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Chapter 83 : Viral Hepatitis
Authors:
Mauro Bendinelli,
Mauro Pistello,
Giulia Freer,
Marialinda Vatteroni,
Fabrizio Maggi
Content Type: Reference
Publication Year:
2006
Category: Immunology
Book DOI:
10.1128/9781555815905
Chapter DOI:
10.1128/9781555815905.ch83
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Viral Hepatitis, Page 1 of 2
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Abstract:
The more recently introduced molecular tests that detect and quantify viral genomes complement the information obtained immunologically and, due to rapid turnaround times and the availability of user-friendly commercial kits, have acquired a key position in both the diagnosis and the follow-up of viral hepatitis. Direct detection of the infectious agent has an ancillary role in the laboratory diagnosis of hepatitis A due to the reliability and ease of anti-hepatitis A virus (HAV) immunoglobulin M (IgM) testing. Viral RNA is tested for mainly by reverse transcriptase PCR (RT-PCR). Certainly more important for laboratory diagnosis and disease management, however, are the so-called hepatitis B e antigen (HBeAg)-minus core or precore mutants of the virus, which are unable to express HBeAg due to a stop codon in the C gene, and the drug-resistant variants that are commonly found in patients undergoing therapy. Qualitative nucleic acid-based tests are most useful in assessing the safety of blood donations but prove useful also when a suspicion of active infection based on serological grounds needs to be confirmed. In this case, it is advisable to retest negative patients several times at intervals of several weeks in order to identify the ones who might have intermittent viremia, as is frequently observed in the course of spontaneous resolution or antiviral therapy.
Citation:
Bendinelli M, Pistello M, Freer G, Vatteroni M, Maggi F.
2006.
Viral Hepatitis,
p 724-745.
In
Detrick B, Hamilton R, Folds J (ed),
Manual of Molecular and Clinical Laboratory Immunology, 7th Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815905.ch83
Figures
Viral Hepatitis
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Citation:
Bendinelli M, Pistello M, Freer G, Vatteroni M, Maggi F.
2006.
Viral Hepatitis,
p 724-745.
In
Detrick B, Hamilton R, Folds J (ed),
Manual of Molecular and Clinical Laboratory Immunology, 7th Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815905.ch83
/content/10.1128/9781555815905.ch83.ch83fig01
FIGURE 1
Typical course of immunovirological events and manifestations of liver damage in symptomatic infection by the enterically transmitted HAV (top) and HEV (bottom). Both viruses produce many more inapparent than symptomatic infections, but the immunovirological events are similar to the ones depicted. Neither virus produces chronic infections.
10.1128/9781555815905/f0726-01_thmb.gif
10.1128/9781555815905/f0726-01.gif
FIGURE 1
Typical course of immunovirological events and manifestations of liver damage in symptomatic infection by the enterically transmitted HAV (top) and HEV (bottom). Both viruses produce many more inapparent than symptomatic infections, but the immunovirological events are similar to the ones depicted. Neither virus produces chronic infections.
Citation:
Bendinelli M, Pistello M, Freer G, Vatteroni M, Maggi F.
2006.
Viral Hepatitis,
p 724-745.
In
Detrick B, Hamilton R, Folds J (ed),
Manual of Molecular and Clinical Laboratory Immunology, 7th Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815905.ch83
/content/10.1128/9781555815905.ch83.ch83fig02
FIGURE 2
Algorithm for use and interpretation of laboratory tests for HAV infection. HAV RNA detection is usually carried out with stool samples.
10.1128/9781555815905/f0727-01_thmb.gif
10.1128/9781555815905/f0727-01.gif
FIGURE 2
Algorithm for use and interpretation of laboratory tests for HAV infection. HAV RNA detection is usually carried out with stool samples.
Citation:
Bendinelli M, Pistello M, Freer G, Vatteroni M, Maggi F.
2006.
Viral Hepatitis,
p 724-745.
In
Detrick B, Hamilton R, Folds J (ed),
Manual of Molecular and Clinical Laboratory Immunology, 7th Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815905.ch83
/content/10.1128/9781555815905.ch83.ch83fig03
FIGURE 3
Typical course of immunovirological events and manifestations of liver damage in symptomatic acute, self-limiting, and chronic HBV infection. The proportion of infections that chronicize is indicated as 15% but in fact varies widely, depending on the patient’s age and other variables (see text). The initial, acute phases are essentially the same, regardless of whether the infection resolves or becomes chronic. The vast majority of HBV infections do not produce overt disease or do so after many years of persistence; however, the immunovirological events are similar to the ones depicted.
10.1128/9781555815905/f0729-01_thmb.gif
10.1128/9781555815905/f0729-01.gif
FIGURE 3
Typical course of immunovirological events and manifestations of liver damage in symptomatic acute, self-limiting, and chronic HBV infection. The proportion of infections that chronicize is indicated as 15% but in fact varies widely, depending on the patient’s age and other variables (see text). The initial, acute phases are essentially the same, regardless of whether the infection resolves or becomes chronic. The vast majority of HBV infections do not produce overt disease or do so after many years of persistence; however, the immunovirological events are similar to the ones depicted.
Citation:
Bendinelli M, Pistello M, Freer G, Vatteroni M, Maggi F.
2006.
Viral Hepatitis,
p 724-745.
In
Detrick B, Hamilton R, Folds J (ed),
Manual of Molecular and Clinical Laboratory Immunology, 7th Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815905.ch83
/content/10.1128/9781555815905.ch83.ch83fig04
FIGURE 4
Algorithm for use and interpretation of laboratory tests for HBV infection. See also
Table 3
.
10.1128/9781555815905/f0731-01_thmb.gif
10.1128/9781555815905/f0731-01.gif
FIGURE 4
Algorithm for use and interpretation of laboratory tests for HBV infection. See also Table 3 .
Citation:
Bendinelli M, Pistello M, Freer G, Vatteroni M, Maggi F.
2006.
Viral Hepatitis,
p 724-745.
In
Detrick B, Hamilton R, Folds J (ed),
Manual of Molecular and Clinical Laboratory Immunology, 7th Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815905.ch83
/content/10.1128/9781555815905.ch83.ch83fig05
FIGURE 5
Typical course of immunovirological events and manifestations of liver damage in symptomatic, acute self-limiting and chronic HCV infection. The initial, acute phases are essentially the same, regardless of whether infection resolves or becomes chronic. HCV has a greater tendency to persist than HBV. The vast majority of both acute and chronic infections do not produce overt disease or do so after many years of persistence; however, the immunovirological events are similar to the ones depicted.
10.1128/9781555815905/f0734-01_thmb.gif
10.1128/9781555815905/f0734-01.gif
FIGURE 5
Typical course of immunovirological events and manifestations of liver damage in symptomatic, acute self-limiting and chronic HCV infection. The initial, acute phases are essentially the same, regardless of whether infection resolves or becomes chronic. HCV has a greater tendency to persist than HBV. The vast majority of both acute and chronic infections do not produce overt disease or do so after many years of persistence; however, the immunovirological events are similar to the ones depicted.
Citation:
Bendinelli M, Pistello M, Freer G, Vatteroni M, Maggi F.
2006.
Viral Hepatitis,
p 724-745.
In
Detrick B, Hamilton R, Folds J (ed),
Manual of Molecular and Clinical Laboratory Immunology, 7th Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815905.ch83
/content/10.1128/9781555815905.ch83.ch83fig06
FIGURE 6
Algorithm for use and interpretation of laboratory tests for HCV infection. Under selected circumstances, HCV-Ag detection and measurement can be used in place of HCV RNA detection. Immunoblotting as a means to confirm positive EIA results is currently skipped by many laboratories, which proceed directly to HCV RNA detection and use confirmation by immunoblotting only for the patients who test HCV RNA negative.
10.1128/9781555815905/f0735-01_thmb.gif
10.1128/9781555815905/f0735-01.gif
FIGURE 6
Algorithm for use and interpretation of laboratory tests for HCV infection. Under selected circumstances, HCV-Ag detection and measurement can be used in place of HCV RNA detection. Immunoblotting as a means to confirm positive EIA results is currently skipped by many laboratories, which proceed directly to HCV RNA detection and use confirmation by immunoblotting only for the patients who test HCV RNA negative.
Citation:
Bendinelli M, Pistello M, Freer G, Vatteroni M, Maggi F.
2006.
Viral Hepatitis,
p 724-745.
In
Detrick B, Hamilton R, Folds J (ed),
Manual of Molecular and Clinical Laboratory Immunology, 7th Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815905.ch83
/content/10.1128/9781555815905.ch83.ch83fig07
FIGURE 7
Typical course of immunovirological events and manifestations of liver damage in symptomatic HDV infection. In concomitant infection (coinfection) of naive individuals with HBV and HDV, HBV markers are affected very little by concurrent HDV replication, and HDV markers may escape detection due to their transient nature. In superinfection of individuals already infected with HBV, HDV replication is particularly florid and may produce transient reductions or unde-tectability of HBV DNA and HBsAg (see text).
10.1128/9781555815905/f0737-01_thmb.gif
10.1128/9781555815905/f0737-01.gif
FIGURE 7
Typical course of immunovirological events and manifestations of liver damage in symptomatic HDV infection. In concomitant infection (coinfection) of naive individuals with HBV and HDV, HBV markers are affected very little by concurrent HDV replication, and HDV markers may escape detection due to their transient nature. In superinfection of individuals already infected with HBV, HDV replication is particularly florid and may produce transient reductions or unde-tectability of HBV DNA and HBsAg (see text).
Citation:
Bendinelli M, Pistello M, Freer G, Vatteroni M, Maggi F.
2006.
Viral Hepatitis,
p 724-745.
In
Detrick B, Hamilton R, Folds J (ed),
Manual of Molecular and Clinical Laboratory Immunology, 7th Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815905.ch83
/content/10.1128/9781555815905.ch83.ch83fig08
FIGURE 8
Algorithm for use and interpretation of laboratory tests for HDV infection. A prerequisite for HDV testing is that the patient is infected with HBV. In regions of high HDV endemicity, HDV testing should be carried out every second or third year or whenever there is an unexplained aggravation of hepatitis. In regions of low endemicity, HDV testing should essentially be limited to IDUs or people returning from areas of endemicity.
10.1128/9781555815905/f0738-01_thmb.gif
10.1128/9781555815905/f0738-01.gif
FIGURE 8
Algorithm for use and interpretation of laboratory tests for HDV infection. A prerequisite for HDV testing is that the patient is infected with HBV. In regions of high HDV endemicity, HDV testing should be carried out every second or third year or whenever there is an unexplained aggravation of hepatitis. In regions of low endemicity, HDV testing should essentially be limited to IDUs or people returning from areas of endemicity.
Citation:
Bendinelli M, Pistello M, Freer G, Vatteroni M, Maggi F.
2006.
Viral Hepatitis,
p 724-745.
In
Detrick B, Hamilton R, Folds J (ed),
Manual of Molecular and Clinical Laboratory Immunology, 7th Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815905.ch83
/content/10.1128/9781555815905.ch83.ch83fig09
FIGURE 9
Algorithm for use and interpretation of laboratory tests for HEV infection. HEV RNA assays should be performed only when there are solid reasons for suspecting HEV infection (see text), on stool samples collected within 2 to 3 weeks from clinical onset.
10.1128/9781555815905/f0739-01_thmb.gif
10.1128/9781555815905/f0739-01.gif
FIGURE 9
Algorithm for use and interpretation of laboratory tests for HEV infection. HEV RNA assays should be performed only when there are solid reasons for suspecting HEV infection (see text), on stool samples collected within 2 to 3 weeks from clinical onset.
Citation:
Bendinelli M, Pistello M, Freer G, Vatteroni M, Maggi F.
2006.
Viral Hepatitis,
p 724-745.
In
Detrick B, Hamilton R, Folds J (ed),
Manual of Molecular and Clinical Laboratory Immunology, 7th Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815905.ch83
References
/content/book/10.1128/9781555815905.ch83
1.
Aggarwal, R.,, D. Kini,, S. Sofat,, S. R. Naik, and , K. Krawczynski. 2000. Duration of viremia and fecal excretion in acute hepatitis. Lancet 356: 1081– 1082.
2.
Allain, J. P. 2004. Occult hepatitis B infection. Transfus. Clin. Biol. 11: 18– 25.
3.
Bendinelli, M.,, M. Pistello,, F. Maggi,, C. Fornai,, G. Freer, and , M. L. Vatteroni. 2001. Molecular properties, biology, and clinical implications of TT virus, a recently identified widespread infectious agent of humans. Clin. Microbiol. Rev. 14: 98– 113.
4.
Berg, T.,, C. Sarrazin,, F. Herrmann,, H. Hinrichsen,, T. Gerlach,, R. Zachoval,, B. Wiedenmann,, U. Hopf, and , S. Zeuzem. 2003. Prediction of treatment outcome in patients with chronic hepatitis C: significance of baseline parameters and viral dynamic during therapy. Hepatology 37: 600– 609.
5.
Bower, W. A.,, O. V. Nainan,, X. Han, and , H. S. Margolis. 2000. Duration of viremia in hepatitis A virus infection. J. Infect. Dis. 182: 12– 17.
6.
Castillo, I.,, M. Pardo,, J. Bartolomé,, N. Ortiz-Movilla,, F. Rodriguez-Inigo,, S. de Lucas,, C. Salas,, J. A. Jimenez-Heffernan,, A. Pérez-Mota,, J. Graus,, J. M. Lopez-Alcorocho, and , V. Carreno. 2004. Occult hepatitis C virus infection in patients in whom the etiology of persistently abnormal results of liver-function tests is unknown. J. Infect. Dis. 189: 7– 14.
7.
Chu, C. J.,, M. Hussain, and , A. S. F. Lok. 2002. Quantitative serum HBV DNA levels during different stages of chronic hepatitis B infection. Hepatology 36: 1408– 1415.
8.
Costa-Mattioli, M.,, A. Di Napoli,, V. Ferrè,, S. Billaudel,, R. Perez-Bercoff, and , J. Cristina. 2003. Genetic variability of hepatitis A. J. Gen. Virol. 84: 3191– 3201.
9.
de Paula, V. S.,, L. M. Villar,, L. M. Morais,, L. L. Lewis-Ximenez,, C. Niel, and , A. M. Gaspar. 2004. Detection of hepatitis A virus RNA in serum during the window period of infection. J. Clin. Virol. 29: 254– 259.
10.
Fried, M. W. 2004. Viral factors affecting the outcome of therapy for chronic hepatitis C. Rev. Gastroenterol. Disord. 4: S8– S13.
11.
Ganem, D., and , A. M. Prince. 2004. Hepatitis B infection— natural history and clinical consequences. N. Engl. J. Med. 350: 1118– 1129.
12.
Hoofnagle, J. H. 2002. Course and outcome of hepatitis C. Hepatology 36: S21– S29.
13.
Huang, Y. H.,, J. C. Wu,, W. Y. Sheng,, T. I. Huo,, E. Y. Chang, and , S. D. Lee. 1998. Diagnostic value of anti-hepatitis D virus (HDV) antibodies revisited: a study of total and IgM anti-HDV compared with detection of HDV-RNA by polymerase chain reaction. J. Gastroenterol. Hepatol. 13: 57– 61.
14.
Jenson, H. B. 2004. The changing picture of hepatitis A in the United States. Curr. Opin. Pediatr. 16: 89– 93.
15.
Lai, C. L.,, V. Ratziu,, M.-F. Yuen, and , T. Poynard. 2003. Viral hepatitis B. Lancet 362: 2089– 2094.
16.
Lanford, R. E.,, B. Guerra,, D. Chavez,, C. Bigger,, K. M. Brasky,, X. H. Wang,, S. C. Ray, and , D. Thomas. 2004. Cross-genotype immunity to hepatitis C virus. J. Virol. 78: 1575– 1581.
17.
Lewis, J. A. 1999. Hepatitis A vaccines, p. 317– 375. In S. Specter (ed.), Viral Hepatitis: Diagnosis, Therapy, and Prevention. Humana Press Inc., Totowa, N.J.
18.
Linnen, J.,, J. Wages, Jr.,, Z. Y. Zhang-Keck,, K. F. Fry,, K. Z. Krawczynski,, H. Alter,, F. Koonin,, M. Gallagher,, M. Alter,, S. Hadziyannis,, P. Karayiannis,, K. Fung,, Y. Nakatsuji,, J. W. K. Shih,, L. Young,, M. Piatak, Jr.,, C. Hoover,, J. Fernandez,, S. Chen,, J. C. Zou,, T. Morris,, K. C. Hyams,, S. Ismay,, J. D. Lifson,, G. Hess,, S. H. K. Foung,, H. Thomas,, D. Bradley,, H. Margolis, and , J. R. Kim. 1996. Molecular cloning and disease association of hepatitis G virus: a transfusion-transmissible agent. Science 271: 505– 508.
19.
Maggi, F.,, M. Pifferi,, F. Tempestini,, C. Fornai,, L. Lanini,, F. Andreoli,, M. L. Vatteroni,, S. Presciuttini,, A. Pietrobelli,, A. Boner,, M. Pistello, and , M. Bendinelli. 2003. TT virus loads and lymphocyte subpopulations in children with acute respiratory diseases. J. Virol. 77: 9081– 9083.
20.
Martinot-Peignoux, M.,, N. Boyer,, M. Colombat,, R. Akremi,, B. N. Pham,, S. Ollivier,, C. Castelnau,, D. Valla,, C. Degott, and , P. Marcellin. 2002. Serum hepatitis B virus DNA levels and liver histology in inactive HBsAg carriers. J. Hepatol. 36: 543– 546.
21.
Maynard, M.,, P. Pradat,, P. Berthillon,, G. Picchio,, N. Voirin,, M. Martinot,, P. Marcelin, and , C. Trepo. 2003. Clinical relevance of total core antigen testing for hepatitis C monitoring and for predicting patients’ response to therapy. J. Viral Hepat. 10: 318– 323.
22.
Mommeja-Martin, H.,, F. Mondou,, M. R. Blum, and , F. Rousseau. 2003. Serum HBV DNA as a marker of efficacy during therapy for chronic HBV infection: analysis and review of the literature. Hepatology 37: 1309– 1319.
23.
Morishima, C.,, M. Chung,, K. W. Ng,, D. J. Brambilla. and , D. R. Gretch. 2004. Strengths and limitations of commercial test for hepatitis C virus RNA quantification. J. Clin. Microbiol. 42: 421– 425.
24.
Nakamoto, Y., and , S. Kaneko. 2003. Mechanisms of viral hepatitis induced liver injury. Curr. Mol. Med. 3: 537– 544.
25.
National Institutes of Health. 2002. NIH consensus statement on management of hepatitis C. NIH Consens. State Sci. Statements Jun 10-12 19: 1– 46. [Online.] http://www.consensus.nih.gov/.
26.
Neumann, U. P.,, T. Berg,, M. Bahra,, G. Puhl,, O. Guckelberger,, J. M. Langrehr, and , P. Neuhaus. 2004. Long-term outcome of liver transplants for chronic hepatitis C: a 10-year follow-up. Transplantation 77: 226– 231.
27.
Nishizawa, T.,, H. Okamoto,, K. Konishi,, H. Yoshizawa,, Y. Miyakawa, and , M. Mayumi. 1997. A novel DNA virus (TTV) associated with elevated transaminase levels in posttransfusion hepatitis of unknown etiology. Biochem. Biophys. Res. Commun. 241: 92– 97.
28.
Nunez, M.,, M. Puoti,, N. Camino, and , V. Soriano. 2003. Treatment of chronic hepatitis B in the human immunodeficiency virus-infected patient: present and future. Clin. Infect. Dis. 37: 1678– 1685.
29.
Pawlotsky, J.-M. 2004. Pathophysiology of hepatitis C infection and related liver disease. Trends Microbiol. 12: 96– 102.
30.
Pham, N. Q.,, S. A. MacParland,, R. M. Mulrooney,, H. Cooksley,, N. V. Naumov, and , T. I. Michalak. 2004. Hepatitis C virus persistence after spontaneous or treatment-induced resolution of hepatitis C. J. Virol. 78: 5867– 5874.
31.
Pistello, M.,, F. Maggi,, C. Fornai,, A. Leonildi,, A. Morrica,, M. L. Vatteroni, and , M. Bendinelli. 1999. Classification of hepatitis C virus type 2 isolates by phylogenetic analysis of core and NS5 region. J. Clin. Microbiol. 37: 2116– 2117.
32.
Pol, S.,, F. Carnet,, B. Nalpas,, J.-L. Lagneau,, H. Fontaine,, J. Serpaggi,, L. Serfaty,, P. Bedossa, and , C. Brechot. 2004. Reversibility of hepatitis C virus-related cirrhosis. Hum. Pathol. 35: 107– 112.
33.
Polish, L. B.,, B. H. Robertson,, B. Khanna,, K. Krawczynski,, J. Spelbring,, F. Olson, and , C. N. Shapiro. 1999. Excretion of hepatitis A virus (HAV) in adults: comparison of immunologic and molecular detection methods and relationship between HAV positivity and infectivity in tamarins. J. Clin. Microbiol. 37: 3615– 3617.
34.
Purcell, R. H.,, H. Nguyen,, M. Shapiro,, R. F. Engle,, S. Govindarajan,, W. C. Blackwelder,, D. C. Wong,, J. P. Prieels, and , S. U. Emerson. 2003. Pre-clinical immuno-genicity and efficacy trial of a recombinant hepatitis E vaccine. Vaccine 2: 2607– 2615.
35.
Ribeiro, R. M.,, A. Lo, and , A. S. Perelson. 2002. Dynamics of hepatitis B virus infection. Microbes Infect. 4: 829– 835.
36.
Rockstroh, J. K., and , U. Spengler. 2004. HIV and hepatitis C virus co-infection. Lancet Infect. Dis. 4: 437– 444.
37.
Sagir, A.,, O. Kirschberg,, T. Heintges,, A. Erhardt, and , D. Haussinger. 2004. SEN virus infection. Rev. Med. Virol. 14: 141– 148.
38.
Schuttler, C. G.,, C. Thomas,, T. Discher,, G. Friese,, J. Lohmeyer,, R. Schuster,, S. Schaefer, and , W. H. Gerlich. 2004. Variable ratio of hepatitis C virus RNA to viral core antigen in patient sera. J. Clin. Microbiol. 45: 1977– 1981.
39.
Simons, J. N.,, T. P. Leary,, G. J. Dawson,, T. J. Pilot-Matias,, A. S. Muerhoff,, G. G. Schlauder,, S. M. Desai, and , I. K. Mushahwar. 1995. Isolation of novel virus-like sequences associated with human hepatitis. Nat. Med. 1: 564– 569.
40.
Smedile, A., and , G. Verme. 1999. Hepatitis D virus. Biology, pathogenesis, epidemiology, clinical description, and therapy, p. 129– 150. In S. Specter (ed.), Viral Hepatitis: Diagnosis, Therapy, and Prevention. Humana Press Inc., Totowa, N.J.
41.
Stapleton, J. T. 2003. GB virus type C/hepatitis G virus. Semin. Liver Dis. 23: 137– 148.
42.
Strader, D. B.,, T. Wright,, D. L. Thomas, and , L. B. Seeff. 2004. Diagnosis, management, and treatment of hepatitis C. Hepatology 39: 1147– 1171.
43.
Taylor, J. M. 2003. Replication of human hepatitis delta virus: recent developments. Trends Microbiol. 11: 185– 190.
44.
Torbenson, M., and , D. L. Thomas. 2002. Occult hepatitis B. Lancet Infect. Dis. 2: 479– 486.
45.
Veillon, P.,, C. Payan,, G. Picchio,, M. Maniez-Montreuil,, P. Guntz, and , F. Lunel. 2003. Comparative evaluation of the total hepatitis C virus core antigen, branched-DNA, and Amplicor Monitor assays in determining viremia for patients with chronic hepatitis C during interferon plus ribavirin combination therapy. J. Clin. Microbiol. 41: 3212– 3220.
46.
Wang, D.,, J. Pearlberg,, Y. T. Liu, and , D. Ganem. 2001. Deleterious effects of hepatitis delta virus replication on host cell proliferation. J. Virol. 75: 3600– 3604.
47.
Wang, Y. C.,, H. Y. Zhang,, N. S. Xia,, G. Peng,, H. Y. Lan,, H. Zhuang,, Y. H. Zhu,, S. W. Li,, K. G. Tian,, W. J. Gu,, J. X. Lin,, X. Wu,, H. M. Li, and , T. J. Harrison. 2002. Prevalence, isolation, and partial sequence analysis of hepatitis E virus from domestic animals in China. J. Med. Virol. 67: 516– 521.
48.
Williams, C. F.,, D. Klinzman,, T. F. Yamashita,, J. Xiang,, P. M. Polgreen,, C. Rinaldo,, C. Liu,, J. Phair,, J. B. Margolick,, D. Zdunek,, G. Hess, and , J. T. Stapleton. 2004. Persistent GB virus C infection and survival in HIV-infected men. N. Engl. J. Med. 350: 981– 990.
49.
Worm, H. C.,, W. H. M. van der Poel, and , G. Brandstaetter. 2002. Hepatitis E: an overview. Microbes Infect. 4: 657– 666.
50.
Wu, J. C.,, I. A. Huang,, Y. H. Huang,, J. Y. Chen, and , I. J. Sheen. 1999. Mixed genotypes infection with hepatitis D virus. J. Med. Virol. 57: 64– 67.
51.
Yamashiro, T.,, K. Nagayama,, N. Enomoto,, H. Watanabe,, T. Miyagi,, H. Nakasone,, H. Sakugawa, and , M. Watanabe. 2004. Quantitation of the level of hepatitis delta virus RNA in serum, by real-time polymerase chain reaction and its possible correlation with the clinical stage of liver disease. J. Infect. Dis. 189: 1151– 1157.
52.
Yu, C.,, R. F. Eagle,, J. P. Bryan,, S. U. Emerson, and , R. H. Purcell. 2003. Detection of immunoglobulin M antibodies to hepatitis E virus by class capture enzyme immunoassay Clin. Diagn. Lab. Immunol. 10: 579– 586.
53.
Yuen, M. F.,, F. Sablon,, H. J. Yuan,, D. K. L. Wong,, C. K. Hui,, B. C. Y. Wong,, A. O. O. Chan, and , C. L. Lai. 2003. Significance of hepatitis B genotype in acute exacerbation, HBeAg seroconversion, cirrhosis-related complications and hepatocellular carcinoma. Hepatology 37: 562– 567.
54.
Zeuzem, S. 2004. Heterogeneous virologic response rates to interferon-based therapy in patients with chronic hepatitis C: who responds less well? Ann. Intern. Med. 140: 346– 355.
Tables
Viral Hepatitis
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Citation:
Bendinelli M, Pistello M, Freer G, Vatteroni M, Maggi F.
2006.
Viral Hepatitis,
p 724-745.
In
Detrick B, Hamilton R, Folds J (ed),
Manual of Molecular and Clinical Laboratory Immunology, 7th Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815905.ch83
/content/10.1128/9781555815905.ch83.ch83tab01
TABLE 1
Viruses discussed in this chapter
TABLE 1
Viruses discussed in this chapter
Citation:
Bendinelli M, Pistello M, Freer G, Vatteroni M, Maggi F.
2006.
Viral Hepatitis,
p 724-745.
In
Detrick B, Hamilton R, Folds J (ed),
Manual of Molecular and Clinical Laboratory Immunology, 7th Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815905.ch83
/content/10.1128/9781555815905.ch83.ch83tab02
TABLE 2
Serum parameters useful for the biochemical evaluation of liver necrosis and function
TABLE 2
Serum parameters useful for the biochemical evaluation of liver necrosis and function
Citation:
Bendinelli M, Pistello M, Freer G, Vatteroni M, Maggi F.
2006.
Viral Hepatitis,
p 724-745.
In
Detrick B, Hamilton R, Folds J (ed),
Manual of Molecular and Clinical Laboratory Immunology, 7th Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815905.ch83
/content/10.1128/9781555815905.ch83.ch83tab03
TABLE 3
Interpretation of immunovirological profiles for HBV
TABLE 3
Interpretation of immunovirological profiles for HBV
Citation:
Bendinelli M, Pistello M, Freer G, Vatteroni M, Maggi F.
2006.
Viral Hepatitis,
p 724-745.
In
Detrick B, Hamilton R, Folds J (ed),
Manual of Molecular and Clinical Laboratory Immunology, 7th Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815905.ch83