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Correction ARTICLE

Front. Cell. Infect. Microbiol., 08 December 2016 | https://doi.org/10.3389/fcimb.2016.00178

Corrigendum: Hemorrhagic Fever with Renal Syndrome: Pathogenesis and Clinical Picture

Hong Jiang1, Hong Du1, Li M. Wang2, Ping Z. Wang1* and Xue F. Bai1*
  • 1Center for Infectious Diseases, Tangdu Hospital, Fourth Military Medical University, Xi'an, China
  • 2Department of Microbiology, School of Basic Medicine, Fourth Military Medical University, Xi'an, China

A corrigendum on
Hemorrhagic Fever with Renal Syndrome: Pathogenesis and Clinical Picture

by Jiang, H., Du, H., Wang, L. M., Wang, P. Z., and Bai, X. F. (2016). Front. Cell. Infect. Microbiol. 6:1. doi: 10.3389/fcimb.2016.00001

Due to an oversight the authors did not cite the original source for Figures 1, 2. Figure 1 was adapted from Figure 5 of Schönrich et al. (2008). The revised figure caption should read:

Left side: Normal endothelial cells (EC), no vascular leakage occurs. Right side: EC were infected with hantaviruses. ZO-1, VEGFR2, VE-cadherin on EC were altered. High hantavirus RNA load result in severe vascular leakage. Virus-infected ECs be cleared by virus-specific CTLs leading to vascular damage. Owing to acute thrombocytopenia, there are not sufficient platelets available to repair “holes” in the EC barrier, resulting in vascular leakage. In addition, cytokines produced during the innate response against pathogenic hantaviruses like TNF-α could enhance vascular permeability. Adapted from Schönrich et al. (2008).

Figure 2 was adapted from Figure 2 of Schönrich et al. (2015). The revised figure caption should read:

Monocytes, macrophages, NK cells, and Lymphocytes produce various cytokines/chemokines which directly or indirectly increase vascular permeability. The humoral pattern recognition receptor PTX3 and antibodies activate complement. Activated complement components induce cytoskeletal rearrangement in EC further increasing dysfunction of the EC barrier. TLRs recognize Hantavirus and mediate the innate response. Virus-infected ECs were cleared by virus-specific CTLs leading to vascular leakage. B cells produce several subclass antibodies, while only the neutralizing antibodies against G1 and G2 is beneficial to decrease the viruses, then decrease vascular leakage. Adapted from Schönrich et al. (2015).

This does not affect the scientific conclusions of this article in any way. The authors apologize for this oversight.

Conflict of Interest Statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

References

Schönrich, G., Krüger, D. H., and Raftery, M. J. (2015). Hantavirus-induced disruption of the endothelial barrier: neutrophils are on the payroll. Front. Microbiol. 6:222. doi: 10.3389/fmicb.2015.00222

PubMed Abstract | CrossRef Full Text | Google Scholar

Schönrich, G., Rang, A., Lütteke, N., Raftery, M. J., Charbonnel, N., and Ulrich, R. G. (2008). Hantavirus-induced immunity in rodent reservoirs and humans. Immunol. Rev. 225, 163–189. doi: 10.1111/j.1600-065X.2008.00694.x

PubMed Abstract | CrossRef Full Text | Google Scholar

Keywords: hantavirus, hemorrhagic fever with renal syndrome, Bunyavirus, hantaan virus, pathogenesis

Citation: Jiang H, Du H, Wang LM, Wang PZ and Bai XF (2016) Corrigendum: Hemorrhagic Fever with Renal Syndrome: Pathogenesis and Clinical Picture. Front. Cell. Infect. Microbiol. 6:178. doi: 10.3389/fcimb.2016.00178

Received: 05 April 2016; Accepted: 22 November 2016;
Published: 08 December 2016.

Edited and reviewed by: Shinichiro Kurosawa, Boston University School of Medicine, USA

Copyright © 2016 Jiang, Du, Wang, Wang and Bai. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Ping Z. Wang, wangpz63@126.com
Xue F. Bai, xfbai2011@163.com