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Viruses
Special Issues
Post-viral Superinfection: Revising the Role of Pathogens and the Host
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Post-viral Superinfection: Revising the Role of Pathogens and the Host

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Animal Viruses".

Deadline for manuscript submissions: closed (15 September 2021) | Viewed by 11421

Special Issue Editors

Dr. Victor Huber

E-Mail Website
Guest Editor
Division of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, SD 57069, USA
Interests: influenza virus; antiviral immunity; influenza–bacterium coinfections; antiviral vaccine development
Dr. Agnieszka Rynda-Apple

E-Mail Website
Guest Editor
Department of Microbiology and Immunology, Montana State University, 109 Lewis Hall, Bozeman, MT 59717, USA
Interests: antiviral immunity; pattern recognition; innate immunity; type I IFN responses; post-influenza bacterial infections

Special Issue Information

Dear Colleagues,

Infections with viral, bacterial or fungal pathogens are common complications of respiratory viral infections, including those caused by influenza, parainfluenza viruses, coronaviruses and RSV, to name a few. Additionally, some chronic viral infections have been known to be complicated by superinfections. It is generally accepted that the resolution of these secondary infections is impaired by the primary virus itself, via a virus-mediated inhibitory effect restricting or otherwise altering the induction of appropriate innate and/or adaptive immune responses, or even virus-induced host tissue damage. Furthermore, secondary pathogens exacerbate this distorted immune response in ways that are damaging and even detrimental to the host. This Special Issue will focus on various mechanisms utilized by either primary viruses or secondary pathogens to delay, restrict or prevent host recovery.

Dr. Victor Huber
Dr. Agnieszka Rynda-Apple
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

  • superinfections
  • secondary infections
  • antiviral defense
  • innate immunity to viral infections
  • innate immunity to bacterial infections
  • innate immunity to fungal infections

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Published Papers (3 papers)

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Research

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11 pages, 1723 KiB  
Article
IFN-γ Attenuates Eosinophilic Inflammation but Is Not Essential for Protection against RSV-Enhanced Asthmatic Comorbidity in Adult Mice
by Abenaya Muralidharan, Md Bashir Uddin, Christopher Bauer, Wenzhe Wu, Xiaoyong Bao and Keer Sun
Viruses 2022, 14(1), 147; https://doi.org/10.3390/v14010147 - 14 Jan 2022
Cited by 4 | Viewed by 2694
Abstract
The susceptibility to respiratory syncytial virus (RSV) infection in early life has been associated with a deficient T-helper cell type 1 (Th1) response. Conversely, healthy adults generally do not exhibit severe illness from RSV infection. In the current study, we investigated whether Th1 [...] Read more.
The susceptibility to respiratory syncytial virus (RSV) infection in early life has been associated with a deficient T-helper cell type 1 (Th1) response. Conversely, healthy adults generally do not exhibit severe illness from RSV infection. In the current study, we investigated whether Th1 cytokine IFN-γ is essential for protection against RSV and RSV-associated comorbidities in adult mice. We found that, distinct from influenza virus, prior RSV infection does not induce significant IFN-γ production and susceptibility to secondary Streptococcus pneumoniae infection in adult wild-type (WT) mice. In ovalbumin (OVA)-induced asthmatic mice, RSV super-infection increases airway neutrophil recruitment and inflammatory lung damage but has no significant effect on OVA-induced eosinophilia. Compared with WT controls, RSV infection of asthmatic Ifng−/− mice results in increased airway eosinophil accumulation. However, a comparable increase in eosinophilia was detected in house dust mite (HDM)-induced asthmatic Ifng−/− mice in the absence of RSV infection. Furthermore, neither WT nor Ifng−/− mice exhibit apparent eosinophil infiltration during RSV infection alone. Together, these findings indicate that, despite its critical role in limiting eosinophilic inflammation during asthma, IFN-γ is not essential for protection against RSV-induced exacerbation of asthmatic inflammation in adult mice. Full article
(This article belongs to the Special Issue Post-viral Superinfection: Revising the Role of Pathogens and the Host)
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20 pages, 2882 KiB  
Article
Successive Inoculations of Pigs with Porcine Reproductive and Respiratory Syndrome Virus 1 (PRRSV-1) and Swine H1N2 Influenza Virus Suggest a Mutual Interference between the Two Viral Infections
by Juliette Bougon, Céline Deblanc, Patricia Renson, Stéphane Quéguiner, Stéphane Gorin, Sophie Mahé, Mireille Le Dimna, Nicolas Barbier, Frédéric Paboeuf, Gaëlle Simon and Olivier Bourry
Viruses 2021, 13(11), 2169; https://doi.org/10.3390/v13112169 - 27 Oct 2021
Cited by 9 | Viewed by 2568
Abstract
Porcine reproductive and respiratory syndrome virus (PRRSV) and swine influenza A virus (swIAV) are major pathogens of the porcine respiratory disease complex, but little is known on their interaction in super-infected pigs. In this study, we investigated clinical, virological and immunological outcomes of [...] Read more.
Porcine reproductive and respiratory syndrome virus (PRRSV) and swine influenza A virus (swIAV) are major pathogens of the porcine respiratory disease complex, but little is known on their interaction in super-infected pigs. In this study, we investigated clinical, virological and immunological outcomes of successive infections with PRRSV-1 and H1N2 swIAV. Twenty-four specific pathogen-free piglets were distributed into four groups and inoculated either with PRRSV at study day (SD) 0, or with swIAV at SD8, or with PRRSV and swIAV one week apart at SD0 and SD8, respectively, or mock-inoculated. In PRRSV/swIAV group, the clinical signs usually observed after swIAV infection were attenuated while higher levels of anti-swIAV antibodies were measured in lungs. Concurrently, PRRSV multiplication in lungs was significantly affected by swIAV infection, whereas the cell-mediated immune response specific to PRRSV was detected earlier in blood, as compared to PRRSV group. Moreover, levels of interferon (IFN)-α measured from SD9 in the blood of super-infected pigs were lower than those measured in the swIAV group, but higher than in the PRRSV group at the same time. Correlation analyses suggested an important role of IFN-α in the two-way interference highlighted between both viral infections. Full article
(This article belongs to the Special Issue Post-viral Superinfection: Revising the Role of Pathogens and the Host)
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Review

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15 pages, 862 KiB  
Review
Disease Tolerance during Viral-Bacterial Co-Infections
by Tarani Kanta Barman and Dennis W. Metzger
Viruses 2021, 13(12), 2362; https://doi.org/10.3390/v13122362 - 25 Nov 2021
Cited by 6 | Viewed by 5163
Abstract
Disease tolerance has emerged as an alternative way, in addition to host resistance, to survive viral-bacterial co-infections. Disease tolerance plays an important role not in reducing pathogen burden, but in maintaining tissue integrity and controlling organ damage. A common co-infection is the synergy [...] Read more.
Disease tolerance has emerged as an alternative way, in addition to host resistance, to survive viral-bacterial co-infections. Disease tolerance plays an important role not in reducing pathogen burden, but in maintaining tissue integrity and controlling organ damage. A common co-infection is the synergy observed between influenza virus and Streptococcus pneumoniae that results in superinfection and lethality. Several host cytokines and cells have shown promise in promoting tissue protection and damage control while others induce severe immunopathology leading to high levels of morbidity and mortality. The focus of this review is to describe the host cytokines and innate immune cells that mediate disease tolerance and lead to a return to host homeostasis and ultimately, survival during viral-bacterial co-infection. Full article
(This article belongs to the Special Issue Post-viral Superinfection: Revising the Role of Pathogens and the Host)
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