The present study was conducted to evaluate and compare the viral load and genotypes of hepatitis E virus (HEV) in acute liver failure (ALF) with that of acute viral hepatitis among pregnant and nonpregnant women. The trial included a total of 100 fulminant hepatic failure (FHF) and 150 acute viral hepatitis (AVH) patients (50, 75 pregnant and 50, 75 nonpregnant, respectively). 

Evidences suggest higher incidence and mortality rate in pregnant women with FHF due to HEV, particularly in women of Asian countries. Pregnancy is considered as an altered state of sex steroid hormones and immunity. There is a rising evidence of increasing occurrence of hepatitis E in developing countries including India. Moreover, a direct effect of steroid hormones is seen on the replication via their impact on viral regulatory elements. Besides the increased prevalence of hepatitis E, folate deficiency is found in pregnant women of Asia that results in reduced immunocompetence causing a greater risk of multiple viral infections and higher viral load.

The result showed that out of total enrolled patients with FHF and AVH, 56% and 29.3% pregnant and 14% and 16% nonpregnant, respectively, were HEV RNA-positive. HEV viral load in FHF pregnant women was 5.87 x 10(4)+/- 1.5 x 10(5) microL/mL in comparison 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 reported genotype 1.

Based on these observations, it can be concluded that HEV viral load was found to be remarkably higher in pregnant patients in contrast to the nonpregnant. Therefore, pregnancy is regarded as a risk factor for viral replication. Furthermore, the viral copies of HEV in FHF pregnant women were substantially higher in comparison to AVH pregnant women, suggestive of an association to the severity of the disease in these patients. The authors also identified only one genotype (genotype 1), therefore, in the absence of other genotypes in this population, the effect of genotype could not be adequately determined.

Source: Am J Gastroenterol. 2008 Oct;103(10):2495-501.