**2. Aspects of HBV morphology**

Hepatitis B virus belongs to the family of *Hepadnaviridae* in the genus *Orthohepadnavirus*, and it is known to have a very high transmissibility [14, 15]. It is a hepatotropic DNA virus which also includes duck hepatitis B virus (DHBV) and woodchuck hepatitis B virus (WHBV) [16]. HBV is partially double-stranded with a circular DNA that is composed of an outer envelope containing hepatitis B surface antigen (HBsAg) and an inner nucleocapsid consisting of hepatitis B envelope antigen (HBeAg) and hepatitis B core antigen (HBcAg) of approximately 3.2 kb, generated from an intermediate RNA through reverse transcription that encodes

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*Traveler's Infections: Overview of Hepatitis B Virus Infection*

four partially overlapping open reading frames (ORF): surface (S), encoding the viral surface protein; core (C) encoding core; polymerase protein; and pDNA and X genera as seen in **Figure 1** [17, 18]. The virus infects the liver of Hominoidae including humans and causes an inflammation called hepatitis. The disease was formally

The cardinal feature of HBV replication cycle is the replication of the DNA genome by reverse transcription, when virions bind susceptible cell-surface receptors and IgA receptors on liver cells following of RNA intermediate [18, 20]. The viral genome is transported into the nucleus, and it is then converted into a covalently closed circular double-stranded HBV DNA (cccDNA) molecule which acts as the transcriptional template for the host RNA polymerase II machinery that synthesizes polyadenylated and four capped mRNAs which encode the envelope structural proteins, viral core and the precore; polymerase; and X non-structural viral proteins [20]. A 3.5-kb genome length RNA is one of the major HBV transcripts which is translated to synthesize the viral core and polymerase proteins and also plays role as a pregenomic RNA that is encapsidated with the polymerase by the core protein in the cytoplasm of the liver cells. The replication of the viral agent usually happens entirely within these capsids by reverse transcription of the pregenomic RNA to synthesize a single-strand DNA copy that serves as the template for the second strand DNA produced, synthesizing a circular double-stranded DNA [21]. The viral capsids that contain the double-stranded DNA traffic either to the nucleus where amplification occurs or the viral cccDNA genome to stabilize intranuclear pool of transcriptional templates or to the endoplasmic reticulum, where they acquire the viral envelope proteins, bud into the lumen, and exit the cell as virions that can infect

*DOI: http://dx.doi.org/10.5772/intechopen.92174*

known as "serum hepatitis" [19].

**3. How HBV replicates**

other cells [22, 23].

infection [27].

HCC [8, 29].

**4. Pathogenesis and clinical features of HBV infection**

Hepatitis B virus gets entry into the bloodstream and targets the liver cells [24]. The hepatocytes which are infected are distended, and the cytoplasm assumes a ground appearance that is glassy. The virus is not cytopathic, and injury of the liver in HBV chronic infection is due to immunological responses [8, 25]. Although, the virus has a long incubation period of 45–180 days, replication starts few days after infection. The infection can be acute, an unexpected sickness with a mild-tosevere course followed by comprehensive resolve [26]. On the other hand, if the cell-mediated immune reaction is feeble, the infection does not resolve, and chronic hepatitis arises with an extended course of active disease or silent asymptomatic

About 30–80% adults of acute HBV infection shows symptoms (1% fulminant hepatitis), whereas less than 1 year old children shows no symptoms [28]. Symptoms of HBV infection include malaise, dark urine, fever, nausea, jaundice, pale stools, right upper quadrant pain, and anorexia. The risk of chronic infection of HBV is hinged on the duration of acquisition [26]. About 90% of infected neonates, 30–50% of children aged 1–4 years, and 1–10% of acutely infected adults result to persistent infection. There are approximately 15–40% with persistent infection that leads to advanced liver disease, cirrhosis, and/or

**Figure 1.** *Morphology of hepatitis B virus [16, 18].*

four partially overlapping open reading frames (ORF): surface (S), encoding the viral surface protein; core (C) encoding core; polymerase protein; and pDNA and X genera as seen in **Figure 1** [17, 18]. The virus infects the liver of Hominoidae including humans and causes an inflammation called hepatitis. The disease was formally known as "serum hepatitis" [19].
