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Viral Infection and Immunogenetics
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Viral Infection and Immunogenetics

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (20 June 2023) | Viewed by 3764

Special Issue Editor

Dr. Candice Brinkmeyer-Langford

E-Mail Website
Guest Editor
Department of Veterinary Integrative Biosciences, School of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843, USA
Interests: genetics/genomics; roles of genetic diversity in neurodegenerative diseases; gene x environment interactions in diseases; virus-induced neurological conditions
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Viral infections provoke immune responses that are coordinated, in part, by the genetic background of the infected host. The effectiveness of different immune responses is influenced by the myriad of genes and proteins involved, as well as the functional elements responsible for modulating their expression. Viruses themselves can impact the effectiveness of the immune response, in some cases by hijacking the defense mechanisms of the host. Genetic diversity, therefore, is key to the differences in the abilities of hosts to defend against viral infections and to protect themselves from potential adverse consequences, such as autoimmunity.

The prime goal of this Special Issue, to be published in the International Journal of Molecular Sciences, is to highlight novel research elucidating the complex immune interactions associated with viral infections. Basic, translational, and computational research studies, as well as studies using new, paradigm-shifting methods, are encouraged.

Dr. Candice Brinkmeyer-Langford
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • genetic diversity
  • immune response
  • viral infection
  • gene expression
  • protein expression
  • immune evasion
  • autoimmunity
  • cytotoxicity
  • major histocompatibility complex (MHC)
  • inflammation
  • innate immunity
  • viral antigens

Published Papers (2 papers)

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Research

16 pages, 1740 KiB  
Article
Baseline Gait and Motor Function Predict Long-Term Severity of Neurological Outcomes of Viral Infection
by Moumita Karmakar, Aracely A. Pérez Gómez, Raymond J. Carroll, Koedi S. Lawley, Katia A. Z. Amstalden, C. Jane Welsh, David W. Threadgill and Candice Brinkmeyer-Langford
Int. J. Mol. Sci. 2023, 24(3), 2843; https://doi.org/10.3390/ijms24032843 - 02 Feb 2023
Viewed by 1563
Abstract
Neurological dysfunction following viral infection varies among individuals, largely due to differences in their genetic backgrounds. Gait patterns, which can be evaluated using measures of coordination, balance, posture, muscle function, step-to-step variability, and other factors, are also influenced by genetic background. Accordingly, to [...] Read more.
Neurological dysfunction following viral infection varies among individuals, largely due to differences in their genetic backgrounds. Gait patterns, which can be evaluated using measures of coordination, balance, posture, muscle function, step-to-step variability, and other factors, are also influenced by genetic background. Accordingly, to some extent gait can be characteristic of an individual, even prior to changes in neurological function. Because neuromuscular aspects of gait are under a certain degree of genetic control, the hypothesis tested was that gait parameters could be predictive of neuromuscular dysfunction following viral infection. The Collaborative Cross (CC) mouse resource was utilized to model genetically diverse populations and the DigiGait treadmill system used to provide quantitative and objective measurements of 131 gait parameters in 142 mice from 23 CC and SJL/J strains. DigiGait measurements were taken prior to infection with the neurotropic virus Theiler’s Murine Encephalomyelitis Virus (TMEV). Neurological phenotypes were recorded over 90 days post-infection (d.p.i.), and the cumulative frequency of the observation of these phenotypes was statistically associated with discrete baseline DigiGait measurements. These associations represented spatial and postural aspects of gait influenced by the 90 d.p.i. phenotype score. Furthermore, associations were found between these gait parameters with sex and outcomes considered to show resistance, resilience, or susceptibility to severe neurological symptoms after long-term infection. For example, higher pre-infection measurement values for the Paw Drag parameter corresponded with greater disease severity at 90 d.p.i. Quantitative trait loci significantly associated with these DigiGait parameters revealed potential relationships between 28 differentially expressed genes (DEGs) and different aspects of gait influenced by viral infection. Thus, these potential candidate genes and genetic variations may be predictive of long-term neurological dysfunction. Overall, these findings demonstrate the predictive/prognostic value of quantitative and objective pre-infection DigiGait measurements for viral-induced neuromuscular dysfunction. Full article
(This article belongs to the Special Issue Viral Infection and Immunogenetics)
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13 pages, 1199 KiB  
Article
Activation of Early Proinflammatory Responses by TBEV NS1 Varies between the Strains of Various Subtypes
by Elizaveta Starodubova, Ksenia Tuchynskaya, Yulia Kuzmenko, Anastasia Latanova, Vera Tutyaeva, Vadim Karpov and Galina Karganova
Int. J. Mol. Sci. 2023, 24(2), 1011; https://doi.org/10.3390/ijms24021011 - 05 Jan 2023
Viewed by 1565
Abstract
Tick-borne encephalitis (TBE) is an emerging zoonosis that may cause long-term neurological sequelae or even death. Thus, there is a growing interest in understanding the factors of TBE pathogenesis. Viral genetic determinants may greatly affect the severity and consequences of TBE. In this [...] Read more.
Tick-borne encephalitis (TBE) is an emerging zoonosis that may cause long-term neurological sequelae or even death. Thus, there is a growing interest in understanding the factors of TBE pathogenesis. Viral genetic determinants may greatly affect the severity and consequences of TBE. In this study, nonstructural protein 1 (NS1) of the tick-borne encephalitis virus (TBEV) was tested as such a determinant. NS1s of three strains with similar neuroinvasiveness belonging to the European, Siberian and Far-Eastern subtypes of TBEV were studied. Transfection of mouse cells with plasmids encoding NS1 of the three TBEV subtypes led to different levels of NS1 protein accumulation in and secretion from the cells. NS1s of TBEV were able to trigger cytokine production either in isolated mouse splenocytes or in mice after delivery of NS1 encoding plasmids. The profile and dynamics of TNF-α, IL-6, IL-10 and IFN-γ differed between the strains. These results demonstrated the involvement of TBEV NS1 in triggering an immune response and indicated the diversity of NS1 as one of the genetic factors of TBEV pathogenicity. Full article
(This article belongs to the Special Issue Viral Infection and Immunogenetics)
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