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Circadian clock proteins BMAL1 and CLOCK may control herpes virus entry into nerve cells by affecting NECTIN-1
Updated
Abstract
Essence
and may regulate HSV-1 nerve-cell entry by rhythmically increasing the receptor.
Evidence
Mouse brain transcriptomics, serum-shocked cell infection assays, overexpression, luciferase reporter assays, ChIP, and CLOCK inhibition showed rhythmic NECTIN-1 expression, HSV-1 DNA variation near NECTIN-1 timing, BMAL1/CLOCK promoter binding, and CLK8 suppression of infection.
Caveat
The antiviral implication is based on mouse tissue analyses and cell models, with no clinical test of circadian timing or BMAL1/CLOCK-targeted HSV-1 therapy.
Simplified
Key numbers
2.5×
Increase in Expression
Overexpression of in SH-SY5Y cells.
50%
Reduction in Infection
Inhibition rate observed in viral plaque assays with treatment.