Does hepatitis E viral load and genotypes influence the final outcome of acute live failure during pregnancy?

Kar, P. ; Jilani, N. ; Husain, S. A. ; Pasha, S. T. ; Anand, R. ; Rai, A. ; Das, B. C. (2008) Does hepatitis E viral load and genotypes influence the final outcome of acute live failure during pregnancy? American Journal of Gastroenterology, 103 . pp. 2495-2501. ISSN 0002-9270

Full text not available from this repository.


Background: Hepatitis E is a major health problem in developing countries including India. The incidence and mortality rate in pregnant women with fulminant hepatic failure (FHF) due to hepatitis E virus (HEV) has been reported to be significantly higher, specifically in Asian women. Pregnancy is usually associated with an altered status of sex steroid hormones and immunity. Steroid hormones directly influence the replication through their effects on viral regulatory elements. Moreover, pregnant women in Asia generally suffer from folate deficiency, which is known to cause reduced immunocompetence leading to greater risk of multiple viral infections and higher viral load. Objectives: To correlate and analyze the viral load and genotypes of HEV in acute liver failure with that of acute viral hepatitis among pregnant and nonpregnant women. Materials and Methods: A total of 100 FHF and 150 acute viral hepatitis (AVH) patients (50, 75 pregnant and 50, 75 nonpregnant, respectively), were included in the study. These cases were evaluated on the basis of history, clinical examination, liver function profile, and serological test of hepatitis A, B, C, and E using commercially available ELISA kits. Quantification of HEV RNA-positive samples was carried out. Results: Out of 100 FHF and 150 acute viral hepatitis (AVH) patients, 28 (56%) and 22 (29.3%) pregnant and 7 (14%) and 8 (16%) nonpregnant, respectively, were HEV RNA-positive. HEV viral load in FHF pregnant women was 5.87 × 10(4)+/− 1.5 × 10(5) microL/mL as compared to AVH pregnant women 343.29 +/− 216.44 microL/mL and FHF and AVH nonpregnant 199.2 +/− 225.5 microL/mL and 13.83 +/− 7.8 microL/mL, respectively. Sequencing data of all the positive samples of FHF and AVH pregnant and nonpregnant women showed genotype 1. Conclusion: HEV viral load was found to be significantly higher (P < 0.05) in pregnant patients compared to the nonpregnant. Pregnancy appears to be a risk factor for viral replication. The viral copies of HEV in FHF pregnant women were comparatively higher when compared to AVH pregnant women, which may be related to the severity of the disease in these patients. We could detect only one genotype (genotype 1) in our study population. Thus in the absence of other genotypes in this population, the impact of genotype could not be adequately assessed in this study.

Item Type:Article
Source:Copyright of this article belongs to Nature Publishing Group.
ID Code:74607
Deposited On:17 Dec 2011 11:22
Last Modified:17 Dec 2011 11:22

Repository Staff Only: item control page