Functional and developmental effects of Zika virus (ZIKV) infection and hydroxychloroquine (HCQ) treatment on the murine placenta were measured using MRI and oxygen enhancement to assess placental volume and oxygenation. HCQ treatment helps to prevent adverse placental volume outcomes earlier in gestation, but late-gestation results are similar to those of ZIKV-infected dams. R1 and R2* measurements show that HCQ has a significant effect on placental oxygenation throughout gestation, whereas ZIKV does not significantly affect these metrics.
Murine placentas consist of both maternal and fetal structures that can be visualized via MRI and histology (Fig. 1). Placental volumes of ZIKV-infected animals were smaller than those of healthy controls at both time points (Fig. 2). At E15.5, mean placental volumes were 0.060 cm3 (ZIKV-infected) vs. 0.063 cm3 (healthy). At E18.5, the means were 0.059 cm3 vs. 0.066 cm3, respectively. In healthy/HCQ-treated animals, mean volumes were 0.065 cm3 (E15.5) vs. 0.071 cm3 (E18.5); in the ZIKV-infected/HCQ-treated animals, 0.063 cm3 (E15.5) vs. 0.058 cm3 (E18.5).
Figure 3 shows that the average R1 values at both time points, and under both breathing-gas conditions, are similar for control and ZIKV-infected animals in the absence of HCQ treatment, with average R1 values of 0.55-0.59 s-1. In HCQ-treated animals, both ZIKV-infected and uninfected, R1 increased significantly, with an average R1 of > 0.7 s-1 for all cases.
Figure 4 shows average R2* values across time points and under both breathing-gas conditions for each cohort. On room air, both cohorts showed increased R2* values from E15.5 to E18.5 (84 s-1 vs. 119 s-1 or 43% increase for healthy dams; 87 s-1 vs. 110 s-1 or 27% increase for ZIKV-infected). For HCQ-treated animals, there was no significant change in baseline R2* across gestation.
Figure 5 shows the change in R2* (air- carbogen) at both gestational ages. The mean change in R2* for healthy and ZIKV-infected dams was 15-20 s-1 on both days. Similarly, the R2* change in ZIKV-infected/HCQ-treated dams decreased from 23 s-1 (E15.5) to 9 s-1 (E18.5), while for healthy/HCQ-treated dams the change was ~3 s-1 on both days.
The smaller placental volumes in infected dams (Fig. 2) suggest that ZIKV inhibits proper development of the murine placenta across gestation. Additionally, ZIKV-infected placentas show no change in mean volume from E15.5 to E18.5, compared with a 3% increase observed in healthy dams. At E15.5, mean placental volumes in ZIKV-infected/HCQ-treated animals are equivalent to those of healthy dams at E15.5, but by E18.5 is comparable to ZIKV without treatment. This suggests that while HCQ may initially preserve placental development in ZIKV-infected animals, without sustained treatment the late-gestation adverse outcomes are unaffected.
Somewhat surprisingly, HCQ treatment had a
larger effect on placental relaxation parameters, R1 and R2*,
than did ZIKV infection (Figs. 3 – 5). The increase of R1 in both
healthy and ZIKV-infected animals following HCQ treatment could suggest increased
oxygenation of the placental tissue. Both healthy and ZIKV mice show
significant R2* increases with aging, an effect
eliminated by HCQ treatment. At both gestational ages, carbogen breathing produced
a significant decrease in R2* in untreated healthy and
ZIKV-infected mice, but not healthy/HCQ-treated animals. At E15.5, a similar decrease
in R2* in response to carbogen is observed for
ZIKV-infected/HCQ-treated mice, an effect that is lost at E18.5. In untreated
mice, changes in R1 and R2* from E15.5 and
E18.5 reflect expected changes in O2 content and utilization
associated with placental aging. The mechanism
by which HCQ affects R1 and R2* values in
healthy and ZIKV-infected animals, and its differential effects on aging, are the
subject of ongoing research.
Research supported, in part, by Mallinckrodt Institute of Radiology Pilot Fund 18-016 (WUSM), the Howard Hughes Medical Institute, and National Institutes of Health grants R01 HD086323, 5T32 EB014855, and R01 HD091218. Valuable discussions with Professor Joseph JH Ackerman, Washington University in St Louis, and Professor Bin Cao, Xiameng University, are gratefully acknowledged. Special thanks to the Center for Reproductive Health Sciences at Washington University School of Medicine for assistance with histopathological processing of tissue samples.