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Microorganisms
Special Issues
Innate Immunity to Retroviral Infection
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Innate Immunity to Retroviral Infection

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Medical Microbiology".

Deadline for manuscript submissions: closed (31 October 2020) | Viewed by 18840

Special Issue Editor

Prof. Dr. Masaaki Miyazawa

E-Mail Website
Guest Editor
1. Department of Immunology, Faculty of Medicine, Kindai University, 377-2 Ohno-Higashi, Osakasayama 589-8511, Japan
2. Research and Development Center for Nasal Mucosal Vaccine, Shin Nippon Biomedical Laboratories, Ltd., 2438 Miyanoura, Kagoshima 891-1394, Japan
Interests: host restriction factors; retroviruses; APOBEC3; epitopes; CD4-positive T-lymphocyte; vaccine strategies; resistance to infection; immune regulatory genes; autoimmune diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

To protect their genomes from insistent attacks by retroviruses, mammals have acquired several strategies that restrict the integration of reverse transcribed proviruses. These include intracellular and extracellular factors interacting with viral genomes and intermediates of reverse transcription, viral proteins, or products of cellular responses to infection that jointly impede the process of retroviral replication. These factors may also function as the basis on which acquired immune responses can work more efficiently.

In this Special Issue of Microorganisms, we intend to provide to the wider academic readership updated and integrated views on molecular mechanisms and physiological roles of innate immune responses against retroviral infections. Subjects of discussion will include, but are not limited to, cellular factors that interfere with early processes of retroviral entry, uncoating or intracellular trafficking of preintegration complexes, nucleic acid sensors that detect viral genomes and/or reverse transcribed DNA, APOBEC3 proteins and their viral countermeasures, and target molecules of recognition utilized by natural killer cells and complements. Interactions between innate and acquired immune responses can also be discussed, provided that roles of innate responses are described in more detail.

For this purpose, we cordially invite you to submit comprehensive review papers, research articles, and/or concise commentary papers related to the above subjects. Short articles written by younger colleagues of yours are also welcomed.

We are looking forward to receiving your contributions to this Special Issue soon.

Prof. Dr. Masaaki Miyazawa
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 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. Microorganisms 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 2700 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

  • retroviruses
  • innate immunity
  • host restriction factors
  • intracellular immunity
  • nucleic acid sensors
  • APOBEC3
  • natural killer cells
  • complement
  • resistence to infection

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Published Papers (4 papers)

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Review

23 pages, 936 KiB  
Review
Deaminase-Independent Mode of Antiretroviral Action in Human and Mouse APOBEC3 Proteins
by Yoshiyuki Hakata and Masaaki Miyazawa
Microorganisms 2020, 8(12), 1976; https://doi.org/10.3390/microorganisms8121976 - 12 Dec 2020
Cited by 14 | Viewed by 3555
Abstract
Apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3 (APOBEC3) proteins (APOBEC3s) are deaminases that convert cytosines to uracils predominantly on a single-stranded DNA, and function as intrinsic restriction factors in the innate immune system to suppress replication of viruses (including retroviruses) and movement [...] Read more.
Apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3 (APOBEC3) proteins (APOBEC3s) are deaminases that convert cytosines to uracils predominantly on a single-stranded DNA, and function as intrinsic restriction factors in the innate immune system to suppress replication of viruses (including retroviruses) and movement of retrotransposons. Enzymatic activity is supposed to be essential for the APOBEC3 antiviral function. However, it is not the only way that APOBEC3s exert their biological function. Since the discovery of human APOBEC3G as a restriction factor for HIV-1, the deaminase-independent mode of action has been observed. At present, it is apparent that both the deaminase-dependent and -independent pathways are tightly involved not only in combating viruses but also in human tumorigenesis. Although the deaminase-dependent pathway has been extensively characterized so far, understanding of the deaminase-independent pathway remains immature. Here, we review existing knowledge regarding the deaminase-independent antiretroviral functions of APOBEC3s and their molecular mechanisms. We also discuss the possible unidentified molecular mechanism for the deaminase-independent antiretroviral function mediated by mouse APOBEC3. Full article
(This article belongs to the Special Issue Innate Immunity to Retroviral Infection)
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34 pages, 1670 KiB  
Review
Retroviral Restriction Factors and Their Viral Targets: Restriction Strategies and Evolutionary Adaptations
by Guney Boso and Christine A. Kozak
Microorganisms 2020, 8(12), 1965; https://doi.org/10.3390/microorganisms8121965 - 11 Dec 2020
Cited by 21 | Viewed by 4441
Abstract
The evolutionary conflict between retroviruses and their vertebrate hosts over millions of years has led to the emergence of cellular innate immune proteins termed restriction factors as well as their viral antagonists. Evidence accumulated in the last two decades has substantially increased our [...] Read more.
The evolutionary conflict between retroviruses and their vertebrate hosts over millions of years has led to the emergence of cellular innate immune proteins termed restriction factors as well as their viral antagonists. Evidence accumulated in the last two decades has substantially increased our understanding of the elaborate mechanisms utilized by these restriction factors to inhibit retroviral replication, mechanisms that either directly block viral proteins or interfere with the cellular pathways hijacked by the viruses. Analyses of these complex interactions describe patterns of accelerated evolution for these restriction factors as well as the acquisition and evolution of their virus-encoded antagonists. Evidence is also mounting that many restriction factors identified for their inhibition of specific retroviruses have broader antiviral activity against additional retroviruses as well as against other viruses, and that exposure to these multiple virus challenges has shaped their adaptive evolution. In this review, we provide an overview of the restriction factors that interfere with different steps of the retroviral life cycle, describing their mechanisms of action, adaptive evolution, viral targets and the viral antagonists that evolved to counter these factors. Full article
(This article belongs to the Special Issue Innate Immunity to Retroviral Infection)
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46 pages, 1632 KiB  
Review
The Role of APOBECs in Viral Replication
by Wendy Kaichun Xu, Hyewon Byun and Jaquelin P. Dudley
Microorganisms 2020, 8(12), 1899; https://doi.org/10.3390/microorganisms8121899 - 30 Nov 2020
Cited by 26 | Viewed by 4672
Abstract
Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like (APOBEC) proteins are a diverse and evolutionarily conserved family of cytidine deaminases that provide a variety of functions from tissue-specific gene expression and immunoglobulin diversity to control of viruses and retrotransposons. APOBEC family expansion has been documented [...] Read more.
Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like (APOBEC) proteins are a diverse and evolutionarily conserved family of cytidine deaminases that provide a variety of functions from tissue-specific gene expression and immunoglobulin diversity to control of viruses and retrotransposons. APOBEC family expansion has been documented among mammalian species, suggesting a powerful selection for their activity. Enzymes with a duplicated zinc-binding domain often have catalytically active and inactive domains, yet both have antiviral function. Although APOBEC antiviral function was discovered through hypermutation of HIV-1 genomes lacking an active Vif protein, much evidence indicates that APOBECs also inhibit virus replication through mechanisms other than mutagenesis. Multiple steps of the viral replication cycle may be affected, although nucleic acid replication is a primary target. Packaging of APOBECs into virions was first noted with HIV-1, yet is not a prerequisite for viral inhibition. APOBEC antagonism may occur in viral producer and recipient cells. Signatures of APOBEC activity include G-to-A and C-to-T mutations in a particular sequence context. The importance of APOBEC activity for viral inhibition is reflected in the identification of numerous viral factors, including HIV-1 Vif, which are dedicated to antagonism of these deaminases. Such viral antagonists often are only partially successful, leading to APOBEC selection for viral variants that enhance replication or avoid immune elimination. Full article
(This article belongs to the Special Issue Innate Immunity to Retroviral Infection)
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21 pages, 7884 KiB  
Review
The Role of Toll-Like Receptors in Retroviral Infection
by Edward P. Browne
Microorganisms 2020, 8(11), 1787; https://doi.org/10.3390/microorganisms8111787 - 14 Nov 2020
Cited by 41 | Viewed by 5775
Abstract
Toll-like receptors (TLRs) are key pathogen sensing receptors that respond to diverse microbial ligands, and trigger both innate and adaptive immune responses to infection. Since their discovery, a growing body of evidence has pointed to an important role for TLRs in retroviral infection [...] Read more.
Toll-like receptors (TLRs) are key pathogen sensing receptors that respond to diverse microbial ligands, and trigger both innate and adaptive immune responses to infection. Since their discovery, a growing body of evidence has pointed to an important role for TLRs in retroviral infection and pathogenesis. These data suggest that multiple TLRs contribute to the anti-retroviral response, and that TLR engagement by retroviruses can have complex and divergent outcomes for infection. Despite this progress, numerous questions remain about the role of TLRs in retroviral infection. In this review, I summarize existing evidence for TLR-retrovirus interactions and the functional roles these receptors play in immunity and pathogenesis, with particular focus on human immunodeficiency virus (HIV). Full article
(This article belongs to the Special Issue Innate Immunity to Retroviral Infection)
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