Host–Pathogen Interactions and Pathogenesis

A special issue of Biology (ISSN 2079-7737).

Deadline for manuscript submissions: 31 July 2025 | Viewed by 3001

Special Issue Editors

Department of Immunology and Microbiology, University of Colorado School of Medicine, Anschutz Campus, Aurora, CO 80045, USA
Interests: infection biology; host-pathogen interaction; gene regulation; cell signaling; drug discovery; redox biology

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Guest Editor
Department of Microbiology, Central University of Rajasthan, Ajmer 305817, India
Interests: human microbiome; host-pathogen interactions; Mycobacterium tuberculosis: dormancy and persistence; drug designing; vaccine development

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Guest Editor
Department of Biochemistry, School of Chemical and Life Sciences, Jamia Hamdard, New Delhi 110062, India
Interests: infection biology; tuberculosis; host-pathogen interaction

Special Issue Information

Dear Colleagues, 

The forthcoming Special Issue on Host–Pathogen Interactions and Pathogenesis is poised to be a ground-breaking compilation of cutting-edge research situated at the nexus of microbiology, immunology, and disease pathogenesis. Its primary objective is to unravel the intricate dynamics governing the relationships between hosts and pathogens, shedding light on the underlying mechanisms driving infection and disease progression.

We are pleased to invite you to this special issue which aims to contribute to a comprehensive overview of the current state of research in the dynamic field of host–pathogen interactions. By synthesizing diverse perspectives and featuring ground-breaking studies, the issue aims to contribute significantly to our understanding of infectious diseases. Moreover, it seeks to pave the way for future advancements in the prevention and treatment of infectious diseases by fostering collaboration and knowledge exchange among researchers.

The special aims to include following themes (but not limited to) for Submissions:

  1. Molecular Insights into Interactions: This theme invites studies delving into the molecular intricacies of host–pathogen interactions, exploring the strategies employed by pathogens to exploit host cellular machinery and the intricate defense mechanisms mounted by hosts.
  2. Emerging Pathogens and Global Health: Researchers are encouraged to spotlight research on emerging pathogens and their global health impact, addressing challenges posed by these agents and proposing strategies for surveillance, prevention, and control.
  3. Immunomodulation and Pathogenesis: A central theme exploring the immunomodulatory tactics employed by pathogens to establish and sustain infection, offering valuable insights for the development of targeted therapeutic interventions.
  4. Technological Advances and Methodological Innovations: This theme showcases the latest technological and methodological innovations, from advanced imaging techniques to high-throughput omics approaches, expanding our understanding of pathogenesis.

In this Special Issue, original research articles and reviews are welcome.

Dr. Sashi Kant
Dr. Deeksha Tripathi
Dr. Saurabh Pandey
Guest Editors

Manuscript Submission Information

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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. Biology 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

  • host-pathogen dynamics
  • infectious disease mechanisms
  • virulence factors
  • microbial interactions
  • pathogenicity
  • emerging pathogens
  • immunological response
  • immunomodulation tactics
  • infection prevention
  • disease pathophysiology

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Published Papers (2 papers)

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Research

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18 pages, 4925 KiB  
Article
Mycobacterium tuberculosis PE_PGRS38 Enhances Intracellular Survival of Mycobacteria by Inhibiting TLR4/NF-κB-Dependent Inflammation and Apoptosis of the Host
by Hayan Ullah, Xiaoxia Shi, Ayaz Taj, Lin Cheng, Qiulong Yan, Shanshan Sha, Ahmad, Jian Kang, Muhammad Haris, Xiaochi Ma and Yufang Ma
Biology 2024, 13(5), 313; https://doi.org/10.3390/biology13050313 - 30 Apr 2024
Cited by 1 | Viewed by 1686
Abstract
Mycobacterium tuberculosis (Mtb) ranks as the most lethal human pathogen, able to fend off repeated attacks by the immune system or medications. PE_PGRS proteins are hallmarks of the pathogenicity of Mtb and contribute to its antigenic diversity, virulence, and persistence during infection. M. [...] Read more.
Mycobacterium tuberculosis (Mtb) ranks as the most lethal human pathogen, able to fend off repeated attacks by the immune system or medications. PE_PGRS proteins are hallmarks of the pathogenicity of Mtb and contribute to its antigenic diversity, virulence, and persistence during infection. M. smegmatis is a nonpathogenic mycobacterium that naturally lacks PE_PGRS and is used as a model to express Mtb proteins. PE_PGRS has the capability to evade host immune responses and enhance the intracellular survival of M. smegmatis. Despite the intense investigations into PE_PGRS proteins, their role in tuberculosis remains elusive. We engineered the recombinant M. smegmatis strain Ms-PE_PGRS38. The result shows that PE_PGRS38 is expressed in the cell wall of M. smegmatis. PE_PGRS38 contributes to biofilm formation, confers permeability to the cell wall, and shows variable responses to exogenous stresses. PE_PGRS38 downregulated TLR4/NF-κB signaling in RAW264.7 macrophages and lung tissues of infected mice. In addition, PE_PGRS38 decreased NLRP3-dependent IL-1β release and limited pathogen-mediated inflammasome activity during infection. Moreover, PE_PGRS38 inhibited the apoptosis of RAW264.7 cells by downregulating the expression of apoptotic markers including Bax, cytochrome c, caspase-3, and caspase-9. In a nutshell, our findings demonstrate that PE_PGRS38 is a virulence factor for Mtb that enables recombinant M. smegmatis to survive by resisting and evading the host’s immune responses during infection. Full article
(This article belongs to the Special Issue Host–Pathogen Interactions and Pathogenesis)
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Review

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15 pages, 1320 KiB  
Review
Insight into the Interaction Mechanism of Pseudorabies Virus Infection
by Xiaoyong Chen and Ziding Yu
Biology 2024, 13(12), 1013; https://doi.org/10.3390/biology13121013 - 4 Dec 2024
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Abstract
The pseudorabies virus (PRV), also known as suid alphaherpesvirus 1 (SuAHV-1), has garnered significant attention due to its broad host range and the economic losses it incurs in the swine industry. This review aims to provide a comprehensive understanding of the intricate virus–host [...] Read more.
The pseudorabies virus (PRV), also known as suid alphaherpesvirus 1 (SuAHV-1), has garnered significant attention due to its broad host range and the economic losses it incurs in the swine industry. This review aims to provide a comprehensive understanding of the intricate virus–host interactions during PRV infection, focusing on the evasion strategies of the virus against the host responses. We also summarize the mechanisms by which PRV manipulates the host cell machinery to facilitate its replication and spread, while simultaneously evading detection and clearance by the immune system. Furthermore, we discuss the latest advancements, such as metabolic, autophagic, and apoptotic pathways in studying these interactions, highlighting the role of various cellular factors and pathways in elucidating virus–host dynamics. By integrating these insights, the article aims to provide a comprehensive overview of the molecular mechanisms underlying PRV pathogenesis and host response, paving the way for the development of novel therapeutic strategies against this virus. Full article
(This article belongs to the Special Issue Host–Pathogen Interactions and Pathogenesis)
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