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Review
. 2019 Jun;48(2):259-279.
doi: 10.1016/j.gtc.2019.02.007. Epub 2019 Apr 1.

Laboratory Diagnosis and Monitoring of Viral Hepatitis

Kunatum Prasidthrathsint  1 , Jack T Stapleton  2
Affiliations
Review

Laboratory Diagnosis and Monitoring of Viral Hepatitis

Kunatum Prasidthrathsint et al. Gastroenterol Clin North Am. 2019 Jun.

Abstract

Many microbes, toxins, autoimmune diseases, and neoplastic diseases may cause liver inflammation; however, 5 viruses whose main pathogenesis is liver disease are referred to as hepatitis A, B, C, D, and E viruses. These viruses cause a significant burden of global illness. With the exception of hepatitis A virus, all may cause chronic infection potentially leading to cirrhosis and hepatocellular carcinoma. Excellent serologic and nucleic acid detection methods are available for determining the precise cause and, in some cases, the duration of infection. Diagnostics are critical for identifying individuals needing treatment and for monitoring the treatment success.

Keywords: Hepatitis A; Hepatitis B; Hepatitis C; Hepatitis D; Hepatitis E; Viral diagnostics; Viral hepatitis.

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Figures

Figure 1.
Figure 1.
Schematic of the kinetics of viral, serologic, and clinical findings in hepatitis A virus infection.
Figure 2.
Figure 2.
HBV virus particles. A. The infectious (Dane) particle contains surface antigen (HBsAg), the partially double stranded (ds) DNA genome (ss = single strand), the viral RNA dependent, DNA polymerase, and the core antigen (HBcAg). HBsAg is released into serum as spherical particles (B) or tubular structures (C). These particles do not carry viral DNA, HBcAg or the viral polymerase.
Figure 3.
Figure 3.
Viral and serologic findings in acute hepatitis B virus infection. HBsAg = hepatitis B virus surface antigen. Anti-HBsAg = anti-hepatitis B surface antibodies. Anti-HBc = anti-hepatitis B core antibodies. “Window” is time between between positive surface antigen and antibody that will not be detected unless anti-HBc antibodies are measured.
Figure 4.
Figure 4.
Viral and serologic findings in chronic hepatitis B virus infection. HBsAg = hepatitis B virus surface antigen. Anti-HBc = anti-hepatitis B core antibodies.
Figure 5.
Figure 5.
Hepatitis C virus genome organization (top), polyprotein structure (middle), and processing (bottom). The 5′ and 3′ untranslated regions contain highly structured, stem-loop regions.
Figure 6.
Figure 6.
Schematic of the kinetics of viral and serologic findings in hepatitis D virus co-infection with HBV in a self-limited HBV infection. Since hepatitis B surface antigen (HBsAg) serves as the surface envelope protein for HDV, it must be present when HDV RNA is detected. Hepatitis delta virus antigen = HDV Ag, HBV serology as in Figure 3.
Figure 7.
Figure 7.
Schematic of the kinetics of viral and serologic findings in hepatitis D virus superinfection of a person with chronic HBV infection. Since hepatitis B surface antigen (HBsAg) serves as the surface envelope protein for HDV, it must be present when HDV RNA is detected. HBV serology as in Figure 4.
Figure 8.
Figure 8.
Viral and serologic findings in acute hepatitis E virus infection.
See this image and copyright information in PMC

References

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