Antiviral Effects of Menthol on Coxsackievirus B
by
David J.R. Taylor 1,†, Syed M. Hamid 1,†, Allen M. Andres 1,†, Hannaneh Saadaeijahromi 1, Honit Piplani 1, Juliana F. Germano 1, Yang Song 1, Savannah Sawaged 1
, Ralph Feuer 2, Stephen J. Pandol 3 and Jon Sin 1,*
David J.R. Taylor 1,†, Syed M. Hamid 1,†, Allen M. Andres 1,†, Hannaneh Saadaeijahromi 1, Honit Piplani 1, Juliana F. Germano 1, Yang Song 1, Savannah Sawaged 1, Ralph Feuer 2, Stephen J. Pandol 3 and Jon Sin 1,*
1
The Smidt Heart Institute and the Barbra Streisand Women’s Heart Center, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA
2
The Integrated Regenerative Research Institute (IRRI) at San Diego State University, San Diego State University, San Diego, CA 92182, USA
3
Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA
*
Author to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Viruses 2020, 12(4), 373; https://doi.org/10.3390/v12040373
Received: 16 March 2020 / Revised: 24 March 2020 / Accepted: 25 March 2020 / Published: 28 March 2020
(This article belongs to the Section Animal Viruses)
Coxsackievirus B (CVB) is a common human enterovirus that causes systemic infection but specifically replicates to high titers in the pancreas. It was reported that certain viruses induce mitochondrial fission to support infection. We documented that CVB triggers mitochondrial fission and blocking mitochondrial fission limits infection. The transient receptor potential channels have been implicated in regulating mitochondrial dynamics; namely, the heat and capsaicin receptor transient receptor potential cation channel subfamily V member 1 (TRPV1) contributes to mitochondrial depolarization and fission. When we transiently warmed HeLa cells to 39 °C prior to CVB exposure, infection was heightened, whereas cooling cells to 25 °C reduced infection. Inducing “cold” by stimulating transient receptor potential cation channel subfamily M member 8 (TRPM8) with menthol led to reduced infection and also resulted in lower levels of mitochondrial fission during infection. Additionally, menthol stabilized levels of mitochondrial antiviral signaling (MAVS) which is known to be tied to mitochondrial dynamics. Taken together, this highlights a novel pathway wherein CVB relies on TRPV1 to initiate proviral mitochondrial fission, which may contribute to the disruption of antiviral immunity. TRPM8 has been shown to antagonize TRPV1, and thus we hypothesize that stimulating TRPM8 blocks TRPV1-mediated mitochondrial fragmentation following CVB exposure and attenuates infection.
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Keywords:
mitochondria; coxsackievirus; antiviral; pancreas; menthol
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MDPI and ACS Style
Taylor, D.J.; Hamid, S.M.; Andres, A.M.; Saadaeijahromi, H.; Piplani, H.; Germano, J.F.; Song, Y.; Sawaged, S.; Feuer, R.; Pandol, S.J.; Sin, J. Antiviral Effects of Menthol on Coxsackievirus B. Viruses 2020, 12, 373.
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