# SARS‐CoV‐2 Chronic Intervillositis: Variations of Maternal Antiviral Response

## TL;DR

This study explores how SARS-CoV-2 infection affects placental inflammation during pregnancy, finding a link between viral load and immune response.

## Contribution

The study reveals new insights into the placental immune response to SARS-CoV-2, highlighting the role of B lymphocytes and viral load variability.

## Key findings

- A significant association was found between SARS-CoV-2 viral load and the severity of chronic histiocytic intervillositis (CHI).
- CD20-positive B lymphocytes were present in all cases with diffuse CHI but absent in non-inflammatory cases.
- Electron microscopy detected viral particles in samples negative for PCR and CHI, suggesting ongoing inflammation despite undetectable virus.

## Abstract

Placental compromise is a determining factor in the outcome of pregnancies complicated by maternal SARS‐CoV‐2 infection. Chronic histiocytic intervillositis (CHI) is the initial response to SARS‐CoV‐2 infection, but the underlying mechanisms are poorly understood. The aim of this study was to assess the extent and composition of the placental inflammatory response and to explore the relationship between the severity of inflammation and viral levels in the placenta.

Placentas from 43 women who tested positive for SARS‐CoV‐2 infection at the time of delivery at a single tertiary medical center (8/2020 to 10/2022) were evaluated using quantitative reverse transcription polymerase chain reaction (qRT‐PCR), histopathological, ultrastructural, and in situ hybridization studies.

There was a significant association between viral load and severity of CHI with notable involvement of CD20‐positive B lymphocytes (100% in patients with diffuse CHI vs 0% in the patients with no inflammation). Both PCR‐positive and PCR‐negative placentas exhibited varying degrees of inflammation. Electron microscopy confirmed viral particles in PCR‐ and CHI‐negative samples, Additionally, mean gestational age at delivery was significantly lower in the PCR‐positive patients.

These findings highlight the complex interplay between maternal SARS‐CoV‐2 infection and placental inflammation. The inflammatory response may extend beyond the presence of the virus per se, and viral load differences linked to individual immune response variability may influence the development of inflammation. Further research is needed to elucidate the mechanisms by which SARS‐CoV‐2 impacts maternal and neonatal health outcomes and provide insight into the implications of viral infections during pregnancy.