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Pathogens
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Pathogenesis of Viral Diseases
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Pathogenesis of Viral Diseases

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Viral Pathogens".

Deadline for manuscript submissions: closed (31 May 2023) | Viewed by 7567

Special Issue Editor

Dr. Lei Wei

E-Mail Website
Guest Editor
1. Center for Infectious Diseases Research, Westlake University, Hangzhou 310024, Zhejiang, China
2. School of Life Sciences, Westlake University, Hangzhou 310024, Zhejiang, China
3. Westlake Institute for Advanced Study, Hangzhou 310024, Zhejiang, China
Interests: virus–host interaction; hepatitis B virus; mechanism of viral replication; anti-viral targets and therapies

Special Issue Information

Dear Colleagues,

The current pandemic has alerted the world to the unprecedented challenges posed by emerging and re-emerging pathogenic viruses. Viral pathogens cause a variety of infectious diseases in their hosts through a complex process called viral pathogenesis, which involves extensive host–virus interactions on both the cellular and systemic levels. These interactions include viral entry, replication, dissemination, and host immune responses, the combinations of which determine virus and host tissue tropisms, the occurrence of viral pathogenesis, and the form and the severity of diseases.

The understanding of how various human and zoonotic viruses lead to pathogenesis is key to alleviating severe infection-related illnesses, reducing deaths, and curbing infection. To advance our understanding of virus–host interaction and the pathogenesis of various emerging and re-emerging viruses, many key questions relating to specific viruses remain to be fully explored. These questions include, but are not limited to, the following:

  • How are viral host and organ tropism determined?
  • How does viral infection affect various functions of infected cells or tissues?
  • How do host immune responses combat viral infection, and how do viruses evade host immune responses?
  • How do host immune responses contribute to pathogenesis and immunopathogenesis?
  • What are the potential strategies to combat viral pathogenesis?

In this Special Issue, we aim to discuss these questions by assembling a collection of original research, review articles, and case reports that highlight the recent advances in understanding the pathogenesis of various human and zoonotic viruses of your expertise. We cordially invite you to submit manuscripts related to these topics.

Dr. Lei Wei
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. Pathogens 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

  • human virus
  • zoonotic virus
  • pathogenesis
  • virus–host interaction
  • disease
  • host and tissue tropism
  • immunopathogenesis
  • immune responses

Published Papers (3 papers)

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Research

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11 pages, 2286 KiB  
Communication
Activation of Inflammasome during Bluetongue Virus Infection
by Marie Pourcelot, Rayane Amaral da Silva Moraes, Sandrine Lacour, Aurore Fablet, Grégory Caignard and Damien Vitour
Pathogens 2023, 12(6), 801; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens12060801 - 04 Jun 2023
Cited by 1 | Viewed by 1191
Abstract
Bluetongue virus (BTV), a double-stranded RNA virus belonging to the Sedoreoviridae family, provokes an economically important disease in ruminants. In this study, we show that the production of activated caspase-1 and interleukin 1 beta (IL-1β) is induced in BTV-infected cells. This response seems [...] Read more.
Bluetongue virus (BTV), a double-stranded RNA virus belonging to the Sedoreoviridae family, provokes an economically important disease in ruminants. In this study, we show that the production of activated caspase-1 and interleukin 1 beta (IL-1β) is induced in BTV-infected cells. This response seems to require virus replication since a UV-inactivated virus is unable to activate this pathway. In NLRP3-/- cells, BTV could not trigger further IL-1β synthesis, indicating that it occurs through NLRP3 inflammasome activation. Interestingly, we observed differential activation levels in bovine endothelial cells depending on the tissue origin. In particular, inflammasome activation was stronger in umbilical cord cells, suggesting that these cells are more prone to induce the inflammasome upon BTV infection. Finally, the strength of the inflammasome activation also depends on the BTV strain, which points to the importance of viral origin in inflammasome modulation. This work reports the crucial role of BTV in the activation of the NLRP3 inflammasome and further shows that this activation relies on BTV replication, strains, and cell types, thus providing new insights into BTV pathogenesis. Full article
(This article belongs to the Special Issue Pathogenesis of Viral Diseases)
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17 pages, 6103 KiB  
Article
T-Cell Receptor β Chain and B-Cell Receptor Repertoires in Chronic Hepatitis B Patients with Coexisting HBsAg and Anti-HBs
by Qiao Zhan, Le Chang, Jian Wu, Zhiyuan Zhang, Jinghang Xu, Yanyan Yu, Zhenru Feng and Zheng Zeng
Pathogens 2022, 11(7), 727; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens11070727 - 26 Jun 2022
Cited by 2 | Viewed by 1823
Abstract
Antibodies in response to antigens are related to the immune repertoire of T- and B-cell receptors. However, some patients with chronic hepatitis B (CHB) have coexisting HBsAg and anti-HBsAg antibodies (anti-HBs) that cannot neutralize HBV. We attempted to investigate the repertoires that produce [...] Read more.
Antibodies in response to antigens are related to the immune repertoire of T- and B-cell receptors. However, some patients with chronic hepatitis B (CHB) have coexisting HBsAg and anti-HBsAg antibodies (anti-HBs) that cannot neutralize HBV. We attempted to investigate the repertoires that produce this response in CHB patients. The T-cell receptor β chain (TRB) and B-cell receptor (BCR) repertoires of peripheral blood genomic DNA were analyzed using MiXCR. T-cell receptor (TCR) cluster analysis was carried out by clusTCR, and motifs prediction was selected by Multiple Em for Motif Elicitation (MEME). A total of 76 subjects were enrolled, including 26 HBsAg and anti-HBs coexisting patients with CHB (DP group), 25 anti-HBs single-positive healthy people (SP group), and 25 CHB patients (CHB group). The clone length of BCR in 39, 90 was significantly different among these groups (p = 0.005, 0.036). The motif “CASSLG” in the DP group was significantly higher than SP and CHB groups and may relate to coexistence, and the motif “GAGPLT” was only shown in the SP group and may relate to anti-HB expression. These provide important insights into vaccine development and CHB treatment. Full article
(This article belongs to the Special Issue Pathogenesis of Viral Diseases)
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Review

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22 pages, 3126 KiB  
Review
SARS-CoV-2 and Emerging Foodborne Pathogens: Intriguing Commonalities and Obvious Differences
by Ahmed G. Abdelhamid, Julia N. Faraone, John P. Evans, Shan-Lu Liu and Ahmed E. Yousef
Pathogens 2022, 11(8), 837; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens11080837 - 27 Jul 2022
Viewed by 3772
Abstract
The coronavirus disease 2019 (COVID-19) has resulted in tremendous human and economic losses around the globe. The pandemic is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a virus that is closely related to SARS-CoV and other human and animal coronaviruses. [...] Read more.
The coronavirus disease 2019 (COVID-19) has resulted in tremendous human and economic losses around the globe. The pandemic is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a virus that is closely related to SARS-CoV and other human and animal coronaviruses. Although foodborne diseases are rarely of pandemic proportions, some of the causative agents emerge in a manner remarkably similar to what was observed recently with SARS-CoV-2. For example, Shiga toxin-producing Escherichia coli (STEC), the most common cause of hemolytic uremic syndrome, shares evolution, pathogenesis, and immune evasion similarities with SARS-CoV-2. Both agents evolved over time in animal hosts, and during infection, they bind to specific receptors on the host cell’s membrane and develop host adaptation mechanisms. Mechanisms such as point mutations and gene loss/genetic acquisition are the main driving forces for the evolution of SARS-CoV-2 and STEC. Both pathogens affect multiple body organs, and the resulting diseases are not completely cured with non-vaccine therapeutics. However, SARS-CoV-2 and STEC obviously differ in the nature of the infectious agent (i.e., virus vs. bacterium), disease epidemiological details (e.g., transmission vehicle and symptoms onset time), and disease severity. SARS-CoV-2 triggered a global pandemic while STEC led to limited, but sometimes serious, disease outbreaks. The current review compares several key aspects of these two pathogenic agents, including the underlying mechanisms of emergence, the driving forces for evolution, pathogenic mechanisms, and the host immune responses. We ask what can be learned from the emergence of both infectious agents in order to alleviate future outbreaks or pandemics. Full article
(This article belongs to the Special Issue Pathogenesis of Viral Diseases)
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