|Articles|October 13, 2016

Research Provides Clues to How Zika Virus Breaches the Placental Barrier

New research reveals that in pregnant women, Zika virus infection damages certain cells that affect placental formation and function. Furthermore, herpes simplex virus-2 (HSV-2) infection augments placental sensitivity to Zika virus by enhancing the expression of receptors that allow Zika virus to enter cells.

The findings may help explain the mechanism by which Zika virus breaches the placental barrier to access the fetus. They also suggest that fetuses in pregnant women with HSV-2 infection are at a higher risk for microcephaly and other effects caused by Zika virus.

"Investigators in Brazil have suspected that something more than Zika virus is causing the high intensity and severity of cases. Our study suggests that the immune response to an early infection, HSV-2, may be the additional factor that increases the risk for severity of Zika virus-induced disease," said Dr. Gil Mor, senior author of the American Journal of Reproductive Immunology study.

Source: Wiley
 


Related to this article

Infection preventionists in full PPE with children in DRC.  (Image credit: author with AI)
Nearly 4 months into the DRC's Bundibugyo virus disease outbreak, some indicators suggest transmission may be slowing. But shifting hotspots, treatment-center capacity problems, community deaths, and incomplete surveillance data show why national case totals alone cannot determine whether containment has been achieved.