Abstract
Purpose of Review
Neonatal infection by herpes simplex virus (HSV) 1 or 2 presents a devastating burden to new parents due to the unpredictability of severe clinical outcomes as well as the potential for lifelong viral reactivation. While just under half of neonatal HSV infections have mild clinical impacts akin to the skin lesions observed in adults, the other half of these infants experience viral spread throughout the body (disseminated infection) and/or the brain (central nervous system infection).
Summary
Here we summarize current data on clinical diagnostic measures, antiviral therapy, and known aspects of human host biology that contribute to the distinct neonatal outcomes of HSV infection.
Recent Findings
We then explore recent new data on how viral genetic diversity between infections may impact clinical outcomes. Further research will be critical to build upon these early findings and to provide statistical power to our ability to discern and/or predict the potential clinical course of a given neonatal infection.
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Acknowledgments
We thank the members of the Szpara and Weitzman labs for helpful discussions.
Funding
This research was supported by NIAID grant 1R21AI140443 (MLS) and NINDS grant 1K08NS109332 (LNA), with additional support from the following: startup funds from the Pennsylvania State University (MLS) and a CURE grant from the Pennsylvania (PA) Department of Health (MLS). The PA Department of Health specifically disclaims responsibility for any analyses, interpretations, or conclusions.
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Akhtar, L.N., Szpara, M.L. Viral Genetic Diversity and Its Potential Contributions to the Development and Progression of Neonatal Herpes Simplex Virus (HSV) Disease. Curr Clin Micro Rpt 6, 249–256 (2019). https://doi.org/10.1007/s40588-019-00131-6
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DOI: https://doi.org/10.1007/s40588-019-00131-6