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Special Issue "Host Responses to Viral Infection"

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A special issue of Vaccines (ISSN 2076-393X).

Deadline for manuscript submissions: closed (30 June 2017) | Viewed by 44882

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Special Issue Editors

Dr. Angela L. Rasmussen

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Guest Editor

Center for Global Health Science and Security, Washington, DC 20057, USA
Interests: host response to infection; virus–host interactions; mechanisms of pathogenesis; experimental model development for highly pathogenic viruses
Special Issues, Collections and Topics in MDPI journals

Dr. Juliet Morrison

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Guest Editor

Center for Infection and Immunity, Columbia University, Mailman School of Public Health, New York, NY 10032, USA
Interests: flaviviruses; influenza; RNA viruses; host responses; transcriptomics; tissue deconvolution; prognostic signatures
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue of Vaccines focuses on the many roles of host factors in virus infection and pathogenesis. Viral infection induces vigorous host responses at the genetic, cellular, and organismal levels, which can be hijacked by the virus to facilitate replication or evade antiviral immune responses. Furthermore, although host responses are thought to promote virus clearance, in some cases, unregulated antiviral or inflammatory responses can themselves exacerbate or cause pathology. Recent technological advances in genomic, transcriptomic, proteomic, and metabolomic methods and analyses have dramatically advanced our understanding of the complex, multi-faceted interactions between host and virus that drive infection, pathogenesis, disease outcome, and both long- and short-term immunity. In addition, new models and larger population studies have demonstrated that host susceptibility and functional responses to infection, treatment, or immunization can be very individualized. Thus, developing more effective, personalized means of treating viral pathogens may indicate a precision medicine approach. The contributions included in this Special Issue will review current efforts to elucidate the many ways in which host responses shape virus infection and pathogenesis.

Dr. Angela L. Rasmussen
Dr. Juliet Morrison
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. Vaccines 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

host factors
host responses
omics
virus
host-virus interactions
viral replication
antiviral immunity

Published Papers (6 papers)

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Research

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Open AccessArticle

The Central Conserved Region (CCR) of Respiratory Syncytial Virus (RSV) G Protein Modulates Host miRNA Expression and Alters the Cellular Response to Infection

and

Vaccines 2017, 5(3), 16; https://doi.org/10.3390/vaccines5030016 - 03 Jul 2017

Cited by 22 | Viewed by 4921

Abstract

Respiratory Syncytial Virus (RSV) infects respiratory epithelial cells and deregulates host gene expression by many mechanisms including expression of RSV G protein (RSV G). RSV G protein encodes a central conserved region (CCR) containing a CX3C motif that functions as a fractalkine mimic. Disruption of the CX3C motif (a.a. 182–186) located in the CCR of the G protein has been shown to affect G protein function in vitro and the severity of RSV disease pathogenesis in vivo. We show that infection of polarized Calu3 respiratory cells with recombinant RSV having point mutations in Cys173 and 176 (C173/176S) (rA2-GC12), or Cys186 (C186S) (rA2-GC4) is associated with a decline in the integrity of polarized Calu-3 cultures and decreased virus production. This is accompanied with downregulation of miRNAs let-7f and miR-24 and upregulation of interferon lambda (IFNλ), a primary antiviral cytokine for RSV in rA2-GC12/rA2-GC4 infected cells. These results suggest that residues in the cysteine noose region of RSV G protein can modulate IFN λ expression accompanied by downregulation of miRNAs, and are important for RSV G protein function and targeting. Full article

(This article belongs to the Special Issue Host Responses to Viral Infection)

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Review

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Open AccessReview

Impact of the Respiratory Microbiome on Host Responses to Respiratory Viral Infection

Maxime Pichon

Bruno Lina

and

Laurence Josset

Vaccines 2017, 5(4), 40; https://doi.org/10.3390/vaccines5040040 - 03 Nov 2017

Cited by 23 | Viewed by 5085

Abstract

Viruses are responsible for most of both upper and lower acute respiratory infections (ARIs). The microbiome—the ecological community of microorganisms sharing the body space, which has gained considerable interest over the last decade—is modified in health and disease states. Even if most of these disturbances have been previously described in relation to chronic disorders of the gastrointestinal microbiome, after a short reminder of microbiome characteristics and methods of characterization, this review will describe the impact of the microbiome (mainly respiratory) on host responses to viral ARIs. The microbiome has a direct environmental impact on the host cells but also an indirect impact on the immune system, by enhancing innate or adaptive immune responses. In microbial infections, especially in viral infections, these dramatic modifications could lead to a dramatic impact responsible for severe clinical outcomes. Studies focusing on the microbiome associated with transcriptomic analyses of the host response and deep characterization of the pathogen would lead to a better understanding of viral pathogenesis and open avenues for biomarker development and innovative therapeutics. Full article

(This article belongs to the Special Issue Host Responses to Viral Infection)

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Open AccessReview

Elucidating the Role of Host Long Non-Coding RNA during Viral Infection: Challenges and Paths Forward

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Vaccines 2017, 5(4), 37; https://doi.org/10.3390/vaccines5040037 - 20 Oct 2017

Cited by 9 | Viewed by 4845

Abstract

Research over the past decade has clearly shown that long non-coding RNAs (lncRNAs) are functional. Many lncRNAs can be related to immunity and the host response to viral infection, but their specific functions remain largely elusive. The vast majority of lncRNAs are annotated with extremely limited knowledge and tend to be expressed at low levels, making ad hoc experimentation difficult. Changes to lncRNA expression during infection can be systematically profiled using deep sequencing; however, this often produces an intractable number of candidate lncRNAs, leaving no clear path forward. For these reasons, it is especially important to prioritize lncRNAs into high-confidence “hits” by utilizing multiple methodologies. Large scale perturbation studies may be used to screen lncRNAs involved in phenotypes of interest, such as resistance to viral infection. Single cell transcriptome sequencing quantifies cell-type specific lncRNAs that are less abundant in a mixture. When coupled with iterative experimental validations, new computational strategies for efficiently integrating orthogonal high-throughput data will likely be the driver for elucidating the functional role of lncRNAs during viral infection. This review highlights new high-throughput technologies and discusses the potential for integrative computational analysis to streamline the identification of infection-related lncRNAs and unveil novel targets for antiviral therapeutics. Full article

(This article belongs to the Special Issue Host Responses to Viral Infection)

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Open AccessReview

Host Transcriptional Response to Ebola Virus Infection

Emily Speranza

and

John H Connor

Vaccines 2017, 5(3), 30; https://doi.org/10.3390/vaccines5030030 - 20 Sep 2017

Cited by 15 | Viewed by 6594

Abstract

Ebola virus disease (EVD) is a serious illness that causes severe disease in humans and non-human primates (NHPs) and has mortality rates up to 90%. EVD is caused by the Ebolavirus and currently there are no licensed therapeutics or vaccines to treat EVD. Due to its high mortality rates and potential as a bioterrorist weapon, a better understanding of the disease is of high priority. Multiparametric analysis techniques allow for a more complete understanding of a disease and the host response. Analysis of RNA species present in a sample can lead to a greater understanding of activation or suppression of different states of the immune response. Transcriptomic analyses such as microarrays and RNA-Sequencing (RNA-Seq) have been important tools to better understand the global gene expression response to EVD. In this review, we outline the current knowledge gained by transcriptomic analysis of EVD. Full article

(This article belongs to the Special Issue Host Responses to Viral Infection)

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Open AccessReview

Immune Evasion Strategies during Chronic Hepatitis B and C Virus Infection

Ana Maria Ortega-Prieto

and

Marcus Dorner

Vaccines 2017, 5(3), 24; https://doi.org/10.3390/vaccines5030024 - 01 Sep 2017

Cited by 45 | Viewed by 10941

Abstract

Both hepatitis B virus (HBV) and hepatitis C virus (HCV) infections are a major global healthcare problem with more than 240 million and 70 million infected, respectively. Both viruses persist within the liver and result in progressive liver disease, resulting in liver fibrosis, cirrhosis and hepatocellular carcinoma. Strikingly, this pathogenesis is largely driven by immune responses, unable to clear an established infection, rather than by the viral pathogens themselves. Even though disease progression is very similar in both infections, HBV and HCV have evolved distinct mechanisms, by which they ensure persistence within the host. Whereas HCV utilizes a cloak-and-dagger approach, disguising itself as a lipid-like particle and immediately crippling essential pattern-recognition pathways, HBV has long been considered a “stealth” virus, due to the complete absence of innate immune responses during infection. Recent developments and access to improved model systems, however, revealed that even though it is among the smallest human-tropic viruses, HBV may, in addition to evading host responses, employ subtle immune evasion mechanisms directed at ensuring viral persistence in the absence of host responses. In this review, we compare the different strategies of both viruses to ensure viral persistence by actively interfering with viral recognition and innate immune responses. Full article

(This article belongs to the Special Issue Host Responses to Viral Infection)

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Open AccessReview

The TRIMendous Role of TRIMs in Virus–Host Interactions

and

Vaccines 2017, 5(3), 23; https://doi.org/10.3390/vaccines5030023 - 22 Aug 2017

Cited by 89 | Viewed by 11893

Abstract

The innate antiviral response is integral in protecting the host against virus infection. Many proteins regulate these signaling pathways including ubiquitin enzymes. The ubiquitin-activating (E1), -conjugating (E2), and -ligating (E3) enzymes work together to link ubiquitin, a small protein, onto other ubiquitin molecules or target proteins to mediate various effector functions. The tripartite motif (TRIM) protein family is a group of E3 ligases implicated in the regulation of a variety of cellular functions including cell cycle progression, autophagy, and innate immunity. Many antiviral signaling pathways, including type-I interferon and NF-κB, are TRIM-regulated, thus influencing the course of infection. Additionally, several TRIMs directly restrict viral replication either through proteasome-mediated degradation of viral proteins or by interfering with different steps of the viral replication cycle. In addition, new studies suggest that TRIMs can exert their effector functions via the synthesis of unconventional polyubiquitin chains, including unanchored (non-covalently attached) polyubiquitin chains. TRIM-conferred viral inhibition has selected for viruses that encode direct and indirect TRIM antagonists. Furthermore, new evidence suggests that the same antagonists encoded by viruses may hijack TRIM proteins to directly promote virus replication. Here, we describe numerous virus–TRIM interactions and novel roles of TRIMs during virus infections. Full article

(This article belongs to the Special Issue Host Responses to Viral Infection)

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