**3. How HBV replicates**

*Tourism*

age are usually symptomatic [7]. When present, the typical signs and symptoms of acute infection include malaise, fatigue, poor appetite, nausea, vomiting, abdominal pain, fever, dark urine, light color (clay-colored) stool, joint pain, and jaundice [8]. The overall case fatality ratio of acute infection due to HBV is approximately 1% [9]. People infected with HBV are susceptible to infection with hepatitis D virus; coinfection increases the risk of fulminant hepatitis and rapidly progressive liver disease [10]. Transmission of HBV is mainly through percutaneous or mucosal exposure to HBV-infected blood or bodily fluids including saliva or semen [2]. There are reports of transmission via sexual contact and contaminated medical equipment and

The prevalence of chronic HBV infection is ≥2%, such as in the western Pacific and African regions; expatriates, missionaries, and long-term development workers may be at increased risk for HBV infection in such countries [7, 8]. Serologic markers specific for the viral agent are necessary to diagnose HBV infection and for appropriate clinical management [12]. These markers can differentiate between acute, resolving, and chronic infections. Polymerase chain reaction (PCR) method can further be use to qualitatively or quantitatively detect the amount of HBV DNA in patients' specimen after checking the markers of the virus [13]. All travelers should be screened for HBV infection markers, so that they would not be at risk of

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

through sharing of infected needles and injecting apparatus [11].

acquiring the virus during their stay [7].

**2. Aspects of HBV morphology**

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**Figure 1.**

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

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 other cells [22, 23].
