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A special issue of Vaccines (ISSN 2076-393X). This special issue belongs to the section "Innate and Adaptive Immunity in Vaccination".

Deadline for manuscript submissions: closed (31 August 2020) | Viewed by 62415

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Prof. Masmudur M. Rahman

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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
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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

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Keywords

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

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Published Papers (11 papers)

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Research

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21 pages, 5934 KiB

Open AccessArticle

IFN-I Independent Antiviral Immune Response to Vesicular Stomatitis Virus Challenge in Mouse Brain

by Anurag R. Mishra, Siddappa N. Byrareddy and Debasis Nayak

Vaccines 2020, 8(2), 326; https://doi.org/10.3390/vaccines8020326 - 19 Jun 2020

Cited by 8 | Viewed by 5331

Abstract

Type I interferon (IFN-I) plays a pivotal role during viral infection response in the central nervous system (CNS). The IFN-I can orchestrate and regulate most of the innate immune gene expression and myeloid cell dynamics following a noncytopathic virus infection. However, the role of IFN-I in the CNS against viral encephalitis is not entirely clear. Here we have implemented the combination of global differential gene expression profiling followed by bioinformatics analysis to decipher the CNS immune response in the presence and absence of the IFN-I signaling. We observed that vesicular stomatitis virus (VSV) infection induced 281 gene changes in wild-type (WT) mice primarily associated with IFN-I signaling. This was accompanied by an increase in antiviral response through leukocyte vascular patrolling and leukocyte influx along with the expression of potent antiviral factors. Surprisingly, in the absence of the IFN-I signaling (IFNAR^−/− mice), a significantly higher (1357) number of genes showed differential expression compared to the WT mice. Critical candidates such as IFN-γ, CCL5, CXCL10, and IRF1, which are responsible for the recruitment of the patrolling leukocytes, are also upregulated in the absence of IFN-I signaling. The computational network analysis suggests the presence of the IFN-I independent pathway that compensates for the lack of IFN-I signaling in the brain. The analysis shows that TNF-α is connected maximally to the networked candidates, thus emerging as a key regulator of gene expression and recruitment of myeloid cells to mount antiviral action. This pathway could potentiate IFN-γ release; thereby, synergistically activating IRF1-dependent ISG expression and antiviral response. Full article

(This article belongs to the Special Issue Virus Immune Escape and Host Immune System)

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20 pages, 2300 KiB

Open AccessArticle

Immunogenicity and Efficacy of Zika Virus Envelope Domain III in DNA, Protein, and ChAdOx1 Adenoviral-Vectored Vaccines

by César López-Camacho, Giuditta De Lorenzo, Jose Luis Slon-Campos, Stuart Dowall, Peter Abbink, Rafael A. Larocca, Young Chan Kim, Monica Poggianella, Victoria Graham, Stephen Findlay-Wilson, Emma Rayner, Jennifer Carmichael, Wanwisa Dejnirattisai, Michael Boyd, Roger Hewson, Juthathip Mongkolsapaya, Gavin R. Screaton, Dan H. Barouch, Oscar R. Burrone, Arvind H. Patel and Arturo Reyes-Sandoval Show full author list Hide full author list

Vaccines 2020, 8(2), 307; https://doi.org/10.3390/vaccines8020307 - 16 Jun 2020

Cited by 17 | Viewed by 6190

Abstract

The flavivirus envelope protein domain III (EDIII) was an effective immunogen against dengue virus (DENV) and other related flaviviruses. Whether this can be applied to the Zika virus (ZIKV) vaccinology remains an open question. Here, we tested the efficacy of ZIKV-EDIII against ZIKV infection, using several vaccine platforms that present the antigen in various ways. We provide data demonstrating that mice vaccinated with a ZIKV-EDIII as DNA or protein-based vaccines failed to raise fully neutralizing antibodies and did not control viremia, following a ZIKV challenge, despite eliciting robust antibody responses. Furthermore, we showed that ZIKV-EDIII encoded in replication-deficient Chimpanzee adenovirus (ChAdOx1-EDIII) elicited anti-ZIKV envelope antibodies in vaccinated mice but also provided limited protection against ZIKV in two physiologically different mouse challenge models. Taken together, our data indicate that contrary to what was shown for other flaviviruses like the dengue virus, which has close similarities with ZIKV-EDIII, this antigen might not be a suitable vaccine candidate for the correct induction of protective immune responses against ZIKV. Full article

(This article belongs to the Special Issue Virus Immune Escape and Host Immune System)

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20 pages, 3306 KiB

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

by Irina Isakova-Sivak, Victoria Matyushenko, Ekaterina Stepanova, Anastasia Matushkina, Tatiana Kotomina, Daria Mezhenskaya, Polina Prokopenko, Igor Kudryavtsev, Pavel Kopeykin, Konstantin Sivak and Larisa Rudenko

Vaccines 2020, 8(2), 196; https://doi.org/10.3390/vaccines8020196 - 24 Apr 2020

Cited by 13 | Viewed by 4449

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 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 H2^b-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)

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19 pages, 4321 KiB

Open AccessArticle

Autophagy Promotes Duck Tembusu Virus Replication by Suppressing p62/SQSTM1-Mediated Innate Immune Responses In Vitro

by Zhiqiang Hu, Yuhong Pan, Anchun Cheng, Xingcui Zhang, Mingshu Wang, Shun Chen, Dekang Zhu, Mafeng Liu, Qiao Yang, Ying Wu, Xinxin Zhao, Juan Huang, Shaqiu Zhang, Sai Mao, Xumin Ou, Yanling Yu, Ling Zhang, Yunya Liu, Bin Tian, Leichang Pan, Mujeeb Ur Rehman, Zhongqiong Yin and Renyong Jia Show full author list Hide full author list

Vaccines 2020, 8(1), 22; https://doi.org/10.3390/vaccines8010022 - 13 Jan 2020

Cited by 8 | Viewed by 5205

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 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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27 pages, 758 KiB

Open AccessReview

Challenges for the Newborn Immune Response to Respiratory Virus Infection and Vaccination

by Kali F. Crofts and Martha A. Alexander-Miller

Vaccines 2020, 8(4), 558; https://doi.org/10.3390/vaccines8040558 - 24 Sep 2020

Cited by 10 | Viewed by 7320

Abstract

The initial months of life reflect an extremely challenging time for newborns as a naïve immune system is bombarded with a large array of pathogens, commensals, and other foreign entities. In many instances, the immune response of young infants is dampened or altered, resulting in increased susceptibility and disease following infection. This is the result of both qualitative and quantitative changes in the response of multiple cell types across the immune system. Here we provide a review of the challenges associated with the newborn response to respiratory viral pathogens as well as the hurdles and advances for vaccine-mediated protection. Full article

(This article belongs to the Special Issue Virus Immune Escape and Host Immune System)

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21 pages, 3498 KiB

Open AccessReview

The Molecular Interactions of ZIKV and DENV with the Type-I IFN Response

by Rosa C. Coldbeck-Shackley, Nicholas S. Eyre and Michael R. Beard

Vaccines 2020, 8(3), 530; https://doi.org/10.3390/vaccines8030530 - 14 Sep 2020

Cited by 25 | Viewed by 5398

Abstract

Zika Virus (ZIKV) and Dengue Virus (DENV) are related viruses of the Flavivirus genus that cause significant disease in humans. Existing control measures have been ineffective at curbing the increasing global incidence of infection for both viruses and they are therefore prime targets for new vaccination strategies. Type-I interferon (IFN) responses are important in clearing viral infection and for generating efficient adaptive immune responses towards infection and vaccination. However, ZIKV and DENV have evolved multiple molecular mechanisms to evade type-I IFN production. This review covers the molecular interactions, from detection to evasion, of these viruses with the type-I IFN response. Additionally, we discuss how this knowledge can be exploited to improve the design of new vaccine strategies. Full article

(This article belongs to the Special Issue Virus Immune Escape and Host Immune System)

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14 pages, 973 KiB

Open AccessReview

Hepatitis E Virus: How It Escapes Host Innate Immunity

by Sébastien Lhomme, Marion Migueres, Florence Abravanel, Olivier Marion, Nassim Kamar and Jacques Izopet

Vaccines 2020, 8(3), 422; https://doi.org/10.3390/vaccines8030422 - 28 Jul 2020

Cited by 14 | Viewed by 3631

Abstract

Hepatitis E virus (HEV) is a leading cause of viral hepatitis in the world. It is usually responsible for acute hepatitis, but can lead to a chronic infection in immunocompromised patients. The host’s innate immune response is the first line of defense against a virus infection; there is growing evidence that HEV RNA is recognized by toll-like receptors (TLRs) and retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs), leading to interferon (IFN) production. The IFNs activate interferon-stimulated genes (ISGs) to limit HEV replication and spread. HEV has developed strategies to counteract this antiviral response, by limiting IFN induction and signaling. This review summarizes the advances in our knowledge of intracellular pathogen recognition, interferon and inflammatory response, and the role of virus protein in immune evasion. Full article

(This article belongs to the Special Issue Virus Immune Escape and Host Immune System)

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19 pages, 606 KiB

Open AccessReview

NK Cell Memory to Cytomegalovirus: Implications for Vaccine Development

by Calum Forrest, Ariane Gomes, Matthew Reeves and Victoria Male

Vaccines 2020, 8(3), 394; https://doi.org/10.3390/vaccines8030394 - 20 Jul 2020

Cited by 10 | Viewed by 4830

Abstract

Natural killer (NK) cells are innate lymphoid cells that recognize 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 several 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 evidence suggesting that the same is likely to be true of human cytomegalovirus (HCMV). The importance of NK cells in the context of HCMV infection is underscored by the armory of NK immune evasion genes encoded by HCMV aimed at subverting the NK cell immune response. As such, ongoing studies that have utilized HCMV to investigate NK cell diversity and function have proven instructive. Here, we discuss our current understanding of NK cell memory to viral infection 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 this high-priority pathogen. Full article

(This article belongs to the Special Issue Virus Immune Escape and Host Immune System)

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15 pages, 3511 KiB

Open AccessReview

Myxoma Virus-Encoded Host Range Protein M029: A Multifunctional Antagonist Targeting Multiple Host Antiviral and Innate Immune Pathways

by Masmudur M. Rahman and Grant McFadden

Vaccines 2020, 8(2), 244; https://doi.org/10.3390/vaccines8020244 - 23 May 2020

Cited by 7 | Viewed by 3898

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 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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18 pages, 334 KiB

Open AccessReview

Targeting Host Innate and Adaptive Immunity to Achieve the Functional Cure of Chronic Hepatitis B

by Sayeh Ezzikouri, Mohammad Enamul Hoque Kayesh, Soumaya Benjelloun, Michinori Kohara and Kyoko Tsukiyama-Kohara

Vaccines 2020, 8(2), 216; https://doi.org/10.3390/vaccines8020216 - 11 May 2020

Cited by 17 | Viewed by 4128

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 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)

20 pages, 626 KiB

Open AccessReview

The Role of Extracellular Vesicles in Viral Infection and Transmission

by Lorena Urbanelli, Sandra Buratta, Brunella Tancini, Krizia Sagini, Federica Delo, Serena Porcellati and Carla Emiliani

Vaccines 2019, 7(3), 102; https://doi.org/10.3390/vaccines7030102 - 28 Aug 2019

Cited by 133 | Viewed by 9092

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 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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