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Review
. 2019 Aug 24;11(9):780.
doi: 10.3390/v11090780.

Pulmonary Involvement during the Ebola Virus Disease

Eleonora Lalle  1 , Mirella Biava  1 , Emanuele Nicastri  1 , Francesca Colavita  1 , Antonino Di Caro  1   2 , Francesco Vairo  1   2 , Simone Lanini  1 , Concetta Castilletti  1 , Martin Langer  3 , Alimuddin Zumla  4   5 , Gary Kobinger  6   7   8 , Maria R Capobianchi  1 , Giuseppe Ippolito  9   10
Affiliations
Review

Pulmonary Involvement during the Ebola Virus Disease

Eleonora Lalle et al. Viruses. .

Abstract

Filoviruses have become a worldwide public health concern, especially during the 2013-2016 Western Africa Ebola virus disease (EVD) outbreak-the largest outbreak, both by number of cases and geographical extension, recorded so far in medical history. EVD is associated with pathologies in several organs, including the liver, kidney, and lung. During the 2013-2016 Western Africa outbreak, Ebola virus (EBOV) was detected in the lung of infected patients suggesting a role in lung pathogenesis. However, little is known about lung pathogenesis and the controversial issue of aerosol transmission in EVD. This review highlights the pulmonary involvement in EVD, with a special focus on the new data emerging from the 2013-2016 Ebola outbreak.

Keywords: Ebola virus; Ebola virus disease; lung pathogenesis; respiratory disease.

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Conflict of interest statement

All authors have an interest in global public health and emerging and re-emerging infections. All authors have no other conflict of interest to declare.

Figures

Figure 1
Figure 1
Direct and indirect effects of viral infections of the airway epithelium. Upon entrance into the cell, viruses are recognized by the Toll-like receptor (TLR) on either cell membrane or in endosomes. TLRs activate interferon regulatory factors (IRFs) leading to IFN-α and IFN-β release via the Toll/IL-1 receptor domain-containing adaptor (TRIF). TLR3 stimulates IRF-7 and NF-κB via MyD88 activation, leading to the release of proinflammatory cytokines and the production of IFN-α, -β, and -λ, respectively. Secretion of proinflammatory cytokines and chemokines activate the immune system, through recruitment of eosinophils, neutrophils, macrophages, dendritic cells, T cells, and NK cells. Most respiratory viruses have developed strategies to escape antiviral defense, mainly by interfering with the IFN system or by affecting the epithelium barrier, with the consequence of a loss of integrity and protection. Furthermore, respiratory viruses can perturb (skewed or exaggerated) inflammatory responses and production of soluble mediators.
Figure 2
Figure 2
EBOV pulmonary disease pathogenesis. Arrows show the proposed sequence of events and inverted ‘Ts’ show the blocked mechanisms due to the consequences of viral infection.
See this image and copyright information in PMC

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