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Innate Immunity and Infectious Diseases
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Innate Immunity and Infectious Diseases

A special issue of Medical Sciences (ISSN 2076-3271). This special issue belongs to the section "Immunology and Infectious Diseases".

Deadline for manuscript submissions: closed (31 May 2015) | Viewed by 17694

Special Issue Editor

Dr. Theresa Chang

E-Mail Website
Guest Editor
Department of Microbiology and Molecular Genetics, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ 07103, USA
Interests: mucosal immunity (female reproductive tracts and GI); host–virus interaction; HIV; herpesvirus; human papillomavirus; Zika virus; SARS-CoV-2
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Innate immunity plays a crucial role in the control of viral infection and pathogenesis. At the infection site, immune cells, in concert with multiple factors, including soluble innate mediators, the extracellular matrix, mucosal microbial compositions, and various cell types, respond to viral invasion, leading to innate immune activation. In addition to its initiation of immune response, innate immunity also modulates the subsequent adaptive immune response. As immune activation contributes to viral pathogenesis and disease progression, understanding the interplay between host innate immune response and viral infection will provide insights into the development of effective strategies for prevention and treatment. Primary research manuscripts or review articles related to various aspects of innate immunity in viral infection are invited for this Special Issue.

Dr. Theresa Li-Yun Chang
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. Medical Sciences is an international peer-reviewed open access quarterly 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 1400 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

  • Innate immunity
  • immune activation
  • mucosal tissues
  • microbiota
  • dendritic cells
  • immune cells
  • antimicrobial peptides
  • immune mediators
  • viral infection
  • viral pathogenesis

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Published Papers (2 papers)

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122 KiB  
Review
Limitations of Current in Vivo Mouse Models for the Study of Chikungunya Virus Pathogenesis
by Yi-Hao Chan, Fok-Moon Lum and Lisa Fong Poh Ng
Med. Sci. 2015, 3(3), 64-77; https://doi.org/10.3390/medsci3030064 - 7 Aug 2015
Cited by 10 | Viewed by 9874
Abstract
Chikungunya virus (CHIKV) is an arthropod-borne alphavirus that causes febrile chikungunya fever (CHIKF) in humans. This disease is debilitating and characterized by acute fever onset and chronic incapacitating polyarthralgia. CHIKF pathogenesis remains poorly defined with no approved vaccines and therapies. Recent outbreaks in [...] Read more.
Chikungunya virus (CHIKV) is an arthropod-borne alphavirus that causes febrile chikungunya fever (CHIKF) in humans. This disease is debilitating and characterized by acute fever onset and chronic incapacitating polyarthralgia. CHIKF pathogenesis remains poorly defined with no approved vaccines and therapies. Recent outbreaks in the Caribbean islands have elevated concerns over the possibility of a global pandemic. Tremendous efforts have been made to develop relevant mouse models to enable the study of infection and immunity against this viral disease. Among them, the more common C57BL/6 mouse model demonstrated the ability to recapitulate the symptoms shown in infected humans, including self-limiting arthritis, myositis, and tenosynovitis. This has facilitated the unraveling of some key factors involved in disease pathogenesis of CHIKF. However, the stark differences in immune response between humans and mouse models necessitate the development of an animal model with an immune system that is more genetically similar to the human system for a better representation. In this paper, we aim to uncover the limitations of the C57BL/6 model and discuss alternative mouse models for CHIKV research. Full article
(This article belongs to the Special Issue Innate Immunity and Infectious Diseases)
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Other

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531 KiB  
Commentary
Nucleic Acid Sensors Involved in the Recognition of HBV in the Liver–Specific in vivo Transfection Mouse Models—Pattern Recognition Receptors and Sensors for HBV
by Chean Ring Leong, Hiroyuki Oshiumi, Takayuki Suzuki, Misako Matsumoto and Tsukasa Seya
Med. Sci. 2015, 3(2), 16-24; https://doi.org/10.3390/medsci3020016 - 15 Apr 2015
Cited by 8 | Viewed by 7226
Abstract
Cellular innate immune system recognizing pathogen infection is critical for the host defense against viruses. Hepatitis B virus (HBV) is a DNA virus with a unique life cycle whereby the DNA and RNA intermediates present at different phases. However, it is still unclear [...] Read more.
Cellular innate immune system recognizing pathogen infection is critical for the host defense against viruses. Hepatitis B virus (HBV) is a DNA virus with a unique life cycle whereby the DNA and RNA intermediates present at different phases. However, it is still unclear whether the viral DNA or RNA templates are recognized by the pattern-recognition receptors (PRRs) to trigger host antiviral immune response. Here in this article, we review the recent advances in the progress of the HBV studies, focusing on the nucleic acid sensors and the pathways involved in the recognition of HBV in the liver–specific in vivo transfection mouse models. Hydrodynamic injection transfecting the hepatocytes in the gene-disrupted mouse model with the HBV replicative genome DNA has revealed that IFNAR and IRF3/7 are indispensable in HBV eradication in the mice liver but not the RNA sensing pathways. Interestingly, accumulating evidence of the recent studies has demonstrated that HBV markedly interfered with IFN-β induction and antiviral immunity mediated by the Stimulator of interferon genes (STING), which has been identified as a central factor in foreign DNA recognition and antiviral innate immunity. This review will present the current understanding of innate immunity in HBV infection and of the challenges for clearing of the HBV infection. Full article
(This article belongs to the Special Issue Innate Immunity and Infectious Diseases)
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