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Chapter 21 : Blood-Borne Hepatitis Viruses: Hepatitis Viruses B, C, and D and Candidate Agents of Cryptogenetic Hepatitis

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Blood-Borne Hepatitis Viruses: Hepatitis Viruses B, C, and D and Candidate Agents of Cryptogenetic Hepatitis, Page 1 of 2

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Abstract:

Blood-borne hepatitis viruses include hepatitis B virus (HBV), hepatitis C virus (HCV), and hepatitis D virus (HDV). As their names imply, blood-borne hepatitis viruses impact mainly on the liver. Investigation of patients with these cryptogenetic forms of liver disease using a variety of molecular methods aimed at identifying possible causing agents has led to the discovery of a number of novel viruses. Viruses thus unveiled include GB type C virus now known to be the prototype of a vast array of viruses classified within the novel genus Anellovirus, and others. Although the hepatopathogenic potential of these viruses is much less pronounced than originally proposed or possibly nonexistent, these candidate agents of hepatitis can be borne by blood and because, for some of them, the ability to injure the liver, alone or in association with other agents, is still under scrutiny. Importantly, patients with symptoms of hepatitis can alternate clinical manifestations with variably long periods of remission, and the proportion of individuals who progress to cirrhosis and hepatocellular carcinoma (HCC) is roughly proportional to disease activity. The majority of acutely infected individuals progress to chronic infection with almost no propensity to resolve the infection spontaneously. There are also no indications that HCV or other blood-borne hepatitis viruses can be spread by insect vectors. The current standard of care for acute and chronic infection is pegIFN-α in combination with ribavirin, which leads to permanent clearance of the virus in approximately 60% of patients.

Citation: Bendinelli M, Pistello M, Maggi F, Vatteroni M. 2009. Blood-Borne Hepatitis Viruses: Hepatitis Viruses B, C, and D and Candidate Agents of Cryptogenetic Hepatitis, p 325-362. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch21
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Figures

Image of FIGURE 1
FIGURE 1

Organization of the HBV genome and encoded proteins. The double circle represents the partially duplex DNA genome found within virions and consisting of one nicked complete strand (outer circle) and one incomplete and also nicked strand (inner circle, with the broken line representing the missing segment). However, the functional genome found in infected cells is a cccDNA. The arcs represent the protein products. Abbreviations: c, capsid (core); e, e antigen; L, M, and S, envelope glycoproteins; RT, reverse transcriptase-DNA polymerase; TP, terminal protein. The approximate location in the RT of the YMDD amino acid motif important for resistance to lamivudine is also shown.

Citation: Bendinelli M, Pistello M, Maggi F, Vatteroni M. 2009. Blood-Borne Hepatitis Viruses: Hepatitis Viruses B, C, and D and Candidate Agents of Cryptogenetic Hepatitis, p 325-362. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch21
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Image of FIGURE 2
FIGURE 2

Typical courses of HBV infection. (A) Acute self-limited infection. (B) Infection that does not resolve and becomes chronic. While the virological and immunological events depicted are seen in virtually all patients, clinical symptoms develop in a proportion of infected individuals that varies greatly with age at infection and other parameters (see text). The shaded areas represent the periods during which the markers indicated are demonstrable in the circulation. As described in the text, in an undefined proportion of patients recovered from acute self-limited infection, minute amounts of HBV DNA are demonstrable by sensitive gene amplification techniques well beyond the time periods indicated.

Citation: Bendinelli M, Pistello M, Maggi F, Vatteroni M. 2009. Blood-Borne Hepatitis Viruses: Hepatitis Viruses B, C, and D and Candidate Agents of Cryptogenetic Hepatitis, p 325-362. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch21
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Image of FIGURE 3
FIGURE 3

Algorithm for use and interpretation of laboratory tests for HBV infection (Table 5). Note that exceptions to the diagnostic conclusions indicated exist and that, especially in certain geographic areas, all HBV infections should also be tested for HDV.

Citation: Bendinelli M, Pistello M, Maggi F, Vatteroni M. 2009. Blood-Borne Hepatitis Viruses: Hepatitis Viruses B, C, and D and Candidate Agents of Cryptogenetic Hepatitis, p 325-362. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch21
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Image of FIGURE 4
FIGURE 4

Organization of the HCV genome and encoded proteins (Table 6). C, capsid (core); E, envelope; NS, nonstructural. p7 is a small nonstructural protein composed of two transmembrane domains with putative ion channel activity.

Citation: Bendinelli M, Pistello M, Maggi F, Vatteroni M. 2009. Blood-Borne Hepatitis Viruses: Hepatitis Viruses B, C, and D and Candidate Agents of Cryptogenetic Hepatitis, p 325-362. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch21
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Image of FIGURE 5
FIGURE 5

Typical courses of HCV infection. (A) Acute, self-limited infection. (B) Infection that does not resolve and becomes chronic. While the virological and immunological events depicted are seen in virtually all patients, clinical symptoms develop in a minority. The shaded areas represent the time periods during which viral RNA and viral antigen are demonstrable in the circulation.

Citation: Bendinelli M, Pistello M, Maggi F, Vatteroni M. 2009. Blood-Borne Hepatitis Viruses: Hepatitis Viruses B, C, and D and Candidate Agents of Cryptogenetic Hepatitis, p 325-362. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch21
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Image of FIGURE 6
FIGURE 6

Algorithm for the laboratory diagnosis of HCV infection. Note that, although less sensitive, HCV antigen testing can substitute for HCV RNA testing when this is not available.

Citation: Bendinelli M, Pistello M, Maggi F, Vatteroni M. 2009. Blood-Borne Hepatitis Viruses: Hepatitis Viruses B, C, and D and Candidate Agents of Cryptogenetic Hepatitis, p 325-362. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch21
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Image of FIGURE 7
FIGURE 7

Organization of the HDV genome and encoded proteins. The ellipses represent the genomic and antigenomic circular viral RNA. The shaded segment of the antigenome represents the HDAg gene. A variable proportion of antigenomes is modified by host cell enzymes at a specific nucleotide position, the editing site (diamond), contained in the functional ORF. This editing leads to the substitution, in the HDAg mRNA, of an amber stop codon with a tryptophan codon (W) and results in the readthrough of 19 additional amino acids. By this mechanism, variable proportions of S-HDAg and L-HDAg are produced. The open circle indicates the cleavage site in which the viral RNA autocatalytically cuts and ligates itself (Table 7). The two forms of HDAg have substantially distinct functions (Table 7). Extents of editing and self-cleavage have been reported to be related to the course of infection in experimental animals.

Citation: Bendinelli M, Pistello M, Maggi F, Vatteroni M. 2009. Blood-Borne Hepatitis Viruses: Hepatitis Viruses B, C, and D and Candidate Agents of Cryptogenetic Hepatitis, p 325-362. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch21
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Image of FIGURE 8
FIGURE 8

Typical courses of HDV infection. (A) Typical coinfection. (B) Typical superinfection. The major markers of the helper HBV infection also are shown. The shaded areas represent the time periods the markers indicated are demonstrable in the circulation. HDAg detectability refers to EIA methods.

Citation: Bendinelli M, Pistello M, Maggi F, Vatteroni M. 2009. Blood-Borne Hepatitis Viruses: Hepatitis Viruses B, C, and D and Candidate Agents of Cryptogenetic Hepatitis, p 325-362. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch21
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Image of FIGURE 9
FIGURE 9

Organization of the GBV-C genome and encoded proteins (Table 9). Capsid?, the sequence encoding the capsid protein is still undefined; E, envelope; NS, nonstructural.

Citation: Bendinelli M, Pistello M, Maggi F, Vatteroni M. 2009. Blood-Borne Hepatitis Viruses: Hepatitis Viruses B, C, and D and Candidate Agents of Cryptogenetic Hepatitis, p 325-362. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch21
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Image of FIGURE 10
FIGURE 10

Genome organization of TTV and the related anelloviruses TTMV and TTMDV. The arcs represent the major ORFs identified. Several smaller ORFs may also exist.

Citation: Bendinelli M, Pistello M, Maggi F, Vatteroni M. 2009. Blood-Borne Hepatitis Viruses: Hepatitis Viruses B, C, and D and Candidate Agents of Cryptogenetic Hepatitis, p 325-362. In Specter S, Hodinka R, Young S, Wiedbrauk D (ed), Clinical Virology Manual, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815974.ch21
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