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Viruses
Special Issues
Viruses and Complement
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Viruses and Complement

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Viral Immunology, Vaccines, and Antivirals".

Deadline for manuscript submissions: closed (19 March 2021) | Viewed by 21949

Special Issue Editors

Prof. Dr. Reinhard Würzner

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Guest Editor
Department of Hygiene, Microbiology and Social Medicine, Medical University Innsbruck, A-6020 Innsbruck, Austria
Interests: Complement: activation, inhibition, terminal pathway, deficiencies, polymorphisms, monoclonal antibodies; Candida albicans: 'molecular mimicry', integrin-analogue, complement receptors, adhesion, secreted aspartic proteases, complement evasion; EHEC: virulence factors, influence of complement, HUS
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Peter Lachmann

E-Mail Website
Guest Editor
Department of Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge CB3 0ES, UK
Interests: The study of the complement system; microbial immunology and vaccines; and immunopathology particularly of systemic LE and insect sting allergy

Special Issue Information

Dear colleagues,

There are two major topics to be considered in this special issue: on the one hand the role that complement may play in providing immunity to viruses and, on the other, the role it may play in the pathogenesis of viral disease.

It is generally considered from the study of complement deficiencies that complement plays no major part in resistance to viruses. It is therefore surprising how many viruses express proteins that inhibit complement and understanding the role of these factors is of interest.

The role of complement in pathogenesis is well established. The canonical example is Dengue where a second infection by a different serotype can give rise to dengue haemorrhagic fever which is due to a greatly enhanced infection produced by non-neutralising antibody giving rise to the release of large amounts of virus which form immune complexes give massive complement activation. There are other diseases where similar mechanisms may play a part.

It is during the present pandemic of Covid 19 a topic of great interest to understand the role of complement in  the severe forms of this disease. A very unusual finding has been reported (Gao et al. 2020) that the nucleoprotein of the virus can bind MASP-2 of the lectin pathway. Further mostly reviews on the interaction of SARS-CoV2 and complement have been published. Preliminary results of anti-complement therapy clinical trial (https://clinicaltrials.gov/ct2/show/NCT04288713) suggests that complement may indeed play a significant role in this disease.

This special issue is dealing with the interaction of several viruses and complement, the role of the latter in pathogenesis, possibly leading to prevention of disease, including aspects of complement evasion mechanisms.

In a follow-up, when all manuscripts have been accepted, a description and appreciation of all the contributions will be added here.

Prof. Dr. Reinhard Würzner
Prof. Dr. Sir Peter Lachmann Ϯ
(Ϯ Peter Lachmann 23.12.31-25.12.20 – a personal tribute to an inspiring mentor, same issue)
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Viruses is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

Role of Complement in virus infection:
  • Evidence from Complement deficiencies
  • Virus synthesis of complement inhibitors
  • Lysis of retroviral virions
  • Role of Complement in ADE
  • C5a in recruiting neutrophils
Role of Complement in viral pathogenesis:
  • Dengue
  • SARS-CoV-2
  • Influenza
  • Ebola
  • Cytomegalovirus & Epstein–Barr virus
  • West Nile virus & Zika & Chikungunya
  • Poxvirus
  • HIV

Related Special Issue

Published Papers (7 papers)

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Editorial

Jump to: Research, Review

3 pages, 589 KiB  
Editorial
A Personal Tribute to a Highly Inspiring Mentor, Professor Sir Peter J. Lachmann, 1931–2020
by Reinhard Würzner
Viruses 2021, 13(2), 206; https://0-doi-org.brum.beds.ac.uk/10.3390/v13020206 - 29 Jan 2021
Cited by 1 | Viewed by 1168
Abstract
With great sadness and sympathy for his family, especially for his wife and companion for many decades, Sylvia, I convey the news of the peaceful passing of Professor Sir Peter Lachmann on 26 December 2020, three days after his 89th birthday and after [...] Read more.
With great sadness and sympathy for his family, especially for his wife and companion for many decades, Sylvia, I convey the news of the peaceful passing of Professor Sir Peter Lachmann on 26 December 2020, three days after his 89th birthday and after a Christmas celebration—as far as this was possible these days—in the heart of his family [...] Full article
(This article belongs to the Special Issue Viruses and Complement)

Research

Jump to: Editorial, Review

10 pages, 1500 KiB  
Article
Soliris to Stop Immune-Mediated Death in COVID-19 (SOLID-C19)—A Compassionate-Use Study of Terminal Complement Blockade in Critically Ill Patients with COVID-19-Related Adult Respiratory Distress Syndrome
by Thomas C. Pitts
Viruses 2021, 13(12), 2429; https://0-doi-org.brum.beds.ac.uk/10.3390/v13122429 - 03 Dec 2021
Cited by 10 | Viewed by 2556
Abstract
Eculizumab, a terminal complement (C5)-inhibiting monoclonal antibody, was administered in five mechanically ventilated patients in life-threatening condition due to COVID-19-related acute respiratory distress syndrome (ARDS) between 23 March 2020 and 3 April 2020. Their clinical progress was monitored. The primary endpoint was mortality. [...] Read more.
Eculizumab, a terminal complement (C5)-inhibiting monoclonal antibody, was administered in five mechanically ventilated patients in life-threatening condition due to COVID-19-related acute respiratory distress syndrome (ARDS) between 23 March 2020 and 3 April 2020. Their clinical progress was monitored. The primary endpoint was mortality. One patient was excluded while two passed away. The remaining two patients survived. At the time of this study, the mortality rate in mechanically ventilated COVID-19 patients suffering from ARDS receiving the standard of care as their therapeutic regimen was reportedly as high as 97%. This pilot study demonstrates a 50% mortality rate in patients receiving eculizumab therapy. Full article
(This article belongs to the Special Issue Viruses and Complement)
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15 pages, 1439 KiB  
Article
Systemic Inflammation and Complement Activation Parameters Predict Clinical Outcome of Severe SARS-CoV-2 Infections
by Silke Huber, Mariam Massri, Marco Grasse, Verena Fleischer, Sára Kellnerová, Verena Harpf, Ludwig Knabl, Ludwig Knabl, Sr., Tatjana Heiner, Moritz Kummann, Magdalena Neurauter, Günter Rambach, Cornelia Speth and Reinhard Würzner
Viruses 2021, 13(12), 2376; https://0-doi-org.brum.beds.ac.uk/10.3390/v13122376 - 26 Nov 2021
Cited by 17 | Viewed by 1951
Abstract
Overactivation of the complement system has been characterized in severe COVID-19 cases. Complement components are known to trigger NETosis via the coagulation cascade and have also been reported in human tracheobronchial epithelial cells. In this longitudinal study, we investigated systemic and local complement [...] Read more.
Overactivation of the complement system has been characterized in severe COVID-19 cases. Complement components are known to trigger NETosis via the coagulation cascade and have also been reported in human tracheobronchial epithelial cells. In this longitudinal study, we investigated systemic and local complement activation and NETosis in COVID-19 patients that underwent mechanical ventilation. Results confirmed significantly higher baseline levels of serum C5a (24.5 ± 39.0 ng/mL) and TCC (11.03 ± 8.52 µg/mL) in patients compared to healthy controls (p < 0.01 and p < 0.0001, respectively). Furthermore, systemic NETosis was significantly augmented in patients (5.87 (±3.71) × 106 neutrophils/mL) compared to healthy controls (0.82 (±0.74) × 106 neutrophils/mL) (p < 0.0001). In tracheal fluid, baseline TCC levels but not C5a and NETosis, were significantly higher in patients. Kinetic studies of systemic complement activation revealed markedly higher levels of TCC and CRP in nonsurvivors compared to survivors. In contrast, kinetic studies showed decreased local NETosis in tracheal fluid but comparable local complement activation in nonsurvivors compared to survivors. Systemic TCC and NETosis were significantly correlated with inflammation and coagulation markers. We propose that a ratio comprising systemic inflammation, complement activation, and chest X-ray score could be rendered as a predictive parameter of patient outcome in severe SARS-CoV-2 infections. Full article
(This article belongs to the Special Issue Viruses and Complement)
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12 pages, 519 KiB  
Article
Incorporation of CD55 into the Zika Viral Envelope Contributes to Its Stability against Human Complement
by Zahra Malekshahi, Sarah Bernklau, Britta Schiela, Iris Koske, Zoltan Banki, Karin Stiasny, Claire L. Harris, Reinhard Würzner and Heribert Stoiber
Viruses 2021, 13(3), 510; https://0-doi-org.brum.beds.ac.uk/10.3390/v13030510 - 19 Mar 2021
Cited by 3 | Viewed by 2008
Abstract
The rapid spread of the virus in Latin America and the association of the infection with microcephaly in newborns or Guillain–Barré Syndrome in adults prompted the WHO to declare the Zika virus (ZIKV) epidemic to be an international public health emergency in 2016. [...] Read more.
The rapid spread of the virus in Latin America and the association of the infection with microcephaly in newborns or Guillain–Barré Syndrome in adults prompted the WHO to declare the Zika virus (ZIKV) epidemic to be an international public health emergency in 2016. As the virus was first discovered in monkeys and is spread not only by mosquitos but also from human to human, we investigated the stability to the human complement of ZIKV derived from mosquito (ZIKVInsect), monkey (ZIKVVero), or human cells (ZIKVA549 and ZIKVFibro), respectively. At a low serum concentration (10%), which refers to complement concentrations found on mucosal surfaces, the virus was relatively stable at 37 °C. At higher complement levels (up to 50% serum concentration), ZIKV titers differed significantly depending on the cell line used for the propagation of the virus. While the viral titer of ZIKVInsect decreased about two orders in magnitude, when incubated with human serum, the virus derived from human cells was more resistant to complement-mediated lysis (CML). By virus-capture assay and Western blots, the complement regulator protein CD55 was identified to be incorporated into the viral envelope. Blocking of CD55 by neutralizing Abs significantly increased the sensitivity to human complement. Taken together, these data indicate that the incorporation of CD55 from human cells contributes to the stability of ZIKV against complement-mediated virolysis. Full article
(This article belongs to the Special Issue Viruses and Complement)
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Review

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15 pages, 2339 KiB  
Review
Dengue and the Lectin Pathway of the Complement System
by Romchat Kraivong, Nuntaya Punyadee, M. Kathryn Liszewski, John P. Atkinson and Panisadee Avirutnan
Viruses 2021, 13(7), 1219; https://0-doi-org.brum.beds.ac.uk/10.3390/v13071219 - 24 Jun 2021
Cited by 7 | Viewed by 5060
Abstract
Dengue is a mosquito-borne viral disease causing significant health and economic burdens globally. The dengue virus (DENV) comprises four serotypes (DENV1-4). Usually, the primary infection is asymptomatic or causes mild dengue fever (DF), while secondary infections with a different serotype increase the risk [...] Read more.
Dengue is a mosquito-borne viral disease causing significant health and economic burdens globally. The dengue virus (DENV) comprises four serotypes (DENV1-4). Usually, the primary infection is asymptomatic or causes mild dengue fever (DF), while secondary infections with a different serotype increase the risk of severe dengue disease (dengue hemorrhagic fever, DHF). Complement system activation induces inflammation and tissue injury, contributing to disease pathogenesis. However, in asymptomatic or primary infections, protective immunity largely results from the complement system’s lectin pathway (LP), which is activated through foreign glycan recognition. Differences in N-glycans displayed on the DENV envelope membrane influence the lectin pattern recognition receptor (PRR) binding efficiency. The important PRR, mannan binding lectin (MBL), mediates DENV neutralization through (1) a complement activation-independent mechanism via direct MBL glycan recognition, thereby inhibiting DENV attachment to host target cells, or (2) a complement activation-dependent mechanism following the attachment of complement opsonins C3b and C4b to virion surfaces. The serum concentrations of lectin PRRs and their polymorphisms influence these LP activities. Conversely, to escape the LP attack and enhance the infectivity, DENV utilizes the secreted form of nonstructural protein 1 (sNS1) to counteract the MBL effects, thereby increasing viral survival and dissemination. Full article
(This article belongs to the Special Issue Viruses and Complement)
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29 pages, 4784 KiB  
Review
Complement Proteins as Soluble Pattern Recognition Receptors for Pathogenic Viruses
by Valarmathy Murugaiah, Praveen M. Varghese, Nazar Beirag, Syreeta De Cordova, Robert B. Sim and Uday Kishore
Viruses 2021, 13(5), 824; https://0-doi-org.brum.beds.ac.uk/10.3390/v13050824 - 02 May 2021
Cited by 10 | Viewed by 4688
Abstract
The complement system represents a crucial part of innate immunity. It contains a diverse range of soluble activators, membrane-bound receptors, and regulators. Its principal function is to eliminate pathogens via activation of three distinct pathways: classical, alternative, and lectin. In the case of [...] Read more.
The complement system represents a crucial part of innate immunity. It contains a diverse range of soluble activators, membrane-bound receptors, and regulators. Its principal function is to eliminate pathogens via activation of three distinct pathways: classical, alternative, and lectin. In the case of viruses, the complement activation results in effector functions such as virion opsonisation by complement components, phagocytosis induction, virolysis by the membrane attack complex, and promotion of immune responses through anaphylatoxins and chemotactic factors. Recent studies have shown that the addition of individual complement components can neutralise viruses without requiring the activation of the complement cascade. While the complement-mediated effector functions can neutralise a diverse range of viruses, numerous viruses have evolved mechanisms to subvert complement recognition/activation by encoding several proteins that inhibit the complement system, contributing to viral survival and pathogenesis. This review focuses on these complement-dependent and -independent interactions of complement components (especially C1q, C4b-binding protein, properdin, factor H, Mannose-binding lectin, and Ficolins) with several viruses and their consequences. Full article
(This article belongs to the Special Issue Viruses and Complement)
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22 pages, 2088 KiB  
Review
Virus-Encoded Complement Regulators: Current Status
by Anwesha Sinha, Anup Kumar Singh, Trupti Satish Kadni, Jayati Mullick and Arvind Sahu
Viruses 2021, 13(2), 208; https://0-doi-org.brum.beds.ac.uk/10.3390/v13020208 - 29 Jan 2021
Cited by 7 | Viewed by 3638
Abstract
Viruses require a host for replication and survival and hence are subjected to host immunological pressures. The complement system, a crucial first response of the host immune system, is effective in targeting viruses and virus-infected cells, and boosting the antiviral innate and acquired [...] Read more.
Viruses require a host for replication and survival and hence are subjected to host immunological pressures. The complement system, a crucial first response of the host immune system, is effective in targeting viruses and virus-infected cells, and boosting the antiviral innate and acquired immune responses. Thus, the system imposes a strong selection pressure on viruses. Consequently, viruses have evolved multiple countermeasures against host complement. A major mechanism employed by viruses to subvert the complement system is encoding proteins that target complement. Since viruses have limited genome size, most of these proteins are multifunctional in nature. In this review, we provide up to date information on the structure and complement regulatory functions of various viral proteins. Full article
(This article belongs to the Special Issue Viruses and Complement)
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