A systemic macrophage response is required to contain a peripheral poxvirus infection.

The goal of the innate immune system is to reduce pathogen spread prior to the initiation of an effective adaptive immune response. Following an infection at a peripheral site, virus typically drains through the lymph to the lymph node prior to entering the blood stream and being systemically dissem...

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Main Authors: Michael L Davies, Nikhil J Parekh, Lauren W Kaminsky, Chetna Soni, Irene E Reider, Tracy E Krouse, Matthew A Fischer, Nico van Rooijen, Ziaur S M Rahman, Christopher C Norbury
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2017-06-01
Series:PLoS Pathogens
Online Access:https://doi.org/10.1371/journal.ppat.1006435
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author Michael L Davies
Nikhil J Parekh
Lauren W Kaminsky
Chetna Soni
Irene E Reider
Tracy E Krouse
Matthew A Fischer
Nico van Rooijen
Ziaur S M Rahman
Christopher C Norbury
author_facet Michael L Davies
Nikhil J Parekh
Lauren W Kaminsky
Chetna Soni
Irene E Reider
Tracy E Krouse
Matthew A Fischer
Nico van Rooijen
Ziaur S M Rahman
Christopher C Norbury
author_sort Michael L Davies
collection DOAJ
description The goal of the innate immune system is to reduce pathogen spread prior to the initiation of an effective adaptive immune response. Following an infection at a peripheral site, virus typically drains through the lymph to the lymph node prior to entering the blood stream and being systemically disseminated. Therefore, there are three distinct spatial checkpoints at which intervention to prevent systemic spread of virus can occur, namely: 1) the site of infection, 2) the draining lymph node via filtration of lymph or 3) the systemic level via organs that filter the blood. We have previously shown that systemic depletion of phagocytic cells allows viral spread after dermal infection with Vaccinia virus (VACV), which infects naturally through the skin. Here we use multiple depletion methodologies to define both the spatial checkpoint and the identity of the cells that prevent systemic spread of VACV. Subcapsular sinus macrophages of the draining lymph node have been implicated as critical effectors in clearance of lymph borne viruses following peripheral infection. We find that monocyte populations recruited to the site of VACV infection play a critical role in control of local pathogenesis and tissue damage, but do not prevent dissemination of virus. Following infection with virulent VACV, the subcapsular sinus macrophages within the draining lymph node become infected, but are not exclusively required to prevent systemic spread. Rather, small doses of VACV enter the bloodstream and the function of systemic macrophages, but not dendritic cells, is required to prevent further spread. The results illustrate that a systemic innate response to a peripheral virus infection may be required to prevent widespread infection and pathology following infection with virulent viruses, such as poxviruses.
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spelling doaj-art-60c93d387d494fe385adcd013861985c2025-08-20T02:22:06ZengPublic Library of Science (PLoS)PLoS Pathogens1553-73661553-73742017-06-01136e100643510.1371/journal.ppat.1006435A systemic macrophage response is required to contain a peripheral poxvirus infection.Michael L DaviesNikhil J ParekhLauren W KaminskyChetna SoniIrene E ReiderTracy E KrouseMatthew A FischerNico van RooijenZiaur S M RahmanChristopher C NorburyThe goal of the innate immune system is to reduce pathogen spread prior to the initiation of an effective adaptive immune response. Following an infection at a peripheral site, virus typically drains through the lymph to the lymph node prior to entering the blood stream and being systemically disseminated. Therefore, there are three distinct spatial checkpoints at which intervention to prevent systemic spread of virus can occur, namely: 1) the site of infection, 2) the draining lymph node via filtration of lymph or 3) the systemic level via organs that filter the blood. We have previously shown that systemic depletion of phagocytic cells allows viral spread after dermal infection with Vaccinia virus (VACV), which infects naturally through the skin. Here we use multiple depletion methodologies to define both the spatial checkpoint and the identity of the cells that prevent systemic spread of VACV. Subcapsular sinus macrophages of the draining lymph node have been implicated as critical effectors in clearance of lymph borne viruses following peripheral infection. We find that monocyte populations recruited to the site of VACV infection play a critical role in control of local pathogenesis and tissue damage, but do not prevent dissemination of virus. Following infection with virulent VACV, the subcapsular sinus macrophages within the draining lymph node become infected, but are not exclusively required to prevent systemic spread. Rather, small doses of VACV enter the bloodstream and the function of systemic macrophages, but not dendritic cells, is required to prevent further spread. The results illustrate that a systemic innate response to a peripheral virus infection may be required to prevent widespread infection and pathology following infection with virulent viruses, such as poxviruses.https://doi.org/10.1371/journal.ppat.1006435
spellingShingle Michael L Davies
Nikhil J Parekh
Lauren W Kaminsky
Chetna Soni
Irene E Reider
Tracy E Krouse
Matthew A Fischer
Nico van Rooijen
Ziaur S M Rahman
Christopher C Norbury
A systemic macrophage response is required to contain a peripheral poxvirus infection.
PLoS Pathogens
title A systemic macrophage response is required to contain a peripheral poxvirus infection.
title_full A systemic macrophage response is required to contain a peripheral poxvirus infection.
title_fullStr A systemic macrophage response is required to contain a peripheral poxvirus infection.
title_full_unstemmed A systemic macrophage response is required to contain a peripheral poxvirus infection.
title_short A systemic macrophage response is required to contain a peripheral poxvirus infection.
title_sort systemic macrophage response is required to contain a peripheral poxvirus infection
url https://doi.org/10.1371/journal.ppat.1006435
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