PMID- 27440876
OWN - NLM
STAT- MEDLINE
DCOM- 20170509
LR  - 20181113
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Print)
IS  - 0022-538X (Linking)
VI  - 90
IP  - 19
DP  - 2016 Oct 1
TI  - Herpes Simplex Virus 1 Interaction with Myeloid Cells In Vivo.
PG  - 8661-72
LID - 10.1128/JVI.00881-16 [doi]
AB  - Herpes simplex virus 1 (HSV-1) enters mice via olfactory epithelial cells and 
      then colonizes the trigeminal ganglia (TG). Most TG nerve endings are 
      subepithelial, so this colonization implies subepithelial viral spread, where 
      myeloid cells provide an important line of defense. The outcome of infection of 
      myeloid cells by HSV-1 in vitro depends on their differentiation state; the 
      outcome in vivo is unknown. Epithelial HSV-1 commonly infected myeloid cells, and 
      Cre-Lox virus marking showed nose and lung infections passing through 
      LysM-positive (LysM(+)) and CD11c(+) cells. In contrast, subcapsular sinus 
      macrophages (SSMs) exposed to lymph-borne HSV-1 were permissive only when type I 
      interferon (IFN-I) signaling was blocked; normally, their infection was 
      suppressed. Thus, the outcome of myeloid cell infection helped to determine the 
      HSV-1 distribution: subepithelial myeloid cells provided a route of spread from 
      the olfactory epithelium to TG neurons, while SSMs blocked systemic spread. 
      IMPORTANCE: Herpes simplex virus 1 (HSV-1) infects most people and can cause 
      severe disease. This reflects its persistence in nerve cells that connect to the 
      mouth, nose, eye, and face. Established infection seems impossible to clear. 
      Therefore, we must understand how it starts. This is difficult in humans, but 
      mice show HSV-1 entry via the nose and then spread to its preferred nerve cells. 
      We show that this spread proceeds in part via myeloid cells, which normally 
      function in host defense. Myeloid infection was productive in some settings but 
      was efficiently suppressed by interferon in others. Therefore, interferon acting 
      on myeloid cells can stop HSV-1 spread, and enhancing this defense offers a way 
      to improve infection control.
CI  - Copyright (c) 2016, American Society for Microbiology. All Rights Reserved.
FAU - Shivkumar, Maitreyi
AU  - Shivkumar M
AD  - Division of Virology, Department of Pathology, University of Cambridge, 
      Cambridge, United Kingdom.
FAU - Lawler, Clara
AU  - Lawler C
AD  - School of Chemistry and Molecular Biosciences, University of Queensland and Royal 
      Children's Hospital, Brisbane, Australia.
FAU - Milho, Ricardo
AU  - Milho R
AD  - Division of Virology, Department of Pathology, University of Cambridge, 
      Cambridge, United Kingdom.
FAU - Stevenson, Philip G
AU  - Stevenson PG
AUID- ORCID: 0000-0002-3520-5060
AD  - Division of Virology, Department of Pathology, University of Cambridge, 
      Cambridge, United Kingdom School of Chemistry and Molecular Biosciences, 
      University of Queensland and Royal Children's Hospital, Brisbane, Australia 
      p.stevenson@uq.edu.au.
LA  - eng
GR  - BB/J014419/1/Biotechnology and Biological Sciences Research Council/United 
      Kingdom
GR  - Medical Research Council/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160912
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Herpesvirus 1, Human/*physiology
MH  - Mice, Inbred C57BL
MH  - Myeloid Cells/*virology
MH  - *Viral Tropism
PMC - PMC5021410
EDAT- 2016/07/22 06:00
MHDA- 2017/05/10 06:00
PMCR- 2017/03/12
CRDT- 2016/07/22 06:00
PHST- 2016/05/05 00:00 [received]
PHST- 2016/07/13 00:00 [accepted]
PHST- 2016/07/22 06:00 [entrez]
PHST- 2016/07/22 06:00 [pubmed]
PHST- 2017/05/10 06:00 [medline]
PHST- 2017/03/12 00:00 [pmc-release]
AID - JVI.00881-16 [pii]
AID - 00881-16 [pii]
AID - 10.1128/JVI.00881-16 [doi]
PST - epublish
SO  - J Virol. 2016 Sep 12;90(19):8661-72. doi: 10.1128/JVI.00881-16. Print 2016 Oct 1.