
major global health problem. It can cause chronic
infection and puts people at high risk of death from
cirrhosis and liver cancer.
VIROLOGY
 HBV virion is approximately 42 nM in

diameter and comprised of 3.2 kb partially
double-stranded relaxed, circular DNA
(rcDNA) genome within a nucleocapsid
(core) that is surrounded by a lipid bilayer
studded with complexes of viral
glycoproteins . The nucleocapsid is a 27 nm
diameter icosahedron assembled from 240
viral capsid proteins and packages a single
copy of viral genomic DNA and DNA
polymerase that is covalently linked to the 5’
end of minus strand DNA .There is evidence
that cellular proteins, including chaperones
and protein kinases, are also packaged inside
of nucleocapsids .
THE NUCLEOCAPSID IS
ENVELOPED DURING ITS
BUDDING FROM THE
ENDOPLASMIC RETICULUM
AND THE ENVELOPE
MEMBRANE CONTAINS THREE
VIRAL GLYCOPROTEINS,
CALLED LARGE (L, LHBS),
MEDIUM (M, MHBS) AND SMALL
(S, SHBS) SURFACE ANTIGENS
THAT ARE TRANSLATED FROM
THE DIFFERENT IN-FRAME
STARTING CODONS WITHIN
THE SAME OPEN READING
FRAME
 The hepatitis B virus can survive outside the body for at least 7
days. During this time, the virus can still cause infection if it
enters the body of a person who is not protected by the vaccine.
The incubation period of the hepatitis B virus is 75 days on
average, but can vary from 30 to 180 days. The virus may be
detected within 30 to 60 days after infection and can persist and
develop into chronic hepatitis B.
The ways of transmission :
 Sexual
 percutaneous
 Perinatal
 Blood transfusion
 Organ transplantation


Has two forms : Acute and Chronic
 After HBV infection, the incubation period
lasts from one to four months. A prodromal phase
may appear before acute hepatitis develops.
 The symptomatology is more constitutional and includes the following:
 Anorexia
 Nausea
 Vomiting
 Low-grade fever
 Myalgia
 Fatigability
 Jaundice
 Disordered gustatory acuity and smell sensations (aversion to food and
cigarettes)
 Right upper quadrant and epigastric pain (intermittent, mild to moderate)
Most patients with chronic HBV (CHB) are clinically asymptomatic. Some may have
nonspecific symptoms such as fatigue. In most instances, significant clinical symptoms
will develop only if liver disease progresses to decompensated cirrhosis. In addition,
extrahepatic manifestations may
cause symptoms. Accordingly, a physical exam will be normal in most instances. In
advanced liver disease there may be clinical signs of chronic liver disease including
splenomegaly, spider angioma, caput medusae, palmar erythema, testicular atrophy,
gynecomastia. In patients with decompensated cirrhosis, jaundice, ascites, peripheral
edema, and encephalopathy may be present.
Laboratory testing shows mild to moderate elevation in serum AST and ALT in most
patients, whereas normal transaminases occur rarely. During exacerbation, serum ALT
concentration may be as high as 50 times the upper limit of normal
Most patients with chronic HBV (CHB) are clinically asymptomatic. Some may have
nonspecific symptoms such as fatigue. In most instances, significant clinical symptoms
will develop only if liver disease progresses to decompensated cirrhosis. In addition,
extrahepatic manifestations may
cause symptoms. Accordingly, a physical exam will be normal in most instances. In
advanced liver disease there may be clinical signs of chronic liver disease including
splenomegaly, spider angioma, caput medusae, palmar erythema, testicular atrophy,
gynecomastia. In patients with decompensated cirrhosis, jaundice, ascites, peripheral
edema, and encephalopathy may be present.
Laboratory testing shows mild to moderate elevation in serum AST and ALT in most
patients, whereas normal transaminases occur rarely. During exacerbation, serum ALT
concentration may be as high as 50 times the upper limit of normal
Diagnosis
The physical examination findings in hepatitis B disease vary from minimal to impressive
(in patients with hepatic decompensation), according to the stage of the disease.
Examination in patients with acute hepatitis may demonstrate the following:
 Low-grade fever
 Jaundice (10 days after appearance of constitutional symptomatology; lasts 1-3 mo)
 Hepatomegaly (mildly enlarged, soft liver)
 Splenomegaly (5-15%)
signs of chronic liver disease include the following:
 Hepatomegaly
 Splenomegaly
 Muscle wasting
 Palmar erythema
 Spider angiomas
 Vasculitis (rarely)
 Hepatomegaly
 Splenomegaly
 Muscle wasting
 Palmar erythema
 Spider angiomas
 Hepatomegaly
 Splenomegaly
 Muscle wasting
 Palmar erythema
 Spider angiomas
Laboratory studies
The following laboratory tests may be used to assess various stages of hepatitis B disease:
General Tests
 Alanine aminotransferase and/or aspartate aminotransferase levels
 Alkaline phosphatase levels
 Gamma-glutamyl transpeptidase levels
 Total and direct serum bilirubin levels
 Albumin level
 Hematologic and coagulation studies (eg, platelet count, complete blood count [CBC],
international normalized ratio)
 Ammonia levels
 Erythrocyte sedimentation rate
Specific diagnostic serology tests for HBV
are :
 Hepatitis B surface antigen (HBsAg)

 Hepatitis B e antigen (HBeAg)
 Hepatitis B core antibody (anti-HBc) immunoglobulin M (IgM)
 anti-HBc IgG
 Hepatitis B e antibody (anti-HBe)
 hepatitis B virus (HBV) dezoxyribonucleic acid (DNA)
Treatement
Treatment : strategy is different for chronic and acute hepatitis.
 For acute phase general treatment strategy is supportive treatment

(dezintoxication, vitaminotheraphy, antipyretics …
 For chronic forms there exists direct antiviral drugs , such as : Tenofovir,
entekavir, lamivudine, interferon …
Treatment with direct antivirals is not definite yet for how long can be lasted,
according the nowadays situation, if DAADirect-acting antiviral has
started ,should be continued for life long.
DAA treatment is indicated for those patients:Direct-acting antiviral
 who has viral load > 2000 IU/ml

 HBeAg (+)
 With delta virus superinfection
 Severe Stage of fibrosis F3, F4
 In family anamnesis genetic predisposition to Hepatocellular carcinoma (HCC)
 ALT level above upper normal value (elevated Alt level )
Aim of DAA treatment is to prevent complications, fibrosis progression , prolong life duration , improve
life quality, prevent development of HCC, prevent extrahepatic manifestations.
Prevention :For Hep. B there exists specific vaccine which is
indicated for any person who is not vaccinated at any age. Vaccine
course contains 3 dose of HBV vaccine I/Muscular administration

HDV INFECTION
 Hepatitis delta is the most severe form of viral hepatitis in humans. The
hepatitis delta virus (HDV) is a defective RNA virus which requires the
hepatitis B virus (HBV) surface antigen (HBsAg) for complete replication and
transmission, while the full extent of the HBV helper function is unexplored
(Rizzetto 1983, Taylor 2012). Hence, HDV occurs only in HBsAg positive
individuals either as acute coinfection or as superinfection in patients with
chronic HBV Several studies have shown that chronic HDV infection leads
to more severe liver disease than chronic HBV monoinfection, with an
accelerated course of fibrosis progression, possibly a slightly increased risk of
hepatocellular carcinoma and early decompensation in the setting of
established cirrhosis.
 Simultaneous HBV and HDV infection has also been shown to be more severe than
infection with HBV alone .
 So far, only interferon α treatment has been shown to exert some antiviral activity
against HDV and has been linked to improve the clinical long-term outcome .Data on
the use of pegylated interferon (PEG-IFN) confirm earlier findings, leading to
prolonged virological off-treatment responses in about one quarter of patients but
long-term HDV RNA relapses may occur .Thus, HBsAg clearance should be the
preferred endpoint of interferonbased therapies of HDV. Alternative treatment
options including HBV entry inhibitors and prenylation inhibitors are currently in
early clinical development.

Hep B can be with or without Hep D(delta). Hep D can’t exist

into the human body without HBV , as it uses HBsAg for self
complication

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HBV INFECTIONMAIN

 HBV virion is approximately 42 nM in

 Hepatitis B surface antigen (HBsAg)

Treatment : strategy is different for chronic and acute hepatitis.

 For acute phase general treatment strategy is supportive treatment

 who has viral load > 2000 IU/ml

Hep B can be with or without Hep D(delta). Hep D can’t exist

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