Hepatitis E laboratory tests

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]

Overview

Hepatitis E cannot be distinguished from other types of hepatitis based on clinical manifestations alone. Although blood markers of liver injury, such as elevated aminotransferases may be identified, definitive diagnosis of hepatitis E is done by serologic tests.

Laboratory Findings

Every patient with acute or chronic hepatitis, which cannot be explained by other causes, should be tested for hepatitis E.[1] Unfortunately, the different available assays show different specificity and sensitivity, and are only available at certain centers.[2]

Throughout the course of infection, serologic markers will vary according to the stage of the disease:[2][3][1]

Laboratory findings
Stage of Infection Findings
Incubation period
Symptom onset
Recovery
  • Viral clearance
  • Increase of IgG titers (detectable for years to life)
  • Decrease of IgM levels (detectable for 3 to 12 months)
  • HEV detected in stool during the initial period of recovery

The detection of increased levels of anti-HEV IgG may therefore indicate recent HEV infection.[1] Several assays are based on the HEV genotype, therefore, even though the specificity may be high, sensitivity of different tests for the remaining genotypes may be lower.[1]

Immunocompromised patients may have a delayed immune response to HEV, and hence delayed seroconversion. Therefore, these patients should be tested for HEV RNA.[4] The RNA of the virus may be detected in blood and stool for several weeks, and quantified in order to evaluate the response to treatment[1][5]

Enzyme Immunoassays

Enzyme immunoassays are directed for the ORF2 and ORF3 proteins. These tests have low sensitivity and specificity, requiring further improvements.[6]

RT-PCR

Amplification techniques allow for the identification of HEV nucleic acids. These techniques allow:[6]

Amplification techniques may have low sensitivity because when performed, viral load in blood and feces may be low or unidentifiable.[6]

References

  1. 1.0 1.1 1.2 1.3 1.4 Wedemeyer H, Pischke S, Manns MP (2012). "Pathogenesis and treatment of hepatitis e virus infection". Gastroenterology. 142 (6): 1388–1397.e1. doi:10.1053/j.gastro.2012.02.014. PMID 22537448.
  2. 2.0 2.1 Hoofnagle JH, Nelson KE, Purcell RH (2012). "Hepatitis E." N Engl J Med. 367 (13): 1237–44. doi:10.1056/NEJMra1204512. PMID 23013075.
  3. Kamar N, Bendall R, Legrand-Abravanel F, Xia NS, Ijaz S, Izopet J; et al. (2012). "Hepatitis E." Lancet. 379 (9835): 2477–88. doi:10.1016/S0140-6736(11)61849-7. PMID 22549046.
  4. Pischke S, Suneetha PV, Baechlein C, Barg-Hock H, Heim A, Kamar N; et al. (2010). "Hepatitis E virus infection as a cause of graft hepatitis in liver transplant recipients". Liver Transpl. 16 (1): 74–82. doi:10.1002/lt.21958. PMID 19866448.
  5. Baylis SA, Hanschmann KM, Blümel J, Nübling CM, HEV Collaborative Study Group (2011). "Standardization of hepatitis E virus (HEV) nucleic acid amplification technique-based assays: an initial study to evaluate a panel of HEV strains and investigate laboratory performance". J Clin Microbiol. 49 (4): 1234–9. doi:10.1128/JCM.02578-10. PMC 3122834. PMID 21307208.
  6. 6.0 6.1 6.2 Aggarwal R, Jameel S (2011). "Hepatitis E." Hepatology. 54 (6): 2218–26. doi:10.1002/hep.24674. PMID 21932388.

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