Decreased expression of equine herpesvirus-1 early and late genes in the placenta of naturally aborted equine fetuses.

This research investigates the decreased expression of certain genes in the placenta of horse fetuses naturally aborted due to equine herpesvirus-1 (EHV-1) infection. The study found that although the placenta expressed an immediate-early gene at a comparable level to the fetal lungs, other genes’ expression was significantly lower, possibly leading to reduced production of viral offspring and diminished immune reaction.

Background

Equine herpesvirus-1 (EHV-1) is a major cause of natural abortions in horses. The virus is thought to be transmitted to the fetus via the placenta, following an infection in the mother’s blood cells. The researchers in this study examined the gene expression of EHV-1 in the placentas of seven naturally aborted equine fetuses.

Findings on Virus and Gene Expression

• The researchers found no sign of lesions or viral antigens in the fetuses’ placentas, suggesting that the virus does not harm the placenta directly.
• The level of the virus in the placenta was significantly lower than in the fetuses’ lungs, which exhibited signs of pneumonia and typical herpesvirus inclusions.
• Utilizing quantitative dot blot hybridization with immediate-early (IE), early (ICP0), and late (gD and gK) gene-specific probes, the researchers found the placenta expressed the IE gene at a level similar to the fetuses’ lungs.

Differing Gene Expression in the Placenta and Lungs

• However, the placenta’s expression of the ICP0, gD, and gK genes was significantly lower than in the lungs. This finding is significant as it suggests a decrease in these gene expressions in the placenta.
• In-situ hybridization showed that IE and gK RNAs — essential for the virus’s progression — were mostly found in the trophoblasts’ cytoplasm, cells forming the outer layer of a blastocyst, providing nutrients to the embryo and developing into a large part of the placenta.

Implications of Findings

• These findings suggest that the limited production of viral offspring could be attributed to this low level of early and late gene expression.
• Moreover, the lack of immunoreactivity — or the immune system’s response to pathogens — for the viral antigen in EHV-1 infected trophoblasts could be a result of this decreased gene expression.