Infections, Immune Mechanisms and Host-Pathogen Interactions

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Molecular Microbiology and Immunology".

Deadline for manuscript submissions: 31 August 2025 | Viewed by 354

Special Issue Editor


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Guest Editor
Chan Zuckerberg Biohub—San Francisco, San Francisco, CA 94158, USA
Interests: immunology; host–pathogen interactions; vaccines; pathogen discovery; global health

Special Issue Information

Dear Colleagues,

There are a number of ways in which pathogens have evolved to specifically evade detection and clearance by the host immune system. Mechanisms of evasion often evolve over time under circumstances of recurrent host exposure leading to pathogenic adaptations. Mechanisms of immune evasion can include strategies such as reorganizing organelles, manipulating cell signaling pathways, hijacking host cellular metabolism or sequestering into latency. These microbial survival strategies can opportunistically change a commensal bacterium into an invasive pathogen or allow viral persistence and dissemination. The approach used by a microbe can affect the severity and progression of an infection by altering pathogen virulence, interfere with the ability to establish memory responses to prevent subsequent infections or change a pathogen’s transmissibility. Understanding how different mechanisms of evasion lead not only to pathogenesis, but also host colonization, will help to identify new targets for the development of more effective therapeutics and efficacious vaccines.

The purpose of this Special Issue is to bring together a collection of research articles that provide the newest insight into mechanisms of immune evasion and manipulation across viral, parasitic and bacterial species that infect human hosts. Of particular interest are articles highlighting mechanisms in neglected or understudied diseases, including Lassa Fever Virus, Giardia, Cryptosporidium, Schistosomiasis, dengue, chikungunya, Mycobacterium ulcerans, etc. 

Dr. Cristina Tato
Guest Editor

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Keywords

  • immune evasion
  • innate immunity
  • adaptive immunity
  • opportunistic
  • neglected diseases
  • virulence
  • persistence
  • metabolism
  • cytokines
  • therapeutic targets

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Published Papers (1 paper)

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Research

23 pages, 4664 KiB  
Article
Dynamic Interaction Between SARS-CoV-2 and Influenza A Virus Infection in Human Respiratory Tissues and Cells
by John C. W. Ho, Kachun Ng, Rachel H. H. Ching, Malik Peiris, John M. Nicholls, Michael C. W. Chan and Kenrie P. Y. Hui
Microorganisms 2025, 13(5), 988; https://doi.org/10.3390/microorganisms13050988 - 25 Apr 2025
Viewed by 250
Abstract
With the concurrent circulations of SARS-CoV-2 omicron and influenza A viruses in the community, there is evidence showing co-infection with both viruses. However, disease severity may vary due to the complex immunity landscape of the patients and the neutralizing antibody waning status. The [...] Read more.
With the concurrent circulations of SARS-CoV-2 omicron and influenza A viruses in the community, there is evidence showing co-infection with both viruses. However, disease severity may vary due to the complex immunity landscape of the patients and the neutralizing antibody waning status. The intrinsic dynamic relationship and pathological significance for such co-infections remain largely unknown. The replication kinetics and innate immune responses from the co-infections of SARS-CoV-2 (Omicron BA.1 and D614G variant) and influenza A viruses (pandemic H1N1, seasonal H3N2 and highly pathogenic avian H5N1) were characterized in human respiratory tissue explants, human airway, and alveolar epithelial cells. SARS-CoV-2 reduced the replication of influenza A viruses, but not vice versa, during co-infections in human bronchial tissues and airway epithelial cells. In lung tissues, the co-infections showed minimal effects on each other, but the viral replications of the two viruses were mutually reduced except for H1N1pdm in the alveolar epithelial cells irrespective of the enhancement of the ACE2 receptor. Notably, the co-infections showed a significant upregulation of the innate immune responses of SARS-CoV-2 in comparison to single infections in both respiratory epithelial cells, suggesting that co-infections of influenza A viruses potentially lead to more severe damage to the host than SARS-CoV-2 single infections. Full article
(This article belongs to the Special Issue Infections, Immune Mechanisms and Host-Pathogen Interactions)
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