Experimental evidence for a high rate of maternal-fetal transmission of dengue virus in the presence of antibodies in immunocompromised mice

Neutrophil infiltration leads to fetal growth restriction by impairing the placental vasculature in DENV-infected pregnant mice

“…A previous study showed that DENV-3 infection did not result in placental damage or fetal pathology, and another indicated that DENV can be transmitted vertically in a gestation stage-dependent manner similar to ZIKV. 43 , 73 , 74 The difference in the results between our study and the literature was likely related to different mouse models, inoculation routes, pregnancy stages, virulence among serotypes, and viral doses used, which are all important influencing factors of adverse pregnancy outcomes during DENV infection in pregnant mice. Our findings demonstrate the potential for DENV infection to cause critical fetal outcomes during pregnancy and elucidate the possible pathogenesis.…”

Collateral Damage in the Placenta during Viral Infection in Pregnancy: A Possible Mechanism for Vertical Transmission and an Adverse Pregnancy Outcome

“…By becoming a target of infection, this virus can cross the placental barrier and reach the chorion [ 147 ]. With the ability to infect the trophoblasts in the chorionic villi, DENV can induce the activation of the immune system and promote the release of proinflammatory elements such as TNF-α, RANTES/CCL5, MCP1/CCL2, and VEGF/R2 that can alter vascular permeability, disrupting the architecture of the chorionic villi and promoting the spread of the virus to both the placenta and the fetus itself, causing fatal aversions such as fetal death [ 59 , 148 ].…”

The Innate Immune Response in DENV- and CHIKV-Infected Placentas and the Consequences for the Fetuses: A Minireview

“…The expression of TNF-α, IFN-γ, and RANTES was also found in DENV-infected placentas, revealing the maintenance of a pro-inflammatory environment in these cases [ 52 ]. Additionally, in an immunocompromised animal model, DENV vertical transmission was observed in the early stages of pregnancy and associated with an increased antibody-dependent enhancing (ADE) condition, which makes it conceivable that Hofbauer cells and macrophages at the maternal portion expressing Fc-gamma receptors could play an important role in inducing an ADE condition and, consequently, fetal infection [ 161 ]. Regarding CHIKV infections, several virus antigens were found in Hofbauer cells in the placentas of infected pregnant women, evidencing the permissiveness of these cells to infection [ 78 , 138 ].…”

“…In experiments with mice infected with DENV, the decidua exhibited a higher number of genes being upregulated, including caspase (2, 6, 8, and 9), IRF1, and NOS2. In the fetal placenta, there were expressions of complements, such as C4A, C6, and CFB [ 161 ].…”