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Host Immune Responses to RNA Viruses, 2nd Edition
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Host Immune Responses to RNA Viruses, 2nd Edition

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Viral Pathogens".

Deadline for manuscript submissions: 20 May 2025 | Viewed by 25147

Special Issue Editors

Dr. Stephanie Longet

E-Mail Website
Guest Editor
International Center for Infectiology Research—INSERM, GIMAP—University of Saint-Etienne,10 rue de la Marandière, 42270 Saint-Priest-en-Jarez, France
Interests: antibody response; adaptive immune response; viral antibody; vaccine antibody; SARS-CoV-2; Ebola virus; Lassa virus; mucosal immune response
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Miles Carroll

E-Mail Website
Guest Editor
Nuffield Department of Medicine, Wellcome Centre for Human Genetics, University of Oxford, Oxford 5OX3 7BN, UK
Interests: emerging diseases; adaptive immune response; neutralising response; Ebola virus; Marburg virus; Lassa virus; human coronaviruses; Crimean–Congo haemorrhagic fever; vaccine-induced immune response; sero-epidemiology; immune evasion
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

RNA viruses have the ability to infect bacteria, plants, animals and humans. Over the past century, infections due to RNA viruses, including human immunodeficiency virus 1 (HIV-1), influenza virus, rotavirus, West Nile virus, Dengue virus, and measles virus, have been major threats to human health. Furthermore, RNA viruses are often the cause of emerging infectious diseases in humans, with high consequences on healthcare systems and economies. Some examples of RNA viruses which have caused emerging diseases are severe acute respiratory syndrome related (SARS) coronavirus, Middle East respiratory syndrome (MERS) coronavirus and the Ebola virus. The huge global impact of SARS-CoV-2, which emerged in 2019, highlighted the importance of preparation in fighting RNA viruses. A better understanding of host immune responses to RNA viruses is key to define the correlates of protection that are essential to improve or develop therapeutic strategies and vaccine platforms.

A lot of effort has been put into research on RNA viruses such as Poliovirus, HIV-1 and influenza virus for many years, but other RNA viruses, including Chikungunya, Zika, and Nipah viruses, have the potential to become epidemics. Recent advancements in the characterisation of protective immune responses to some RNA viruses, such as Ebola virus or SARS-CoV-2, quickly led to first-generation vaccine development. However, knowledge gaps in relation to host immune responses to a number of RNA viruses still exist. Host-immune factors that lead to the control of infection as well as immune determinants involved in disease severity, or latency and viral reservoirs in particular cases, are not fully understood. In addition, RNA viruses may show a high mutation rate in their host due to the lack of proofreading by their replicases, which can lead to immune evasion. Immune mechanisms against viral evasion are not fully defined. Such information will be crucial to design novel vaccine and therapeutic strategies.

I would like to invite colleagues investigating immune responses to any of the RNA viruses in in vitro or ex vivo models, animal models or humans within the areas of immunology, virology, public health and epidemiology to submit their manuscripts to this Special Issue of Pathogens in the form of original research and reviews. Potential topics include but are not limited to:

  • Characterisation of humoral and cellular responses during RNA virus infections;
  • Dynamics of innate immune response to RNA virus infection;
  • Role of host immune responses in pathogenesis of viral infections;
  • Immune mechanisms against viral escape.

Dr. Stephanie Longet
Prof. Dr. Miles Carroll
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. Pathogens 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 2200 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

  • RNA viruses
  • antibody response
  • cellular response
  • innate response
  • immune evasion
  • viral infections
  • memory response
  • correlates of protection
  • protective response
  • humans
  • animal models
  • public health

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Related Special Issue

Published Papers (8 papers)

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Research

Jump to: Review

15 pages, 3749 KiB  
Article
Differential TLR-ERK1/2 Activity Promotes Viral ssRNA and dsRNA Mimic-Induced Dysregulated Immunity in Macrophages
by Rakshya Shrestha, Paige Marie Johnson, Roshan Ghimire, Cody John Whitley and Rudragouda Channappanavar
Pathogens 2024, 13(12), 1033; https://doi.org/10.3390/pathogens13121033 - 23 Nov 2024
Viewed by 1645
Abstract
RNA virus-induced excessive inflammation and impaired antiviral interferon (IFN-I) responses are associated with severe disease. This innate immune response, also referred to as “dysregulated immunity” is caused by viral single-stranded RNA (ssRNA)- and double-stranded-RNA (dsRNA)-mediated exuberant inflammation and viral protein-induced IFN antagonism. However, [...] Read more.
RNA virus-induced excessive inflammation and impaired antiviral interferon (IFN-I) responses are associated with severe disease. This innate immune response, also referred to as “dysregulated immunity” is caused by viral single-stranded RNA (ssRNA)- and double-stranded-RNA (dsRNA)-mediated exuberant inflammation and viral protein-induced IFN antagonism. However, key host factors and the underlying mechanism driving viral RNA-mediated dysregulated immunity are poorly defined. Here, using viral ssRNA and dsRNA mimics, which activate toll-like receptor 7 (TLR7) and TLR3, respectively, we evaluated the role of viral RNAs in causing dysregulated immunity. We observed that murine bone marrow-derived macrophages (BMDMs), when stimulated with TLR3 and TLR7 agonists, induced differential inflammatory and antiviral cytokine response. TLR7 activation triggered a robust inflammatory cytokine/chemokine induction compared to TLR3 activation, whereas TLR3 stimulation induced significantly increased IFN/IFN stimulated gene (ISG) response relative to TLR7 activation. To define the mechanistic basis for dysregulated immunity, we examined cell-surface and endosomal TLR levels and downstream mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-kB) activation. We identified significantly higher cell-surface and endosomal TLR7 levels compared to TLR3, which were associated with early and robust MAPK (p-ERK1/2, p-P38, and p-JNK) and NF-kB activation in TLR7-stimulated macrophages. Furthermore, blocking EKR1/2 and NF-kB activity reduced TLR3/7-induced inflammatory cytokine/chemokine levels, whereas only ERK1/2 inhibition enhanced viral RNA mimic-induced IFN/ISG responses. Collectively, our results illustrate that high cell-surface and endosomal TLR7 expression and robust ERK1/2 activation drive viral ssRNA mimic-induced excessive inflammatory and reduced IFN/ISG response and blocking ERK1/2 activity would likely mitigate viral-RNA/TLR-induced dysregulated immunity. Full article
(This article belongs to the Special Issue Host Immune Responses to RNA Viruses, 2nd Edition)
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23 pages, 21813 KiB  
Article
mRNA Profiling and Transcriptomics Analysis of Chickens Received Newcastle Disease Virus Genotype II and Genotype VII Vaccines
by Putri Pandarangga, Phuong Thi Kim Doan, Rick Tearle, Wai Yee Low, Yan Ren, Hanh Thi Hong Nguyen, Niluh Indi Dharmayanti and Farhid Hemmatzadeh
Pathogens 2024, 13(8), 638; https://doi.org/10.3390/pathogens13080638 - 30 Jul 2024
Viewed by 1520
Abstract
Newcastle Disease Virus (NDV) genotype VII (GVII) is becoming the predominant strain of NDV in the poultry industry. It causes high mortality even in vaccinated chickens with a common NDV genotype II vaccine (GII-vacc). To overcome this, the killed GVII vaccine has been [...] Read more.
Newcastle Disease Virus (NDV) genotype VII (GVII) is becoming the predominant strain of NDV in the poultry industry. It causes high mortality even in vaccinated chickens with a common NDV genotype II vaccine (GII-vacc). To overcome this, the killed GVII vaccine has been used to prevent NDV outbreaks. However, the debate about vaccine differences remains ongoing. Hence, this study investigated the difference in chickens’ responses to the two vaccines at the molecular level. The spleen transcriptomes from vaccinated chickens reveal that GVII-vacc affected the immune response by downregulating neuroinflammation. It also enhanced a synaptogenesis pathway that operates typically in the nervous system, suggesting a mechanism for the neurotrophic effect of this strain. We speculated that the down-regulated immune system regulation correlated with protecting the nervous system from excess leukocytes and cytokine activity. In contrast, GII-vacc inhibited apoptosis by downregulating PERK/ATF4/CHOP as part of the unfolded protein response pathway but did not affect the expression of the same synaptogenesis pathway. Thus, the application of GVII-vacc needs to be considered in countries where GVII is the leading cause of NDV outbreaks. The predicted molecular signatures may also be used in developing new vaccines that trigger specific genes in the immune system in combating NDV outbreaks. Full article
(This article belongs to the Special Issue Host Immune Responses to RNA Viruses, 2nd Edition)
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14 pages, 3225 KiB  
Article
Newcastle Disease Virus Induces Profound Lymphoid Depletion with Different Patterns of Necroptosis, Necrosis, and Oxidative DNA Damage in Bursa, Spleen, and Other Lymphoid Tissues
by Mohammad Rabiei, Milton M. McAllister, Natalie R. Gassman, Kevin J. Lee, Sydney Acton, Dieter Liebhart, Wai Yee Low and Farhid Hemmatzadeh
Pathogens 2024, 13(8), 619; https://doi.org/10.3390/pathogens13080619 - 26 Jul 2024
Viewed by 1490
Abstract
This study delves into the pathogenesis of virulent genotype VII strains of the Newcastle disease virus (NDV), focusing on experimentally infected birds. Predominant and consistent lesions observed include bursal atrophy and extensive depletion of all lymphoid tissues. Immunohistochemistry (IHC) analysis, targeting apoptosis (Caspase-3), [...] Read more.
This study delves into the pathogenesis of virulent genotype VII strains of the Newcastle disease virus (NDV), focusing on experimentally infected birds. Predominant and consistent lesions observed include bursal atrophy and extensive depletion of all lymphoid tissues. Immunohistochemistry (IHC) analysis, targeting apoptosis (Caspase-3), necroptosis (MLKL), and NDV markers, indicates that bursal atrophy is linked to a non-apoptotic programmed cell death pathway known as “necroptosis”. Repair assisted damage detection (RADD) of the bursa reveal oxidative DNA damage patterns consistent with programmed cell death, aligning with MLKL expression. Contrastingly, in the spleen, our findings suggest that necrosis (non-programmed cell death) predominantly contributes to lymphoid depletion. This conclusion is supported by evidence of karyorrhexis, fibrinous inflammation, RADD analyses, and IHC. Moreover, in addition to being pathogenic in its own right, NDV caused extensive and rapid lymphoid depletion that should be expected to contribute to profound immunosuppression. The elucidation of necroptosis in NDV-infected chickens provides a good rationale to investigate this mechanism in other paramyxoviral diseases such as human measles. Full article
(This article belongs to the Special Issue Host Immune Responses to RNA Viruses, 2nd Edition)
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12 pages, 1621 KiB  
Article
Comparative Study of T-Cell Repertoires after COVID-19 Immunization with Homologous or Heterologous Vaccine Booster
by Elizabeth-Barbara Tatsi, Filippos Filippatos, Thomas Bello, Vasiliki Syriopoulou and Athanasios Michos
Pathogens 2024, 13(4), 284; https://doi.org/10.3390/pathogens13040284 - 27 Mar 2024
Viewed by 1982
Abstract
Sequencing of the T-cell repertoire is an innovative method to assess the cellular responses after immunization. The purpose of this study was to compare T-cell repertoires after COVID-19 immunization with homologous (HOB) and heterologous (HEB) boosting. The study included 20 participants with a [...] Read more.
Sequencing of the T-cell repertoire is an innovative method to assess the cellular responses after immunization. The purpose of this study was to compare T-cell repertoires after COVID-19 immunization with homologous (HOB) and heterologous (HEB) boosting. The study included 20 participants with a median age of 27.5 (IQR:23) years, who were vaccinated with one dose of the Ad26.COV2.S vaccine and were boosted with either Ad26.COV2.S (n = 10) or BNT162b2 (n = 10) vaccine. Analysis of the T-cell receptor beta locus (TCRβ) sequencing one month after the booster dose identified that the HEB compared to the HOB group exhibited a higher number of both total and COVID-19-related functional T-cell rearrangements [mean of total productive rearrangements (TPRs): 63151.8 (SD ± 18441.5) vs. 34915.4 (SD ± 11121.6), p = 0.001 and COVID-19–TPRs: 522.5 (SD ± 178.0) vs. 298.3 (SD ± 101.1), p = 0.003]. A comparison between the HOB and HEB groups detected no statistically significant differences regarding T-cell Simpson clonality [0.021 (IQR:0.014) vs. 0.019 (IQR:0.007)], richness [8734.5 (IQR:973.3) vs. 8724 (IQR:383.7)] and T-cell fraction [0.19 (IQR:0.08) vs. 0.18 (IQR:0.08)]. HEB also exhibited a substantially elevated humoral immune response one month after the booster dose compared to HOB [median antibody titer (IQR): 10115.0 U/mL (6993.0) vs. 1781.0 U/mL (1314.0), p = 0.001]. T-cell repertoire sequencing indicated that HEB had increased SARS-CoV-2-related T-cell rearrangements, which was in accordance with higher humoral responses and possibly conferring longer protection. Data from the present study indicate that the administration of different COVID-19 vaccines as a booster may provide better protection. Full article
(This article belongs to the Special Issue Host Immune Responses to RNA Viruses, 2nd Edition)
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Review

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31 pages, 4696 KiB  
Review
Host Innate Antiviral Response to Influenza A Virus Infection: From Viral Sensing to Antagonism and Escape
by Wenlong An, Simran Lakhina, Jessica Leong, Kartik Rawat and Matloob Husain
Pathogens 2024, 13(7), 561; https://doi.org/10.3390/pathogens13070561 - 3 Jul 2024
Cited by 6 | Viewed by 5591
Abstract
Influenza virus possesses an RNA genome of single-stranded, negative-sensed, and segmented configuration. Influenza virus causes an acute respiratory disease, commonly known as the “flu” in humans. In some individuals, flu can lead to pneumonia and acute respiratory distress syndrome. Influenza A virus (IAV) [...] Read more.
Influenza virus possesses an RNA genome of single-stranded, negative-sensed, and segmented configuration. Influenza virus causes an acute respiratory disease, commonly known as the “flu” in humans. In some individuals, flu can lead to pneumonia and acute respiratory distress syndrome. Influenza A virus (IAV) is the most significant because it causes recurring seasonal epidemics, occasional pandemics, and zoonotic outbreaks in human populations, globally. The host innate immune response to IAV infection plays a critical role in sensing, preventing, and clearing the infection as well as in flu disease pathology. Host cells sense IAV infection through multiple receptors and mechanisms, which culminate in the induction of a concerted innate antiviral response and the creation of an antiviral state, which inhibits and clears the infection from host cells. However, IAV antagonizes and escapes many steps of the innate antiviral response by different mechanisms. Herein, we review those host and viral mechanisms. This review covers most aspects of the host innate immune response, i.e., (1) the sensing of incoming virus particles, (2) the activation of downstream innate antiviral signaling pathways, (3) the expression of interferon-stimulated genes, (4) and viral antagonism and escape. Full article
(This article belongs to the Special Issue Host Immune Responses to RNA Viruses, 2nd Edition)
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20 pages, 391 KiB  
Review
Biomarkers in Detection of Hepatitis C Virus Infection
by Jungreem Woo and Youkyung Choi
Pathogens 2024, 13(4), 331; https://doi.org/10.3390/pathogens13040331 - 17 Apr 2024
Cited by 4 | Viewed by 4442
Abstract
The hepatitis C virus (HCV) infection affects 58 million people worldwide. In the United States, the incidence rate of acute hepatitis C has doubled since 2014; during 2021, this increased to 5% from 2020. Acute hepatitis C is defined by any symptom of [...] Read more.
The hepatitis C virus (HCV) infection affects 58 million people worldwide. In the United States, the incidence rate of acute hepatitis C has doubled since 2014; during 2021, this increased to 5% from 2020. Acute hepatitis C is defined by any symptom of acute viral hepatitis plus either jaundice or elevated serum alanine aminotransferase (ALT) activity with the detection of HCV RNA, the anti-HCV antibody, or hepatitis C virus antigen(s). However, most patients with acute infection are asymptomatic. In addition, ALT activity and HCV RNA levels can fluctuate, and a delayed detection of the anti-HCV antibody can occur among some immunocompromised persons with HCV infection. The detection of specific biomarkers can be of great value in the early detection of HCV infection at an asymptomatic stage. The high rate of HCV replication (which is approximately 1010 to 1012 virions per day) and the lack of proofreading by the viral RNA polymerase leads to enormous genetic diversity, creating a major challenge for the host immune response. This broad genetic diversity contributes to the likelihood of developing chronic infection, thus leading to the development of cirrhosis and liver cancer. Direct-acting antiviral (DAA) therapies for HCV infection are highly effective with a cure rate of up to 99%. At the same time, many patients with HCV infection are unaware of their infection status because of the mostly asymptomatic nature of hepatitis C, so they remain undiagnosed until the liver damage has advanced. Molecular mechanisms induced by HCV have been intensely investigated to find biomarkers for diagnosing the acute and chronic phases of the infection. However, there are no clinically verified biomarkers for patients with hepatitis C. In this review, we discuss the biomarkers that can differentiate acute from chronic hepatitis C, and we summarize the current state of the literature on the useful biomarkers that are detectable during acute and chronic HCV infection, liver fibrosis/cirrhosis, and hepatocellular carcinoma (HCC). Full article
(This article belongs to the Special Issue Host Immune Responses to RNA Viruses, 2nd Edition)
21 pages, 1419 KiB  
Review
Zika Virus—A Reemerging Neurotropic Arbovirus Associated with Adverse Pregnancy Outcomes and Neuropathogenesis
by Kenneth C. Elliott and Joseph J. Mattapallil
Pathogens 2024, 13(2), 177; https://doi.org/10.3390/pathogens13020177 - 15 Feb 2024
Cited by 4 | Viewed by 3566
Abstract
Zika virus (ZIKV) is a reemerging flavivirus that is primarily spread through bites from infected mosquitos. It was first discovered in 1947 in sentinel monkeys in Uganda and has since been the cause of several outbreaks, primarily in tropical and subtropical areas. Unlike [...] Read more.
Zika virus (ZIKV) is a reemerging flavivirus that is primarily spread through bites from infected mosquitos. It was first discovered in 1947 in sentinel monkeys in Uganda and has since been the cause of several outbreaks, primarily in tropical and subtropical areas. Unlike earlier outbreaks, the 2015–2016 epidemic in Brazil was characterized by the emergence of neurovirulent strains of ZIKV strains that could be sexually and perinatally transmitted, leading to the Congenital Zika Syndrome (CZS) in newborns, and Guillain-Barre Syndrome (GBS) along with encephalitis and meningitis in adults. The immune response elicited by ZIKV infection is highly effective and characterized by the induction of both ZIKV-specific neutralizing antibodies and robust effector CD8+ T cell responses. However, the structural similarities between ZIKV and Dengue virus (DENV) lead to the induction of cross-reactive immune responses that could potentially enhance subsequent DENV infection, which imposes a constraint on the development of a highly efficacious ZIKV vaccine. The isolation and characterization of antibodies capable of cross-neutralizing both ZIKV and DENV along with cross-reactive CD8+ T cell responses suggest that vaccine immunogens can be designed to overcome these constraints. Here we review the structural characteristics of ZIKV along with the evidence of neuropathogenesis associated with ZIKV infection and the complex nature of the immune response that is elicited by ZIKV infection. Full article
(This article belongs to the Special Issue Host Immune Responses to RNA Viruses, 2nd Edition)
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30 pages, 2092 KiB  
Review
G-Quadruplexes in the Regulation of Viral Gene Expressions and Their Impacts on Controlling Infection
by Andrew R. Zareie, Prerna Dabral and Subhash C. Verma
Pathogens 2024, 13(1), 60; https://doi.org/10.3390/pathogens13010060 - 8 Jan 2024
Cited by 6 | Viewed by 3702
Abstract
G-quadruplexes (G4s) are noncanonical nucleic acid structures that play significant roles in regulating various biological processes, including replication, transcription, translation, and recombination. Recent studies have identified G4s in the genomes of several viruses, such as herpes viruses, hepatitis viruses, and human coronaviruses. These [...] Read more.
G-quadruplexes (G4s) are noncanonical nucleic acid structures that play significant roles in regulating various biological processes, including replication, transcription, translation, and recombination. Recent studies have identified G4s in the genomes of several viruses, such as herpes viruses, hepatitis viruses, and human coronaviruses. These structures are implicated in regulating viral transcription, replication, and virion production, influencing viral infectivity and pathogenesis. G4-stabilizing ligands, like TMPyP4, PhenDC3, and BRACO19, show potential antiviral properties by targeting and stabilizing G4 structures, inhibiting essential viral life-cycle processes. This review delves into the existing literature on G4’s involvement in viral regulation, emphasizing specific G4-stabilizing ligands. While progress has been made in understanding how these ligands regulate viruses, further research is needed to elucidate the mechanisms through which G4s impact viral processes. More research is necessary to develop G4-stabilizing ligands as novel antiviral agents. The increasing body of literature underscores the importance of G4s in viral biology and the development of innovative therapeutic strategies against viral infections. Despite some ligands’ known regulatory effects on viruses, a deeper comprehension of the multifaceted impact of G4s on viral processes is essential. This review advocates for intensified research to unravel the intricate relationship between G4s and viral processes, paving the way for novel antiviral treatments. Full article
(This article belongs to the Special Issue Host Immune Responses to RNA Viruses, 2nd Edition)
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