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Bernstein, D.I., Bellamy, A.R., Hook, E.W., Levin, M.J., Wald, A., Ewell, M.G., Wolff, P.A., Deal, C.D., Heineman, T.C., Dubin, G. and Belshe, R.B. (2013) Epidemiology, Clinical Presentation, and Antibody Response to Primary Infection with Herpes Simplex Virus Type 1 and Type 2 in Young Women. Clinical Infectious Diseases, 56, 344-351.
https://doi.org/10.1093/cid/cis891

has been cited by the following article:

• TITLE: Kinetics of Candida albicans and Staphylococcus aureus Biofilm Initiation on Herpes Simplex Virus (HSV-1 and HSV-2) Infected Cells

  AUTHORS: Balbina J. Plotkin, Ira M. Sigar, Amber Kaminski, Jessica Kreamer, Brent Ito, Joan Kacmar

  KEYWORDS: Polymicrobic, Microbiome, Biofilm, Adherence, Herpes Simplex Virus, Staphylococcus aureus, Candida albicans

  JOURNAL NAME: Advances in Microbiology, Vol.10 No.11, November 27, 2020

  ABSTRACT: This study examines the kinetics of S. aureus and C. albicans adherence as it relates to HSV replication and corresponding dynamic display of shared receptors. HeLa cells infected for various times with HSV-1 gL86 or HSV-2 333gJ-(MOI 50) were incubated with S. aureus ATCC 25923 or C. albicans yeast and CFU measured. Over time, S. aureus adherence to HSV-1 infected cells was relatively stable for 45 min then decreased to 0.8 of virus-free control, before cycling at 15-to-30 min intervals. In contrast, staphylococcal adherence to HSV-2 infected cells proceeded at a more gradual rate, increasing to control levels at ~105 min before decreasing to a nadir at 165 min. Yeast adherence to HSV-1 infected cells remained relatively unchanged for the first 75 min then increased 2-fold before returning to its original level. This pattern is repeated over the next 90 min. While a similar pattern with C. albicans and HSV-2 was measured, it occurred more rapidly. Our model shows that while the interaction of both HSV-1 and HSV-2 with S. aureus is both dynamic and inhibitory, C. albicans interaction with HSV-2 is more permissive than HSV-1. However, the interaction of both microbes with HSV-infected cells in this model system appears to be independent of α5B1, CD36 and HSP60 viral-regulated receptor expression. These findings indicate that microbiome interactions across taxonomic kingdoms are more complex than previously thought.