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Interplay between Viruses and Host Adaptive Immunity

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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 (20 December 2021) | Viewed by 24585

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Special Issue Editors

Dr. Bumsuk Hahm

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Guest Editor

Departments of Surgery and Molecular Microbiology and Immunology, University of Missouri School of Medicine, Columbia, MO 65212, USA
Interests: viral immunity; RNA virus-host interaction; influenza; LCMV; sphingolipid network
Special Issues, Collections and Topics in MDPI journals

Dr. Young-Jin Seo

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Guest Editor

Department of Life Science, College of Natural Sciences, Chung-Ang University, 84 Heukseok-ro, Dongjak-gu, Seoul 06974, Korea
Interests: anti-viral immunity; Influenza virus; anti-viral CD8+ T cell response

Special Issue Information

Dear Colleagues,

Upon infection with a virus, antigen-specific adaptive immunity develops to eliminate viruses. While antibody responses help neutralize or block viruses from entering into cells, cytotoxic CD8⁺ lymphocytes precisely destroy virus-infected cells to purge viruses from hosts. Further, CD4⁺ helper T cells play a pivotal role during infections by regulating the differentiation of CD8⁺ T and B cells. On the other hand, multiple innate immune cells and cytokines cooperate with T/B cells to eradicate viruses. However, pathogenic viruses often develop strategies to evade or repress the adaptive immunity and persist in hosts. Enormous efforts have been made to regulate adaptive immunity to increase the efficacy of vaccines or therapeutics for the prevention or treatment of viral diseases.

In this Special Issue, emphasis will be placed on the recent scientific advancement as to the interaction between host adaptive immunity and viruses, as well as its applications such as vaccine development against viral diseases including COVID-19. This research will improve our understanding of the host immunity to virus infections and help us design new prophylactic or therapeutic interventions to eliminate pathogenic viruses including HIV, influenza, and SARS-CoV-2. You are cordially invited to contribute unique research or review articles on this theme or related research topics.

Dr. Bumsuk Hahm
Dr. Young-Jin Seo
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

SARS-CoV-2
COVID-19
immune evasion
virus persistence
adaptive immunity
T cells
B cells
lymphocyte
antibody
cytokine
vaccine
cytotoxic T lymphocyte
CD8 T cell
CD4 T cell

Published Papers (7 papers)

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Research

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24 pages, 5048 KiB

Open AccessArticle

Involvement of Th1Th17 Cell Subpopulations in the Immune Responses of Mothers Who Gave Birth to Children with Congenital Zika Syndrome (CZS)

by Iury Amancio Paiva, Débora Familiar-Macedo, Jéssica Badolato-Corrêa, Fabiana Rabe Carvalho, Helver Gonçalves Dias, Alex Pauvolid-Corrêa, Caroline Fernandes dos Santos, Andréa Alice Silva, Elzinandes Leal de Azeredo, Renata Artimos de Oliveira Vianna, Claudete Aparecida Araújo Cardoso, Alba Grifoni, Alessandro Sette, Daniela Weiskopf and Luzia Maria de-Oliveira-Pinto

Viruses 2022, 14(2), 250; https://0-doi-org.brum.beds.ac.uk/10.3390/v14020250 - 26 Jan 2022

Cited by 1 | Viewed by 2778

Abstract

High levels of T helper 17 cell (Th17)-related cytokines have been shown in acute Zika virus (ZIKV) infection. We hypothesized that the high levels of Th17-related cytokines, associated with a regulatory environment during pregnancy, create a favorable milieu for the differentiation of CD4+Th17 cells. We present data from a cross-sectional study on mothers who confirmed ZIKV infection by qRT-PCR and their children. We also recruited non-pregnant women infected with ZIKV in the same period. ZIKV infection occurred between 2015 and 2017. We collected samples for this study between 2018 and 2019, years after the initial infection. We highlight that, after in vitro stimulation with ZIKV CD4 megapool (ZIKV MP), we found a lower frequency of IL-17-producing CD4+ T cells (Th17), especially in the mothers, confirmed by the decrease in IL-17 production in the supernatant. However, a higher frequency of CD4+ IL-17+ IFN-γ+ T cells (Th1Th17) responding to the ZIKV MP was observed in the cells of the mothers and children but not in those of the non-pregnant women. Our data indicate that the priming of CD4 T cells of the Th1Th17 phenotype occurred preferentially in the mothers who gave birth to children with CZS and in the children. Full article

(This article belongs to the Special Issue Interplay between Viruses and Host Adaptive Immunity)

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15 pages, 1341 KiB

Open AccessArticle

Robust and Persistent B- and T-Cell Responses after COVID-19 in Immunocompetent and Solid Organ Transplant Recipient Patients

by Federica Zavaglio, Vanessa Frangipane, Monica Morosini, Elisa Gabanti, Paola Zelini, Josè Camilla Sammartino, Alessandro Ferrari, Marilena Gregorini, Teresa Rampino, Annalia Asti, Elena Seminari, Angela Di Matteo, Barbara Cattadori, Carlo Pellegrini, Stelvio Tonello, Venkata Ramana Mallela, Rosalba Minisini, Manuela Rizzi, Pier Paolo Sainaghi, Federica Meloni, Daniele Lilleri and Fausto Baldanti Show full author list Hide full author list

Viruses 2021, 13(11), 2261; https://0-doi-org.brum.beds.ac.uk/10.3390/v13112261 - 11 Nov 2021

Cited by 12 | Viewed by 2157

Abstract

The development and persistence of SARS-CoV-2-specific immune response in immunocompetent (IC) and immunocompromised patients is crucial for long-term protection. Immune response to SARS-CoV-2 infection was analysed in 57 IC and 15 solid organ transplanted (TX) patients. Antibody responses were determined by ELISA and neutralization assay. T-cell response was determined by stimulation with peptide pools of the Spike, Envelope, Membrane, and Nucleocapsid proteins with a 20-h Activation Induced Marker (AIM) and 7-day lymphoproliferative assays. Antibody response was detected at similar levels in IC and TX patients. Anti-Spike IgG, IgA and neutralizing antibodies persisted for at least one year, while anti-Nucleocapsid IgG declined earlier. Patients with pneumonia developed higher antibody levels than patients with mild symptoms. Similarly, both rapid and proliferative T-cell responses were detected within the first two months after infection at comparable levels in IC and TX patients, and were higher in patients with pneumonia. T-cell response persisted for at least one year in both IC and TX patients. Spike, Membrane, and Nucleocapsid proteins elicited the major CD4⁺ and CD8⁺ T-cell responses, whereas the T-cell response to Envelope protein was negligible. After SARS-CoV-2 infection, antibody and T-cell responses develop rapidly and persist over time in both immunocompetent and transplanted patients. Full article

(This article belongs to the Special Issue Interplay between Viruses and Host Adaptive Immunity)

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13 pages, 14543 KiB

Open AccessArticle

Dose-Dependent Outcome of EBV Infection of Humanized Mice Based on Green Raji Unit (GRU) Doses

by Haiwen Chen, Ling Zhong, Wanlin Zhang, Shanshan Zhang, Junping Hong, Xiang Zhou, Xinyu Zhang, Qisheng Feng, Yixin Chen, Yi-Xin Zeng, Miao Xu, Claude Krummenacher and Xiao Zhang

Viruses 2021, 13(11), 2184; https://0-doi-org.brum.beds.ac.uk/10.3390/v13112184 - 29 Oct 2021

Cited by 5 | Viewed by 2545

Abstract

Humanized mouse models are used as comprehensive small-animal models of EBV infection. Previously, infectious doses of EBV used in vivo have been determined mainly on the basis of TD₅₀ (50% transforming dose), which is a time-consuming process. Here, we determined infectious doses of Akata-EBV-GFP using green Raji units (GRUs), and characterized dose-dependent effects in humanized mice. We defined two outcomes in vivo, including an infection model and a lymphoma model, following inoculation with low or high doses of Akata-EBV-GFP, respectively. Inoculation with a low dose induced primary B cells to become lymphoblastoid cell lines in vitro, and caused latent infection in humanized mice. In contrast, a high dose of Akata-EBV-GFP resulted in primary B cells death in vitro, and fatal B cell lymphomas in vivo. Following infection with high doses, the frequency of CD19⁺ B cells decreased, whereas the percentage of CD8⁺ T cells increased in peripheral blood and the spleen. At such doses, a small part of activated CD8⁺ T cells was EBV-specific CD8⁺ T cells. Thus, GRUs quantitation of Akata-EBV-GFP is an effective way to quantify infectious doses to study pathologies, immune response, and to assess (in vivo) the neutralizing activity of antibodies raised by immunization against EBV. Full article

(This article belongs to the Special Issue Interplay between Viruses and Host Adaptive Immunity)

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22 pages, 3999 KiB

Open AccessArticle

The Monoclonal Antibody Recognized the Open Reading Frame Protein in Porcine Circovirus Type 2-Infected Peripheral Blood Mononuclear Cells

by Ling-Chu Hung

Viruses 2020, 12(9), 961; https://0-doi-org.brum.beds.ac.uk/10.3390/v12090961 - 29 Aug 2020

Cited by 2 | Viewed by 2551

Abstract

The purpose of this study in the context of the open reading frame 3 (ORF3) protein of porcine circovirus type 2 (PCV2) was especially its location and its relation to the capsid protein and the apoptosis protein in PCV2-infected porcine peripheral blood mononuclear cells (PBMCs). To detect the ORF3 protein, monoclonal antibodies (mAbs) were generated in this study. The mAb 7D3 binds to the ORF3 peptide (residues 35–66) and the native ORF3 protein in PCV2-infected PBMCs, as shown by immunofluorescence assay (IFA). The data show that 3–5% of PBMCs were positive for ORF3 protein or p53 protein. Further, 78–82% of PBMCs were positive for the capsid. This study confirmed the ORF3 protein not only colocalized with the capsid protein but also colocalized with the p53 protein in PBMCs. Immunoassays were conducted in this study to detect the capsid protein, the ORF3 protein, anti-capsid IgG, and anti-ORF3 IgG. The data show the correlation (r = 0.758) of the ORF3 protein and the capsid protein in the blood samples from the PCV2-infected herd. However, each anti-viral protein IgG had a different curve of the profile in the same herd after vaccination. Overall, this study provides a blueprint to explore the ORF3 protein in PCV2-infected PBMCs. Full article

(This article belongs to the Special Issue Interplay between Viruses and Host Adaptive Immunity)

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Review

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14 pages, 685 KiB

Open AccessReview

Role of Damage-Associated Molecular Pattern/Cell Death Pathways in Vaccine-Induced Immunity

by Sun Min Lee, Paul Kim, Jinsuh You and Eui Ho Kim

Viruses 2021, 13(12), 2340; https://0-doi-org.brum.beds.ac.uk/10.3390/v13122340 - 23 Nov 2021

Cited by 7 | Viewed by 3415

Abstract

Immune responses induced by natural infection and vaccination are known to be initiated by the recognition of microbial patterns by cognate receptors, since microbes and most vaccine components contain pathogen-associated molecular patterns. Recent discoveries on the roles of damage-associated molecular patterns (DAMPs) and cell death in immunogenicity have improved our understanding of the mechanism underlying vaccine-induced immunity. DAMPs are usually immunologically inert, but can transform into alarming signals to activate the resting immune system in response to pathogenic infection, cellular stress and death, or tissue damage. The activation of DAMPs and cell death pathways can trigger local inflammation, occasionally mediating adaptive immunity, including antibody- and cell-mediated immune responses. Emerging evidence indicates that the components of vaccines and adjuvants induce immunogenicity via the stimulation of DAMP/cell death pathways. Furthermore, strategies for targeting this pathway to enhance immunogenicity are being investigated actively. In this review, we describe various DAMPs and focus on the roles of DAMP/cell death pathways in the context of vaccines for infectious diseases and cancer. Full article

(This article belongs to the Special Issue Interplay between Viruses and Host Adaptive Immunity)

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20 pages, 797 KiB

Open AccessReview

Chronic LCMV Infection Is Fortified with Versatile Tactics to Suppress Host T Cell Immunity and Establish Viral Persistence

by Caleb J. Studstill and Bumsuk Hahm

Viruses 2021, 13(10), 1951; https://0-doi-org.brum.beds.ac.uk/10.3390/v13101951 - 29 Sep 2021

Cited by 3 | Viewed by 4301

Abstract

Ever since the immune regulatory strains of lymphocytic choriomeningitis virus (LCMV), such as Clone 13, were isolated, LCMV infection of mice has served as a valuable model for the mechanistic study of viral immune suppression and virus persistence. The exhaustion of virus-specific T cells was demonstrated during LCMV infection, and the underlying mechanisms have been extensively investigated using LCMV infection in mouse models. In particular, the mechanism for gradual CD8⁺ T cell exhaustion at molecular and transcriptional levels has been investigated. These studies revealed crucial roles for inhibitory receptors, surface markers, regulatory cytokines, and transcription factors, including PD-1, PSGL-1, CXCR5, and TOX in the regulation of T cells. However, the action mode for CD4⁺ T cell suppression is largely unknown. Recently, sphingosine kinase 2 was proven to specifically repress CD4⁺ T cell proliferation and lead to LCMV persistence. As CD4⁺ T cell regulation was also known to be important for viral persistence, research to uncover the mechanism for CD4⁺ T cell repression could help us better understand how viruses launch and prolong their persistence. This review summarizes discoveries derived from the study of LCMV in regard to the mechanisms for T cell suppression and approaches for the termination of viral persistence with special emphasis on CD8⁺ T cells. Full article

(This article belongs to the Special Issue Interplay between Viruses and Host Adaptive Immunity)

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23 pages, 1729 KiB

Open AccessReview

Impact of Microbiota: A Paradigm for Evolving Herd Immunity against Viral Diseases

by Asha Shelly, Priya Gupta, Rahul Ahuja, Sudeepa Srichandan, Jairam Meena and Tanmay Majumdar

Viruses 2020, 12(10), 1150; https://0-doi-org.brum.beds.ac.uk/10.3390/v12101150 - 10 Oct 2020

Cited by 7 | Viewed by 5790

Abstract

Herd immunity is the most critical and essential prophylactic intervention that delivers protection against infectious diseases at both the individual and community level. This process of natural vaccination is immensely pertinent to the current context of a pandemic caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection around the globe. The conventional idea of herd immunity is based on efficient transmission of pathogens and developing natural immunity within a population. This is entirely encouraging while fighting against any disease in pandemic circumstances. A spatial community is occupied by people having variable resistance capacity against a pathogen. Protection efficacy against once very common diseases like smallpox, poliovirus or measles has been possible only because of either natural vaccination through contagious infections or expanded immunization programs among communities. This has led to achieving herd immunity in some cohorts. The microbiome plays an essential role in developing the body’s immune cells for the emerging competent vaccination process, ensuring herd immunity. Frequency of interaction among microbiota, metabolic nutrients and individual immunity preserve the degree of vaccine effectiveness against several pathogens. Microbiome symbiosis regulates pathogen transmissibility and the success of vaccination among different age groups. Imbalance of nutrients perturbs microbiota and abrogates immunity. Thus, a particular population can become vulnerable to the infection. Intestinal dysbiosis leads to environmental enteropathy (EE). As a consequence, the generation of herd immunity can either be delayed or not start in a particular cohort. Moreover, disparities of the protective response of many vaccines in developing countries outside of developed countries are due to inconsistencies of healthy microbiota among the individuals. We suggested that pan-India poliovirus vaccination program, capable of inducing herd immunity among communities for the last 30 years, may also influence the inception of natural course of heterologous immunity against SARS-CoV-2 infection. Nonetheless, this anamnestic recall is somewhat counterintuitive, as antibody generation against original antigens of SARS-CoV-2 will be subdued due to original antigenic sin. Full article

(This article belongs to the Special Issue Interplay between Viruses and Host Adaptive Immunity)

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