The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes COVID-19 and can result in preterm birth or severe disease or death in the mother. The research objective was to quantify the SARS-CoV-2 viral load in placental tissue and evaluate whether the placenta mounts an antiviral innate immune response. Furthermore, the study seeks to understand whether the timing of a COVID-19 infection during pregnancy correlates with viral load at the time of delivery and placental pathology. I, along with the two research technicians I am working closely with, hypothesize that a SARS-CoV-2 infection modulates the placental innate immune pathway in pregnant women and result in high viral loads in the context of placental pathology. The virus may amplify or dampen the innate immune response, significantly impacting viral clearance and potentially inducing substantial injury to maternal and fetal tissue. In the study, I helped extract RNA from two tissue types in the placenta, chorionic villous tissue and chorioamniotic membranes, from pregnant women with and without COVID-19 at different trimesters. I have begun to extract RNA, synthesize complementary DNA (cDNA), and perform quantitative polymerase chain reaction (qPCR) to quantify the viral load of SARS-CoV-2 per mg of tissue. In SARS-CoV-2 positive samples, I have also begun to quantify the relative gene expression of ifnb, mxa, ifit1, and il6, which will allow my team and I to evaluate the innate immune response. Our preliminary results indicate a low, but significant frequency of SARS-CoV-2 in placental tissues with rare high viral loads associated with a significant IL-6 response. I will help analyze our data through visual graphs and statistical analysis once the data is uploaded to the lab’s database. This project will not only improve our understanding of pregnancy pathologies, but also make significant strides in what is known about SARS-CoV-2’s impact on pregnancy health.