Role of the Orphan Transporter SLC35E1 in the Nuclear Egress of Herpes Simplex Virus 1

Abstract

The identification of cellular protein(s) that interact with viral effector proteins and function in important viral procedures is necessary for enhancing our understanding of the mechanics of various viral processes. In this study, we established a new system consisting of interactome screening for the herpes simplex virus 1 (HSV-1) nuclear egress complex (NEC), followed by loss-of-function screening to target the identified putative NEC-interacting cellular proteins to detect a defect in HSV-1 nuclear egress.

RNA helicase DDX3X modulates herpes simplex virus 1 nuclear egress

“…Interestingly, deletion of pU S 3 does not prevent the initial budding step but rather causes the accumulation of enveloped perinuclear virions in nuclear herniations, pointing to the dual role of the viral kinase in the nucleus and perinuclear space during viral egress 42 , 45 , 63 . The cellular p32, TorsinA, SUN2, ESCRT III components ALIX and CHMP4B, VAPB, CD98, protein kinases C and D as well as SCL35E1 have additionally been implicated in herpesviruses nuclear egress 64 – 74 . However many molecular details of this complex nuclear egress pathway remain to be clarified.…”