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Viruses
Special Issues
Viral Evasion or Suppression of Host Immunity
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Viral Evasion or Suppression of Host Immunity

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 (1 March 2020) | Viewed by 52069

Special Issue Editor

Dr. Bumsuk Hahm

E-Mail Website
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

Special Issue Information

Dear Colleagues,

Virologists have been continuously discovering novel mechanisms for virus–host immune interactions. Notably, highly pathogenic viruses pose tremendous challenges to the ideal operation of the host immune system. Thus, it is conceptualized that viruses evolved through frequent mutations to survive in hosts or devised meticulous strategies to suppress host immunity. The brawl between viruses and host immunity is exemplified by seminal findings such as T cell exhaustion caused by chronic virus infections and viral evasion of the formidable interferon response.

In this Special Issue, emphasis will be placed on the recent scientific development of viral tactics to escape or counterattack host innate or adaptive immune responses following infection. This research will increase our understanding of the hostile dialogue between virus and host defense, potentially providing a means to develop intelligent and effective immune therapeutics against viral infections. You are cordially invited to contribute unique research or review articles on this theme or related research topics, which will ultimately improve science and public health.

Dr. Bumsuk Hahm
Guest Editor

Manuscript Submission Information

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Keywords

  • Viral immunity
  • Viral pathogenicity
  • Host defense
  • Innate immunity
  • Adaptive immunity
  • Immune evasion
  • Immune suppression

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Published Papers (12 papers)

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Editorial

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2 pages, 149 KiB  
Editorial
Special Issue “Viral Evasion or Suppression of Host Immunity”
by Bumsuk Hahm
Viruses 2020, 12(6), 656; https://doi.org/10.3390/v12060656 - 18 Jun 2020
Viewed by 1731
Abstract
Viruses have evolved to survive in hosts, presumably by devising meticulous strategies to elude or suppress host immunity [...] Full article
(This article belongs to the Special Issue Viral Evasion or Suppression of Host Immunity)

Research

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13 pages, 970 KiB  
Article
n-3 Polyunsaturated Fatty Acids Impede the TCR Mobility and the TCR–pMHC Interaction of Anti-Viral CD8+ T Cells
by Younghyun Lim, Seyoung Kim, Sehoon Kim, Dong-In Kim, Kyung Won Kang, So-Hee Hong, Sang-Myeong Lee, Hye Ran Koh and Young-Jin Seo
Viruses 2020, 12(6), 639; https://doi.org/10.3390/v12060639 - 12 Jun 2020
Cited by 2 | Viewed by 2370
Abstract
The immune-suppressive effects of omega-3 (n-3) polyunsaturated fatty acids (PUFAs) on T cells have been observed via multiple in vitro and in vivo models. However, the precise mechanism that causes these effects is still undefined. In this study, we investigated whether [...] Read more.
The immune-suppressive effects of omega-3 (n-3) polyunsaturated fatty acids (PUFAs) on T cells have been observed via multiple in vitro and in vivo models. However, the precise mechanism that causes these effects is still undefined. In this study, we investigated whether n-3 PUFAs regulated T cell receptor (TCR) and peptide-major histocompatibility complex (pMHC) interactions. The expansion of anti-viral CD8+ T cells that endogenously synthesize n-3 PUFAs (FAT-1) dramatically decreased upon lymphocytic choriomeningitis virus (LCMV) infection in vivo. This decrease was not caused by the considerable reduction of TCR expression or the impaired chemotactic activity of T cells. Interestingly, a highly inclined and laminated optical sheet (HILO) microscopic analysis revealed that the TCR motility was notably reduced on the surface of the FAT-1 CD8+ T cells compared to the wild type (WT) CD8+ T cells. Importantly, the adhesion strength of the FAT-1 CD8+ T cells to the peptide-MHC was significantly lower than that of the WT CD8+T cells. Consistent with this result, treatment with docosahexaenoic acid (DHA), one type of n-3 PUFA, significantly decreased CD8+ T cell adhesion to the pMHC. Collectively, our results reveal a novel mechanism through which n-3 PUFAs decrease TCR-pMHC interactions by modulating TCR mobility on CD8+ T cell surfaces. Full article
(This article belongs to the Special Issue Viral Evasion or Suppression of Host Immunity)
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21 pages, 4236 KiB  
Article
Autophagy Induced by Simian Retrovirus Infection Controls Viral Replication and Apoptosis of Jurkat T Lymphocytes
by Jingting Zhu, Lingyan Yang, Qibo Zhang, Jia Meng, Zhi-Liang Lu and Rong Rong
Viruses 2020, 12(4), 381; https://doi.org/10.3390/v12040381 - 31 Mar 2020
Cited by 5 | Viewed by 3685
Abstract
Autophagy and apoptosis are two important evolutionarily conserved host defense mechanisms against viral invasion and pathogenesis. However, the association between the two pathways during the viral infection of T lymphocytes remains to be elucidated. Simian type D retrovirus (SRV) is an etiological agent [...] Read more.
Autophagy and apoptosis are two important evolutionarily conserved host defense mechanisms against viral invasion and pathogenesis. However, the association between the two pathways during the viral infection of T lymphocytes remains to be elucidated. Simian type D retrovirus (SRV) is an etiological agent of fatal simian acquired immunodeficiency syndrome (SAIDS), which can display disease features that are similar to acquired immunodeficiency syndrome in humans. In this study, we demonstrate that infection with SRV-8, a newly isolated subtype of SRV, triggered both autophagic and apoptotic pathways in Jurkat T lymphocytes. Following infection with SRV-8, the autophagic proteins LC3 and p62/SQSTM1 interacted with procaspase-8, which might be responsible for the activation of the caspase-8/-3 cascade and apoptosis in SRV-8-infected Jurkat cells. Our findings indicate that autophagic responses to SRV infection of T lymphocytes promote the apoptosis of T lymphocytes, which, in turn, might be a potential pathogenetic mechanism for the loss of T lymphocytes during SRV infection. Full article
(This article belongs to the Special Issue Viral Evasion or Suppression of Host Immunity)
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10 pages, 1861 KiB  
Article
Molecular Basis of the Ternary Interaction between NS1 of the 1918 Influenza A Virus, PI3K, and CRK
by Alyssa Dubrow, Sirong Lin, Nowlan Savage, Qingliang Shen and Jae-Hyun Cho
Viruses 2020, 12(3), 338; https://doi.org/10.3390/v12030338 - 20 Mar 2020
Cited by 7 | Viewed by 3177
Abstract
The 1918 influenza A virus (IAV) caused the worst flu pandemic in human history. Non-structural protein 1 (NS1) is an important virulence factor of the 1918 IAV and antagonizes host antiviral immune responses. NS1 increases virulence by activating phosphoinositide 3-kinase (PI3K) via binding [...] Read more.
The 1918 influenza A virus (IAV) caused the worst flu pandemic in human history. Non-structural protein 1 (NS1) is an important virulence factor of the 1918 IAV and antagonizes host antiviral immune responses. NS1 increases virulence by activating phosphoinositide 3-kinase (PI3K) via binding to the p85β subunit of PI3K. Intriguingly, unlike the NS1 of other human IAV strains, 1918 NS1 hijacks another host protein, CRK, to form a ternary complex with p85β, resulting in hyperactivation of PI3K. However, the molecular basis of the ternary interaction between 1918 NS1, CRK, and PI3K remains elusive. Here, we report the structural and thermodynamic bases of the ternary interaction. We find that the C-terminal tail (CTT) of 1918 NS1 remains highly flexible in the complex with p85β. Thus, the CTT of 1918 NS1 in the complex with PI3K can efficiently hijack CRK. Notably, our study indicates that 1918 NS1 enhances its affinity to p85β in the presence of CRK, which might result in enhanced activation of PI3K. Our results provide structural insight into how 1918 NS1 hijacks two host proteins simultaneously. Full article
(This article belongs to the Special Issue Viral Evasion or Suppression of Host Immunity)
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14 pages, 1784 KiB  
Article
Development of Antibodies with Broad Neutralization Specificities against HIV-1 after Long Term SHIV Infection in Macaques
by Nan Gao, Yanxin Gai, Lina Meng, Chu Wang, Xin Zhang, Wei Wang, Chuan Qin, Xianghui Yu and Feng Gao
Viruses 2020, 12(2), 163; https://doi.org/10.3390/v12020163 - 31 Jan 2020
Cited by 5 | Viewed by 2975
Abstract
Non-human primates (NHP) are the only animal model suitable to evaluate the protection efficacy of HIV-1 vaccines. It is important to understand how and when neutralizing antibodies (nAbs) with specificities similar to those of human broadly neutralizing antibodies (bnAbs) develop in NHPs. To [...] Read more.
Non-human primates (NHP) are the only animal model suitable to evaluate the protection efficacy of HIV-1 vaccines. It is important to understand how and when neutralizing antibodies (nAbs) with specificities similar to those of human broadly neutralizing antibodies (bnAbs) develop in NHPs. To address these questions, we determined plasma neutralization specificities in two macaques which developed neutralization breadth after long-term simian/human immunodeficiency virus (SHIV) infection and identified neutralization escape mutations by analyzing the env sequences from longitudinal plasma samples. Neutralization activities targeting V2, CD4bs, V3 and gp120-gp41 interface only became detectable in week 350 plasma from macaques G1015R and G1020R using 25710 env mutants. When mapped with CAP45 env mutants, only V2 specificity was detected at week 217 and persisted until week 350 in G1015R. Neutralization escape mutations were found in CD4bs and V2 regions. However, all of them were different from those resistant mutations identified for human bnAbs. These results show that nAbs with specificities similar to human bnAbs are only detectable after long-term SHIV infection and that neutralization escape mutations in macaques are different from those found in HIV-1-infected individuals. These findings can have important implications in the best utilization of the NHP model to evaluate HIV-1 vaccines. Full article
(This article belongs to the Special Issue Viral Evasion or Suppression of Host Immunity)
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13 pages, 2177 KiB  
Article
Pseudorabies Virus UL24 Abrogates Tumor Necrosis Factor Alpha-Induced NF-κB Activation by Degrading P65
by Tong-Yun Wang, Yue-Lin Yang, Cong Feng, Ming-Xia Sun, Jin-Mei Peng, Zhi-Jun Tian, Yan-Dong Tang and Xue-Hui Cai
Viruses 2020, 12(1), 51; https://doi.org/10.3390/v12010051 - 2 Jan 2020
Cited by 28 | Viewed by 3297
Abstract
The transcription factor NF-κB plays a critical role in diverse biological processes. The NF-κB pathway can be activated by incoming pathogens and then stimulates both innate and adaptive immunity. However, many viruses have evolved corresponding strategies to balance NF-κB activation to benefit their [...] Read more.
The transcription factor NF-κB plays a critical role in diverse biological processes. The NF-κB pathway can be activated by incoming pathogens and then stimulates both innate and adaptive immunity. However, many viruses have evolved corresponding strategies to balance NF-κB activation to benefit their replication. Pseudorabies virus (PRV) is an economically important pathogen that belongs to the alphaherpesvirus group. There is little information about PRV infection and NF-κB regulation. This study demonstrates for the first time that the UL24 protein could abrogate tumor necrosis factor alpha (TNF-α)-mediated NF-κB activation. An overexpression assay indicated that UL24 inhibits this pathway at or downstream of P65. Furthermore, co-immunoprecipitation analysis demonstrated that UL24 selectively interacts with P65. We demonstrated that UL24 could significantly degrade P65 by the proteasome pathway. For the first time, PRV UL24 was shown to play an important role in NF-κB evasion during PRV infection. This study expands our understanding that PRV can utilize its encoded protein UL24 to evade NF-κB signaling. Full article
(This article belongs to the Special Issue Viral Evasion or Suppression of Host Immunity)
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19 pages, 2580 KiB  
Article
Bovine Viral Diarrhoea Virus Infection Disrupts Uterine Interferon Stimulated Gene Regulatory Pathways During Pregnancy Recognition in Cows
by Zhangrui Cheng, Laura E Brown and D Claire Wathes
Viruses 2020, 12(1), 1; https://doi.org/10.3390/v12010001 - 18 Dec 2019
Cited by 10 | Viewed by 3554
Abstract
In cattle, conceptus-derived interferon tau (IFNT) is the pregnancy recognition (PR) signal. Our previous studies showed that non-cytopathic bovine viral diarrhoea virus (ncpBVDV) infection inhibited IFNT-induced interferon stimulated gene (ISG) expression, potentially causing early embryonic death. This study investigated the effect of bovine [...] Read more.
In cattle, conceptus-derived interferon tau (IFNT) is the pregnancy recognition (PR) signal. Our previous studies showed that non-cytopathic bovine viral diarrhoea virus (ncpBVDV) infection inhibited IFNT-induced interferon stimulated gene (ISG) expression, potentially causing early embryonic death. This study investigated the effect of bovine viral diarrhoea virus (BVDV) infection on upstream regulatory pathways of ISG production using an established PR model. Uterine endometrial cells from 10 apparently healthy and BVDV free cows were cultured and treated with 0 or 100 ng/mL IFNT for 24 h in the presence or absence of ncpBVDV infection. Microarray and pathway analysis were used to determine the IFNT-induced upstream regulators. Expression of the genes associated with the identified pathways were quantified with qPCR. IFNT challenge activated the signalling pathways associated with IFN receptors, JAK1/TYK2, IRFs and STATs and ncpBVDV infection inhibited the activation of IFNT on this pathway. Inhibition of this upstream signalling pathway may thus reduce ISG production to disrupt maternal PR. In addition, the reduction of uterine immunity by ncpBVDV infection may predispose the animals to uterine infection, which in turn impairs their reproductive performance. This provides a mechanism of how BVDV infection leads to early pregnancy failure in cows. Full article
(This article belongs to the Special Issue Viral Evasion or Suppression of Host Immunity)
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Review

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12 pages, 1919 KiB  
Review
The Viral Macrodomain Counters Host Antiviral ADP-Ribosylation
by Yousef M. O. Alhammad and Anthony R. Fehr
Viruses 2020, 12(4), 384; https://doi.org/10.3390/v12040384 - 31 Mar 2020
Cited by 72 | Viewed by 8946
Abstract
Macrodomains, enzymes that remove ADP-ribose from proteins, are encoded by several families of RNA viruses and have recently been shown to counter innate immune responses to virus infection. ADP-ribose is covalently attached to target proteins by poly-ADP-ribose polymerases (PARPs), using nicotinamide adenine dinucleotide [...] Read more.
Macrodomains, enzymes that remove ADP-ribose from proteins, are encoded by several families of RNA viruses and have recently been shown to counter innate immune responses to virus infection. ADP-ribose is covalently attached to target proteins by poly-ADP-ribose polymerases (PARPs), using nicotinamide adenine dinucleotide (NAD+) as a substrate. This modification can have a wide variety of effects on proteins including alteration of enzyme activity, protein–protein interactions, and protein stability. Several PARPs are induced by interferon (IFN) and are known to have antiviral properties, implicating ADP-ribosylation in the host defense response and suggesting that viral macrodomains may counter this response. Recent studies have demonstrated that viral macrodomains do counter the innate immune response by interfering with PARP-mediated antiviral defenses, stress granule formation, and pro-inflammatory cytokine production. Here, we will describe the known functions of the viral macrodomains and review recent literature demonstrating their roles in countering PARP-mediated antiviral responses. Full article
(This article belongs to the Special Issue Viral Evasion or Suppression of Host Immunity)
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14 pages, 2283 KiB  
Review
The Interactions Between HBV and the Innate Immunity of Hepatocytes
by Fayed Attia Koutb Megahed, Xiaoling Zhou and Pingnan Sun
Viruses 2020, 12(3), 285; https://doi.org/10.3390/v12030285 - 5 Mar 2020
Cited by 61 | Viewed by 5766
Abstract
Hepatitis B virus (HBV) infection affects ~350 million people and poses a major public health problem worldwide. HBV is a major cause of cirrhosis and hepatocellular carcinoma. Fewer than 5% of HBV-infected adults (but up to 90% of HBV-infected infants and children) develop [...] Read more.
Hepatitis B virus (HBV) infection affects ~350 million people and poses a major public health problem worldwide. HBV is a major cause of cirrhosis and hepatocellular carcinoma. Fewer than 5% of HBV-infected adults (but up to 90% of HBV-infected infants and children) develop chronic HBV infection as indicated by continued, detectable expression of hepatitis B surface antigen (HBsAg) for at least 6 months after the initial infection. Increasing evidence indicates that HBV interacts with innate immunity signaling pathways of hepatocytes to suppress innate immunity. However, it is still not clear how HBV avoids monitoring by the innate immunity of hepatocytes and whether the innate immunity of hepatocytes can be effective against HBV if re-triggered. Moreover, a deep understanding of virus–host interactions is important in developing new therapeutic strategies for the treatment of HBV infection. In this review, we summarize the current knowledge regarding how HBV represses innate immune recognition, as well as recent progress with respect to in vitro models for studying HBV infection and innate immunity. Full article
(This article belongs to the Special Issue Viral Evasion or Suppression of Host Immunity)
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14 pages, 834 KiB  
Review
Emerging Connections of S1P-Metabolizing Enzymes with Host Defense and Immunity During Virus Infections
by Jennifer J. Wolf, Caleb J. Studstill and Bumsuk Hahm
Viruses 2019, 11(12), 1097; https://doi.org/10.3390/v11121097 - 27 Nov 2019
Cited by 21 | Viewed by 4139
Abstract
The sphingosine 1-phosphate (S1P) metabolic pathway is a dynamic regulator of multiple cellular and disease processes. Identification of the immune regulatory role of the sphingosine analog FTY720 led to the development of the first oral therapy for the treatment of an autoimmune disease, [...] Read more.
The sphingosine 1-phosphate (S1P) metabolic pathway is a dynamic regulator of multiple cellular and disease processes. Identification of the immune regulatory role of the sphingosine analog FTY720 led to the development of the first oral therapy for the treatment of an autoimmune disease, multiple sclerosis. Furthermore, inhibitors of sphingosine kinase (SphK), which mediate S1P synthesis, are being evaluated as a therapeutic option for the treatment of cancer. In conjunction with these captivating discoveries, S1P and S1P-metabolizing enzymes have been revealed to display vital functions during virus infections. For example, S1P lyase, which is known for metabolizing S1P, inhibits influenza virus replication by promoting antiviral type I interferon innate immune responses. In addition, both isoforms of sphingosine kinase have been shown to regulate the replication or pathogenicity of many viruses. Pro- or antiviral activities of S1P-metabolizing enzymes appear to be dependent on diverse virus–host interactions and viral pathogenesis. This review places an emphasis on summarizing the functions of S1P-metabolizing enzymes during virus infections and discusses the opportunities for designing pioneering antiviral drugs by targeting these host enzymes. Full article
(This article belongs to the Special Issue Viral Evasion or Suppression of Host Immunity)
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10 pages, 228 KiB  
Review
Pathogenesis of Hypervirulent Fowl Adenovirus Serotype 4: The Contributions of Viral and Host Factors
by Zeng Wang and Jun Zhao
Viruses 2019, 11(8), 741; https://doi.org/10.3390/v11080741 - 12 Aug 2019
Cited by 42 | Viewed by 4541
Abstract
Since 2015, severe outbreaks of hepatitis-hydropericardium syndrome (HHS), caused by hypervirulent fowl adenovirus serotype 4 (FAdV-4), have emerged in several provinces in China, posing a great threat to poultry industry. So far, factors contributing to the pathogenesis of hypervirulent FAdV-4 have not been [...] Read more.
Since 2015, severe outbreaks of hepatitis-hydropericardium syndrome (HHS), caused by hypervirulent fowl adenovirus serotype 4 (FAdV-4), have emerged in several provinces in China, posing a great threat to poultry industry. So far, factors contributing to the pathogenesis of hypervirulent FAdV-4 have not been fully uncovered. Elucidation of the pathogenesis of FAdV-4 will facilitate the development of effective FAdV-4 vaccine candidates for the control of HHS and vaccine vector. The interaction between pathogen and host defense system determines the pathogenicity of the pathogen. Therefore, the present review highlights the knowledge of both viral and host factors contributing to the pathogenesis of hypervirulent FAdV-4 strains to facilitate the related further studies. Full article
(This article belongs to the Special Issue Viral Evasion or Suppression of Host Immunity)
14 pages, 535 KiB  
Review
Current Findings on Gut Microbiota Mediated Immune Modulation against Viral Diseases in Chicken
by Muhammad Abaidullah, Shuwei Peng, Muhammad Kamran, Xu Song and Zhongqiong Yin
Viruses 2019, 11(8), 681; https://doi.org/10.3390/v11080681 - 25 Jul 2019
Cited by 36 | Viewed by 6425
Abstract
Chicken gastrointestinal tract is an important site of immune cell development that not only regulates gut microbiota but also maintains extra-intestinal immunity. Recent studies have emphasized the important roles of gut microbiota in shaping immunity against viral diseases in chicken. Microbial diversity and [...] Read more.
Chicken gastrointestinal tract is an important site of immune cell development that not only regulates gut microbiota but also maintains extra-intestinal immunity. Recent studies have emphasized the important roles of gut microbiota in shaping immunity against viral diseases in chicken. Microbial diversity and its integrity are the key elements for deriving immunity against invading viral pathogens. Commensal bacteria provide protection against pathogens through direct competition and by the production of antibodies and activation of different cytokines to modulate innate and adaptive immune responses. There are few economically important viral diseases of chicken that perturb the intestinal microbiota diversity. Disruption of microbial homeostasis (dysbiosis) associates with a variety of pathological states, which facilitate the establishment of acute viral infections in chickens. In this review, we summarize the calibrated interactions among the microbiota mediated immune modulation through the production of different interferons (IFNs) ILs, and virus-specific IgA and IgG, and their impact on the severity of viral infections in chickens. Here, it also shows that acute viral infection diminishes commensal bacteria such as Lactobacillus, Bifidobacterium, Firmicutes, and Blautia spp. populations and enhances the colonization of pathobionts, including E. coli, Shigella, and Clostridial spp., in infected chickens. Full article
(This article belongs to the Special Issue Viral Evasion or Suppression of Host Immunity)
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