Special Issue "Virus Immune Escape and Host Immune System"

A special issue of Vaccines (ISSN 2076-393X). This special issue belongs to the section "Immune Mechanisms".

Deadline for manuscript submissions: 31 August 2020.

Special Issue Editor

Prof. Masmudur M. Rahman
Website
Guest Editor
The Biodesign Institute, Center for Immunotherapy, Vaccines, and Virotherapy, Arizona State University, Tempe, AZ 85287, USA
Interests: Virus-host interactions; molecular virology; innate immune signaling pathways; molecular biology; microbiology; cell biology; immunology; oncolytic virotherapy and immunotherapy; cancer biology; development of therapeutic proteins

Special Issue Information

Dear Colleagues,

Virus-host interaction studies is a fascinating area of research. Hosts have numerous counter-measures against virus infections, viruses, on the other hand, have co-evolved to defend the host anti-viral innate and adaptive immune responses. In their natural host, viruses have learned to co-exist with the hosts; however, the same virus could cause severe disease and pathogenesis when infecting a new host. Such incidence might cause a severe burden on society. Recent discoveries made significant progress in finding novel virus-host interactions, more to be discovered and learned in terms of the development of vaccines against new emerging viruses. The understanding of virus-host interaction is particularly important for the recent developments in the use of viruses as potential therapeutics such as oncolytic viruses, gene therapy vectors, cancer vaccines, and treatment of emerging genetic and infectious diseases.

This special issue focuses on the recent findings of viral immune evasion strategies and host counter-measures to prevent virus infection. The goal is to enhance our understanding of the complex and fascinating interaction between the virus and host defense. Understanding virus-host interactions will eventually help to develop effective vaccines and therapeutics against life-threatening viral infections. This special issue invites contribution to these areas of research.

Prof. Masmudur M. Rahman
Guest Editor

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 papers will be 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. Vaccines is an international peer-reviewed open access quarterly 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 1800 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

  • Virus-host interactions
  • Immune evasion
  • Innate immunity Adaptive immunity
  • Host anti-viral defenses
  • Viral pathogenicity Vaccines
  • Immunomodulatory proteins

Published Papers (5 papers)

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Research

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Open AccessArticle
Recombinant Live Attenuated Influenza Vaccine Viruses Carrying Conserved T-cell Epitopes of Human Adenoviruses Induce Functional Cytotoxic T-Cell Responses and Protect Mice against Both Infections
Vaccines 2020, 8(2), 196; https://doi.org/10.3390/vaccines8020196 - 24 Apr 2020
Abstract
Human adenoviruses (AdVs) are one of the most common causes of acute respiratory viral infections worldwide. Multiple AdV serotypes with low cross-reactivity circulate in the human population, making the development of an effective vaccine very challenging. In the current study, we designed a [...] Read more.
Human adenoviruses (AdVs) are one of the most common causes of acute respiratory viral infections worldwide. Multiple AdV serotypes with low cross-reactivity circulate in the human population, making the development of an effective vaccine very challenging. In the current study, we designed a cross-reactive AdV vaccine based on the T-cell epitopes conserved among various AdV serotypes, which were inserted into the genome of a licensed cold-adapted live attenuated influenza vaccine (LAIV) backbone. We rescued two recombinant LAIV-AdV vaccines by inserting the selected AdV T-cell epitopes into the open reading frame of full-length NA and truncated the NS1 proteins of the H7N9 LAIV virus. We then tested the bivalent vaccines for their efficacy against influenza and human AdV5 in a mouse model. The vaccine viruses were attenuated in C57BL/6J mice and induced a strong influenza-specific antibody and cell-mediated immunity, fully protecting the mice against virulent influenza virus infection. The CD8 T-cell responses induced by both LAIV-AdV candidates were functional and efficiently killed the target cells loaded either with influenza NP366 or AdV DBP418 peptides. In addition, high levels of recall memory T cells targeted to an immunodominant H2b-restricted CD8 T-cell epitope were detected in the immunized mice after the AdV5 challenge, and the magnitude of these responses correlated with the level of protection against pulmonary pathology caused by the AdV5 infection. Our findings suggest that the developed recombinant vaccines can be used for combined protection against influenza and human adenoviruses and warrant further evaluation on humanized animal models and subsequent human trials. Full article
(This article belongs to the Special Issue Virus Immune Escape and Host Immune System)
Open AccessArticle
Autophagy Promotes Duck Tembusu Virus Replication by Suppressing p62/SQSTM1-Mediated Innate Immune Responses In Vitro
Vaccines 2020, 8(1), 22; https://doi.org/10.3390/vaccines8010022 - 13 Jan 2020
Cited by 1
Abstract
Duck Tembusu virus (DTMUV) has recently appeared in ducks in China and the key cellular determiners for DTMUV replication in host cells remain unknown. Autophagy is an evolutionarily conserved cellular process that has been reported to facilitate flavivirus replication. In this study, we [...] Read more.
Duck Tembusu virus (DTMUV) has recently appeared in ducks in China and the key cellular determiners for DTMUV replication in host cells remain unknown. Autophagy is an evolutionarily conserved cellular process that has been reported to facilitate flavivirus replication. In this study, we utilized primary duck embryo fibroblast (DEF) as the cell model and found that DTMUV infection triggered LC3-II increase and polyubiquitin-binding protein sequestosome 1 (p62) decrease, confirming that complete autophagy occurred in DEF cells. The induction of autophagy by pharmacological treatment increased DTMUV replication in DEF cells, whereas the inhibition of autophagy with pharmacological treatments or RNA interference decreased DTMUV replication. Inhibiting autophagy enhanced the activation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and interferon regulatory factor 7 (IRF7) pathways and increased the p62 protein level in DTMUV-infected cells. We further found that the overexpression of p62 decreased DTMUV replication and inhibited the activation of the NF-κB and IRF7 pathways, and changes in the NF-κB and IRF7 pathways were consistent with the level of phosphorylated TANK-binding kinase 1 (p-TBK1). Opposite results were found in p62 knockdown cells. In summary, we found that autophagy-mediated p62 degradation acted as a new strategy for DTMUV to evade host innate immunity. Full article
(This article belongs to the Special Issue Virus Immune Escape and Host Immune System)
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Review

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Open AccessReview
Myxoma Virus-Encoded Host Range Protein M029: A Multifunctional Antagonist Targeting Multiple Host Antiviral and Innate Immune Pathways
Vaccines 2020, 8(2), 244; https://doi.org/10.3390/vaccines8020244 - 23 May 2020
Abstract
Myxoma virus (MYXV) is the prototypic member of the Leporipoxvirus genus of the Poxviridae family of viruses. In nature, MYXV is highly restricted to leporids and causes a lethal disease called myxomatosis only in European rabbits (Oryctologous cuniculus). However, MYXV has [...] Read more.
Myxoma virus (MYXV) is the prototypic member of the Leporipoxvirus genus of the Poxviridae family of viruses. In nature, MYXV is highly restricted to leporids and causes a lethal disease called myxomatosis only in European rabbits (Oryctologous cuniculus). However, MYXV has been shown to also productively infect various types of nonrabbit transformed and cancer cells in vitro and in vivo, whereas their normal somatic cell counterparts undergo abortive infections. This selective tropism of MYXV for cancer cells outside the rabbit host has facilitated its development as an oncolytic virus for the treatment of different types of cancers. Like other poxviruses, MYXV possesses a large dsDNA genome which encodes an array of dozens of immunomodulatory proteins that are important for host and cellular tropism and modulation of host antiviral innate immune responses, some of which are rabbit-specific and others can function in nonrabbit cells as well. This review summarizes the functions of one such MYXV host range protein, M029, an ortholog of the larger superfamily of poxvirus encoded E3-like dsRNA binding proteins. M029 has been identified as a multifunctional protein involved in MYXV cellular and host tropism, antiviral responses, and pathogenicity in rabbits. Full article
(This article belongs to the Special Issue Virus Immune Escape and Host Immune System)
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Open AccessReview
Targeting Host Innate and Adaptive Immunity to Achieve the Functional Cure of Chronic Hepatitis B
Vaccines 2020, 8(2), 216; https://doi.org/10.3390/vaccines8020216 - 11 May 2020
Abstract
Despite the availability of an effective preventive vaccine for hepatitis B virus (HBV) for over 38 years, chronic HBV (CHB) infection remains a global health burden with around 257 million patients. The ideal treatment goal for CHB infection would be to achieve complete [...] Read more.
Despite the availability of an effective preventive vaccine for hepatitis B virus (HBV) for over 38 years, chronic HBV (CHB) infection remains a global health burden with around 257 million patients. The ideal treatment goal for CHB infection would be to achieve complete cure; however, current therapies such as peg-interferon and nucleos(t)ide analogs are unable to achieve the functional cure, the newly set target for HBV chronic infection. Considering the fact functional cure has been accepted as an endpoint in the treatment of chronic hepatitis B by scientific committee, the development of alternative therapeutic strategies is urgently needed to functionally cure CHB infection. A promising target for future therapeutic strategies is immune modulation to restore dysfunctional HBV-specific immunity. In this review, we provide an overview of the progress in alternative therapeutic strategies, including immune-based therapeutic approaches that enhance host innate and adaptive immunity to achieve and increase the functional cure from CHB infection. Full article
(This article belongs to the Special Issue Virus Immune Escape and Host Immune System)
Open AccessReview
The Role of Extracellular Vesicles in Viral Infection and Transmission
Vaccines 2019, 7(3), 102; https://doi.org/10.3390/vaccines7030102 - 28 Aug 2019
Cited by 4
Abstract
Extracellular vesicles (EVs) have been found to be released by any type of cell and can be retrieved in every circulating body fluid, namely blood (plasma, serum), saliva, milk, and urine. EVs were initially considered a cellular garbage disposal tool, but later it [...] Read more.
Extracellular vesicles (EVs) have been found to be released by any type of cell and can be retrieved in every circulating body fluid, namely blood (plasma, serum), saliva, milk, and urine. EVs were initially considered a cellular garbage disposal tool, but later it became evident that they are involved in intercellular signaling. There is evidence that viruses can use EV endocytic routes to enter uninfected cells and hijack the EV secretory pathway to exit infected cells, thus illustrating that EVs and viruses share common cell entry and biogenesis mechanisms. Moreover, EVs play a role in immune response against viral pathogens. EVs incorporate and spread both viral and host factors, thereby prompting or inhibiting immune responses towards them via a multiplicity of mechanisms. The involvement of EVs in immune responses, and their potential use as agents modulating viral infection, will be examined. Although further studies are needed, the engineering of EVs could package viral elements or host factors selected for their immunostimulatory properties, to be used as vaccines or tolerogenic tools in autoimmune diseases. Full article
(This article belongs to the Special Issue Virus Immune Escape and Host Immune System)
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: NK cell memory to cytomegalovirus: implications for vaccine development
Authors: 1 Calum Forrest; 1 Ariane Gomes; 1 Matthew Reeves; 2 Victoria Male
Affiliation: 1 Institute for Immunity and Transplantation, UCL, Royal Free Campus, London NW3 2PF, UK
2 Department of Metabolism, Digestion & Reproduction, Imperial College, Chelsea & Westminster Campus, London, UK
Abstract: Natural killer (NK) cells are innate lymphoid cells that recognise and eliminate virally infected and cancerous cells. Members of the innate immune system are not usually considered to mediate immune memory, but over the past decade evidence has emerged that NK cells can do this in a number of contexts. Of these, the best-understood and most-widely accepted is the response to cytomegaloviruses, with strong evidence for memory to murine cytomegalovirus (MCMV) and several lines of investigation suggesting that the same is likely to be true of human cytomegalovirus (HCMV). The importance of NK cells in the context of CMV infection is underscored by the armoury of NK immune evasion genes encoded by CMV aimed at subverting the NK cell immune response. As such ongoing studies that have utilised CMV to investigate NK cell diversity and function have proven instructive. Here, we discuss our current understanding of NK cell memory with a focus on the response to cytomegaloviruses. We will then discuss the implications that this will have for the development of a vaccine against HCMV with particular emphasis on how a strategy that can harness the innate immune system and NK cells could be crucial for the development of a vaccine against in this high priority medical pathogen.

Title: Adaptation of H2N2 influenza viruses with different receptor specificities to MDCK cells: implications for the development of a cell-based pandemic H2N2 influenza vaccine
Authors: Victoria Matyushenko; Irina Isakova-Sivak; Ekaterina Stepanova; Larisa Rudenko
Affiliation: Department of Virology, Institute of Experimental Medicine, Saint Petersburg, 197376 Russia
Abstract: H2N2 influenza viruses caused a pandemic in 1957 due to the adaptation of avian influenza hemagglutinin from avian-type α2,3 to human-type α2,6 receptor specificity. These viruses have not circulated among humans for more than 50 years but are still found in avian reservoir, indicating their pandemic potential. It is known that at the beginning of a pandemic wave viruses with α2,3 and α2,6 receptor specificities can co-circulate, and the selection of one or another isolate for the development of a better pandemic influenza vaccine should be based on strong scientific evidence. Although the vast majority of influenza vaccines are produced in eggs, mammalian cell culture may be a preferred substrate for the production of pandemic influenza vaccines. Here we studied two variants of A/Singapore/1/57 (H2N2) virus which differed by their receptor specificity defined by three residues in the HA1 molecule: E156, Q226, G228 (Sing/EQG) for α2,3 avian-type and K156, L226, S228 (Sing/KLS) for α2,6 human-type receptor specificity. We conducted serial passaging of these viruses on MDCK cells and analyzed growth properties of plaque-purified clones in vitro and in vivo, as well as their immunogenicity and cross-reactivity in a mouse model. Adaptation to MDCK cells significantly increased viral titers in MDCK cells; however their receptor specificity was not affected. Viruses with α2,6 receptor specificity generated higher homologous HAI and IgG antibody titers compared to the viruses with α2,3 receptor specificity, but these antibodies could react only with the α2,6 viruses. In contrast, antibody induced by viruses with α2,3 receptor specificity had broad reactivity against all studied viruses. Although we detected an escape mutation P221S in a MDCK-adapted Sing/EQG variant, this mutant virus still induced serum antibodies with broad reactivity. The results of our study indicate that in the case of a new transmission of H2N2 avian influenza viruses to the human population and co-circulation of viruses with both receptor specificities, the variant with α2,3 specificity should be selected for the development of cross-reactive influenza vaccines.

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