scholarly journals Brain immune cells undergo cGAS/STING-dependent apoptosis during herpes simplex virus type 1 infection to limit type I IFN production

2021 ◽  
Vol 131 (1) ◽  
Author(s):  
Line S. Reinert ◽  
Ahmad S. Rashidi ◽  
Diana N. Tran ◽  
Georgios Katzilieris-Petras ◽  
Astrid K. Hvidt ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Type ◽  
Immune Cells ◽  
Herpes Simplex Virus Type ◽  
Type I ◽  
Type I Ifn ◽  
Simplex Virus

Participation of Type I Interferon in the Decreased Virulence of the UL13 Gene-Deleted Mutant of Herpes Simplex Virus Type 1

2001 ◽  
Vol 21 (5) ◽  
pp. 279-285 ◽  
Author(s):  
Taiichiro Shibaki ◽  
Tatsuo Suzutani ◽  
Itsuro Yoshida ◽  
Masahiro Ogasawara ◽  
Masanobu Azuma
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Type I Interferon ◽  
Type I ◽  
Simplex Virus

scholarly journals An N-Terminal Domain of Herpes Simplex Virus Type I gE Is Capable of Forming Stable Complexes with gI

2001 ◽  
Vol 75 (23) ◽  
pp. 11897-11901 ◽  
Author(s):  
Syed Monem Rizvi ◽  
Malini Raghavan
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Domain Boundary ◽  
Stable Complex ◽  
Type I ◽  
Terminal Domain ◽  
Simplex Virus

ABSTRACT Using limited proteolytic analyses, we show that gE present in soluble herpes simplex virus type 1 gE-gI complexes is cleaved into a C-terminal (CgE) and an N-terminal (NgE) domain. The domain boundary is in the vicinity of residue 188 of mature gE. NgE, but not CgE, forms a stable complex with soluble gI.

scholarly journals Local Immune Control of Latent Herpes Simplex Virus Type 1 in Ganglia of Mice and Man

2021 ◽  
Vol 12 ◽  
Author(s):  
Anthony J. St. Leger ◽  
David M. Koelle ◽  
Paul R. Kinchington ◽  
Georges Michel G. M. Verjans
Keyword(s):  
T Cells ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Epithelial Cells ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Type I ◽  
Simplex Virus ◽  
Hsv 1

Herpes simplex virus type 1 (HSV-1) is a prevalent human pathogen. HSV-1 genomes persist in trigeminal ganglia neuronal nuclei as chromatinized episomes, while epithelial cells are typically killed by lytic infection. Fluctuations in anti-viral responses, broadly defined, may underlay periodic reactivations. The ganglionic immune response to HSV-1 infection includes cell-intrinsic responses in neurons, innate sensing by several cell types, and the infiltration and persistence of antigen-specific T-cells. The mechanisms specifying the contrasting fates of HSV-1 in neurons and epithelial cells may include differential genome silencing and chromatinization, dictated by variation in access of immune modulating viral tegument proteins to the cell body, and protection of neurons by autophagy. Innate responses have the capacity of recruiting additional immune cells and paracrine activity on parenchymal cells, for example via chemokines and type I interferons. In both mice and humans, HSV-1-specific CD8 and CD4 T-cells are recruited to ganglia, with mechanistic studies suggesting active roles in immune surveillance and control of reactivation. In this review we focus mainly on HSV-1 and the TG, comparing and contrasting where possible observational, interventional, and in vitro studies between humans and animal hosts.

Role of herpes simplex virus type 1 (HSV-1) in the pathogenesis of peptic ulcer disease

2001 ◽  
Vol 120 (5) ◽  
pp. A136-A137
Author(s):  
K TSAMAKIDES ◽  
E PANOTOPOULOU ◽  
D DIMITROULOPOULOS ◽  
M CHRISTOPOULO ◽  
D XINOPOULOS ◽  
...  
Keyword(s):  
Peptic Ulcer ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Peptic Ulcer Disease ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Ulcer Disease ◽  
Simplex Virus
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