T-Cell tropism of simian varicella virus during primary infection.
Varicella-zoster virus (VZV) causes varicella, establishes a life-long latent infection of ganglia and reactivates to cause herpes zoster. The cell types that transport VZV from the respiratory tract to skin and ganglia during primary infection are unknown. Clinical, pathological, virological and im...
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2013
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oai:doaj.org-article:9ef5e8b8b3264166ab28287ee248d2c42021-11-18T06:05:39ZT-Cell tropism of simian varicella virus during primary infection.1553-73661553-737410.1371/journal.ppat.1003368https://doaj.org/article/9ef5e8b8b3264166ab28287ee248d2c42013-05-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23675304/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Varicella-zoster virus (VZV) causes varicella, establishes a life-long latent infection of ganglia and reactivates to cause herpes zoster. The cell types that transport VZV from the respiratory tract to skin and ganglia during primary infection are unknown. Clinical, pathological, virological and immunological features of simian varicella virus (SVV) infection of non-human primates parallel those of primary VZV infection in humans. To identify the host cell types involved in virus dissemination and pathology, we infected African green monkeys intratracheally with recombinant SVV expressing enhanced green fluorescent protein (SVV-EGFP) and with wild-type SVV (SVV-wt) as a control. The SVV-infected cell types and virus kinetics were determined by flow cytometry and immunohistochemistry, and virus culture and SVV-specific real-time PCR, respectively. All monkeys developed fever and skin rash. Except for pneumonitis, pathology produced by SVV-EGFP was less compared to SVV-wt. In lungs, SVV infected alveolar myeloid cells and T-cells. During viremia the virus preferentially infected memory T-cells, initially central memory T-cells and subsequently effector memory T-cells. In early non-vesicular stages of varicella, SVV was seen mainly in perivascular skin infiltrates composed of macrophages, dendritic cells, dendrocytes and memory T-cells, implicating hematogenous spread. In ganglia, SVV was found primarily in neurons and occasionally in memory T-cells adjacent to neurons. In conclusion, the data suggest the role of memory T-cells in disseminating SVV to its target organs during primary infection of its natural and immunocompetent host.Werner J D OuwendijkRavi MahalingamRik L de SwartBart L HaagmansGeert van AmerongenSarah GetuDon GildenAlbert D M E OsterhausGeorges M G M VerjansPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 9, Iss 5, p e1003368 (2013) |
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Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 |
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Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 Werner J D Ouwendijk Ravi Mahalingam Rik L de Swart Bart L Haagmans Geert van Amerongen Sarah Getu Don Gilden Albert D M E Osterhaus Georges M G M Verjans T-Cell tropism of simian varicella virus during primary infection. |
description |
Varicella-zoster virus (VZV) causes varicella, establishes a life-long latent infection of ganglia and reactivates to cause herpes zoster. The cell types that transport VZV from the respiratory tract to skin and ganglia during primary infection are unknown. Clinical, pathological, virological and immunological features of simian varicella virus (SVV) infection of non-human primates parallel those of primary VZV infection in humans. To identify the host cell types involved in virus dissemination and pathology, we infected African green monkeys intratracheally with recombinant SVV expressing enhanced green fluorescent protein (SVV-EGFP) and with wild-type SVV (SVV-wt) as a control. The SVV-infected cell types and virus kinetics were determined by flow cytometry and immunohistochemistry, and virus culture and SVV-specific real-time PCR, respectively. All monkeys developed fever and skin rash. Except for pneumonitis, pathology produced by SVV-EGFP was less compared to SVV-wt. In lungs, SVV infected alveolar myeloid cells and T-cells. During viremia the virus preferentially infected memory T-cells, initially central memory T-cells and subsequently effector memory T-cells. In early non-vesicular stages of varicella, SVV was seen mainly in perivascular skin infiltrates composed of macrophages, dendritic cells, dendrocytes and memory T-cells, implicating hematogenous spread. In ganglia, SVV was found primarily in neurons and occasionally in memory T-cells adjacent to neurons. In conclusion, the data suggest the role of memory T-cells in disseminating SVV to its target organs during primary infection of its natural and immunocompetent host. |
format |
article |
author |
Werner J D Ouwendijk Ravi Mahalingam Rik L de Swart Bart L Haagmans Geert van Amerongen Sarah Getu Don Gilden Albert D M E Osterhaus Georges M G M Verjans |
author_facet |
Werner J D Ouwendijk Ravi Mahalingam Rik L de Swart Bart L Haagmans Geert van Amerongen Sarah Getu Don Gilden Albert D M E Osterhaus Georges M G M Verjans |
author_sort |
Werner J D Ouwendijk |
title |
T-Cell tropism of simian varicella virus during primary infection. |
title_short |
T-Cell tropism of simian varicella virus during primary infection. |
title_full |
T-Cell tropism of simian varicella virus during primary infection. |
title_fullStr |
T-Cell tropism of simian varicella virus during primary infection. |
title_full_unstemmed |
T-Cell tropism of simian varicella virus during primary infection. |
title_sort |
t-cell tropism of simian varicella virus during primary infection. |
publisher |
Public Library of Science (PLoS) |
publishDate |
2013 |
url |
https://doaj.org/article/9ef5e8b8b3264166ab28287ee248d2c4 |
work_keys_str_mv |
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