Format

Send to

Choose Destination
Virology. 2017 Dec;512:187-193. doi: 10.1016/j.virol.2017.09.020. Epub 2017 Oct 2.

Adverse fetal outcomes in pregnant rabbits experimentally infected with rabbit hepatitis E virus.

Author information

1
Department of Infectious Diseases, College of Veterinary Medicine, Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul 05029, Republic of Korea.
2
Department of Food and Nutrition, School of Food Science and Technology, Chung-Ang University, Ansung 17546, Republic of Korea.
3
Korea Zoonosis Research Institute, Chonbuk National University, Jeonju 54896, Republic of Korea.
4
Department of Infectious Diseases, College of Veterinary Medicine, Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul 05029, Republic of Korea. Electronic address: ischoi@konkuk.ac.kr.

Abstract

Hepatitis E virus (HEV) causes severe hepatitis in pregnant women, with associated poor fetal outcomes. To study HEV viral pathogenesis, pregnant rabbits were infected with low- and high-dose rabbit HEV at 2 weeks gestation. HEV was identified in the serum, feces, and liver tissue of infected rabbits, and dose-dependent fetal mortality rates ranging from 67% to 80% were observed. The aspartate transaminase (AST)/alanine transaminase ratio was significantly higher (P < 0.01) in high-dose infected rabbits than low-dose infected and negative control rabbits 14 days post infection (dpi). Tumor necrosis factor-α (TNF-α) was significantly higher in low-dose (P < 0.01) and high-dose infected rabbits (P < 0.001) than in negative controls 7 dpi. High-dose HEV-infected rabbits produced significantly more interferon-γ (IFN-γ; P < 0.05) than negative control rabbits at 7 and 14 dpi. High levels of AST, TNF-α, and IFN-γ may substantially influence adverse fetal outcomes in pregnant rabbits infected with high-dose HEV.

KEYWORDS:

Aspartate transaminase; Fetal mortality; Hepatitis E virus; Interferon-γ; Pregnancy; Rabbit; Tumor necrosis factor-α

PMID:
28982029
DOI:
10.1016/j.virol.2017.09.020
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center