An Investigation of Teratogenic Viruses: Analyzing the Implications of Congenital Infections on Viral Transmission Dynamics

Abstract

Teratogenic viruses, viruses which have the capability to infect a fetus congenitally, persist as a prevalent health threat globally. Since their first documentation, researchers and physicians alike have sought to uncover the molecular mechanisms of pathology and understand a virus can develop the traits necessary to cross the physical and immunologic barrier of the maternal-fetal interface and produce profound congenital defects. Although more is being discovered in regard to the mechanisms of teratogenic infections, the potential contribution that teratogenic viruses can make to the overall transmission dynamics of a virus has remained poorly studied. This has left an entire subset of potentially meaningful additions to overall disease dynamics unacknowledged in epidemiology and global health practices. Here, we hypothesized that teratogenic effects do have an impact on the transmission dynamics of a virus. In this study we explore rubella, a well-known teratogenic virus, which results in Congenital Rubella Syndrome (CRS) when a fetus is infected in utero. Using Susceptible- Exposed-Infectious- Recovered (SEIR) mathematical modeling, with viral parameters obtained through a systematic literature review, we explored teratogenic rubella at different transmission rates and observe if teratogenic infections are able to induce direct infections and propagate the spread and persistence of a virus in a population in a significant manner. We analyzed the viral transmission dynamics using statistical methods from results produced by the model. We observed that teratogenic infections from rubella were able to serve as meaningful constituents of the overall disease persistence in a population, verifying that teratogenic infections have the capability to effect transmission dynamics. Further, we observed that higher teratogenic transmission rates had progressively stronger performance in terms of disease persistence and spread, suggesting that there is likely evolutionary selection for teratogenic viruses at higher beta values, but likely only to a certain capacity. Holistically our study establishes that teratogenic infections contribute meaningfully to viral spread and persistence and act a reservoir for novel infections in a population. Further, this research provides critical insight into the selection of teratogenic effects evolutionarily for a virus, as well as the transmission rates that teratogenic rubella likely needs to adopt to favor this selection.