Special Issue "Filovirus: Replication, Disease Pathogenesis and Host Immune Responses"

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Viral Pathogens".

Deadline for manuscript submissions: closed (15 December 2020).

Special Issue Editor

Dr. Priya Luthra
Guest Editor
Trudeau Research Network, Viral Diseases Research and Translational Science Program Trudeau Institute, Saranac Lake, NY 12983, USA
Interests: RNA viruses; filoviruses; virus–host interactions; innate immune responses; viral pathogenesis; infectious disease

Special Issue Information

Dear Colleagues,

The members of the filovirus family, such as Ebolavirus and Marburgvirus are highly pathogenic etiological agents associated with systemic and potentially fatal diseases. The unprecedented scale of the 2013–2016 Ebola virus (EBOV) outbreak in West Africa resulted in over 28,000 confirmed cases, over 11,000 deaths, and was classified by WHO as a Public Health Emergency of International Concern [1,2]. Currently, the Democratic Republic of Congo (DRC) is experiencing their tenth EBOV outbreak, with the first reported case dating back to August 2018. The outbreak is in the northeast region of the DRC, which shares a border with Uganda and Sudan and has already accounted for over 2000 reported cases and 1500 deaths, making it the second-largest EBOV epidemic [3,4]. Similarly, Marburgviruses (MARV) has caused devastating outbreaks, albeit with lower case numbers. These situations demonstrate that these viruses are a serious threat to public health, highlighting the urgent need for effective treatments. Filovirus disease is characterized by systemic virus replication, innate immune suppression, and inflam­matory responses detrimental to the host [5,6]. Damage to host tissues and organs following infection often result in hypotension, vascular leakage, and disseminated intravascular coagulation, all contributing to the high morbidity and mortality rates associated with ebolavirus outbreaks [7]. Despite the tremendous advancement in development of vaccines and therapeutics against EBOV and MARV, a specific treatment has yet to be approved.

Major discoveries have elucidated the underlying pathogenic mechanisms of filoviruses; however, there remain unaddressed questions pertaining to the paradoxical host responses, including an insufficient understanding of how filoviruses access immune privileged sites and key host factors that contribute to virus pathogenesis. Reports on the innate immune evasion functions of interferon antagonists such as EBOV and MARV VP35, EBOV VP24, and MARV VP40 illustrate their role in disease severity [8]. However, it is still unclear how these proteins suppress cellular immunity and the role of filovirus virus–host protein interactions in host adaptive immunity and pathogenesis. It is noteworthy that recent insights into virus–host interactions, viral pathogenesis, and host immune responses are leading to both the identification and development of additional countermeasures to combat virus infection. This Special Issue is devoted to expanding upon the current body of knowledge to highlight and identify new findings in these important areas. Timely contributions in the form of original research and review articles on filovirus replication, disease pathogenesis and protection, host immune modulations, and other related hot topics are hereby solicited for consideration of publication in this Special Issue.


  1. Agua-Agum J, Allegranzi B, Ariyarajah A, Aylward RB, Blake IM, Barboza P, Bausch D, Brennan RJ, Clement P, Coffey P, Cori A, Donnelly CA, Dorigatti I, Drury P, Durski K, Dye C, Eckmanns T, Ferguson NM, Fraser C, Garcia E, Garske T, Gasasira A, Gurry C, Gutierrez GJ, Hamblion E, Hinsley W, Holden R, Holmes D, Hugonnet S, Jombart T, Kelley E, Santhana R, Mahmoud N, Mills HL, Mohamed Y, Musa E, Naidoo D, Nedjati-Gilani G, Newton E, Norton I, Nouvellet P, Perkins D, Perkins M, Riley S, Schumacher D, Shah A, Tang M, Varsaneux O, Van Kerkhove MD, Team WER. After Ebola in West Africa - Unpredictable Risks, Preventable Epidemics. New Engl J Med. 2016;375(6):587-96. doi: 10.1056/NEJMsr1513109. PubMed PMID: WOS:000382193100015.<Go to ISI>://WOS:000382193100015
  2. Labouba I, Leroy EM. Ebola outbreaks in 2014. J Clin Virol. 2015;64:109-10. Epub 2015/01/17. doi: 10.1016/j.jcv.2014.12.012. PubMed PMID: 25591390.https://www.ncbi.nlm.nih.gov/pubmed/25591390
  3. Nguyen VK. An Epidemic of Suspicion - Ebola and Violence in the DRC. N Engl J Med. 2019;380(14):1298-9. Epub 2019/03/07. doi: 10.1056/NEJMp1902682. PubMed PMID: 30840790.https://www.ncbi.nlm.nih.gov/pubmed/30840790
  4. Nsio J, Kapetshi J, Makiala S, Raymond F, Tshapenda G, Boucher N, Corbeil J, Okitandjate A, Mbuyi G, Kiyele M, Mondonge V, Kikoo MJ, Van Herp M, Barboza P, Petrucci R, Benedetti G, Formenty P, Muyembe Muzinga B, Ilunga Kalenga O, Ahuka S, Fausther-Bovendo H, Ilunga BK, Kobinger GP, Muyembe JT. 2017 Outbreak of Ebola Virus Disease in Northern Democratic Republic of Congo. J Infect Dis. 2019. Epub 2019/04/04. doi: 10.1093/infdis/jiz107. PubMed PMID: 30942884.https://www.ncbi.nlm.nih.gov/pubmed/30942884
  5. Malvy D, McElroy AK, de Clerck H, Gunther S, van Griensven J. Ebola virus disease. Lancet. 2019;393(10174):936-48. Epub 2019/02/20. doi: 10.1016/S0140-6736(18)33132-5. PubMed PMID: 30777297.https://www.ncbi.nlm.nih.gov/pubmed/30777297
  6. Rougeron V, Feldmann H, Grard G, Becker S, Leroy EM. Ebola and Marburg haemorrhagic fever. J Clin Virol. 2015;64:111-9. Epub 2015/02/11. doi: 10.1016/j.jcv.2015.01.014. PubMed PMID: 25660265.https://www.ncbi.nlm.nih.gov/pubmed/25660265
  7. Reynard S, Journeaux A, Gloaguen E, Schaeffer J, Varet H, Pietrosemoli N, Mateo M, Baillet N, Laouenan C, Raoul H, Mullaert J, Baize S. Immune parameters and outcomes during Ebola virus disease. JCI Insight. 2019;4(1). Epub 2019/01/11. doi: 10.1172/jci.insight.125106. PubMed PMID: 30626757; PMCID: PMC6485372.https://www.ncbi.nlm.nih.gov/pubmed/30626757
  8. Messaoudi I, Amarasinghe GK, Basler CF. Filovirus pathogenesis and immune evasion: insights from Ebola virus and Marburg virus. Nat Rev Microbiol. 2015;13(11):663-76. Epub 2015/10/07. doi: 10.1038/nrmicro3524. PubMed PMID: 26439085; PMCID: PMC5201123.https://www.ncbi.nlm.nih.gov/pubmed/26439085

Dr. Priya Luthra
Guest Editor

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  • Newly discovered filoviruses
  • Filovirus replication mechanisms
  • Filovirus disease pathogenesis
  • Filovirus protein–host protein interactions
  • Filovirus immune evasion
  • Immunity to filoviruses
  • Filovirus vaccine
  • Antivirals against filovirus
  • Animal models of filovirus disease

Published Papers (1 paper)

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Open AccessArticle
A Conserved Tryptophan in the Ebola Virus Matrix Protein C-Terminal Domain Is Required for Efficient Virus-Like Particle Formation
Pathogens 2020, 9(5), 402; https://doi.org/10.3390/pathogens9050402 - 22 May 2020
Cited by 1
The Ebola virus (EBOV) harbors seven genes, one of which is the matrix protein eVP40, a peripheral protein that is sufficient to induce the formation of virus-like particles from the host cell plasma membrane. eVP40 can form different structures to fulfil different functions [...] Read more.
The Ebola virus (EBOV) harbors seven genes, one of which is the matrix protein eVP40, a peripheral protein that is sufficient to induce the formation of virus-like particles from the host cell plasma membrane. eVP40 can form different structures to fulfil different functions during the viral life cycle, although the structural dynamics of eVP40 that warrant dimer, hexamer, and octamer formation are still poorly understood. eVP40 has two conserved Trp residues at positions 95 and 191. The role of Trp95 has been characterized in depth as it serves as an important residue in eVP40 oligomer formation. To gain insight into the functional role of Trp191 in eVP40, we prepared mutations of Trp191 (W191A or W191F) to determine the effects of mutation on eVP40 plasma membrane localization and budding as well as eVP40 oligomerization. These in vitro and cellular experiments were complemented by molecular dynamics simulations of the wild-type (WT) eVP40 structure versus that of W191A. Taken together, Trp is shown to be a critical amino acid at position 191 as mutation to Ala reduces the ability of VP40 to localize to the plasma membrane inner leaflet and form new virus-like particles. Further, mutation of Trp191 to Ala or Phe shifted the in vitro equilibrium to the octamer form by destabilizing Trp191 interactions with nearby residues. This study has shed new light on the importance of interdomain interactions in stability of the eVP40 structure and the critical nature of timing of eVP40 oligomerization for plasma membrane localization and viral budding. Full article
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