Immunity and Viral Immune Evasion Strategies: Recent Insights

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Virology".

Deadline for manuscript submissions: 30 September 2025 | Viewed by 145

Special Issue Editors


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Guest Editor
Laboratory of Virology, Department of Molecular Medicine, Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Sapienza University of Rome, 00185 Rome, Italy
Interests: virus–host interaction; antiviral immunity; virus interferon resistance; flavivirus, HIV; respiratory infectious diseases; cystic fibrosis; COVID-19 pathogenesis
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Guest Editor
Department of Molecular Medicine, Laboratory of Virology, Sapienza University of Rome, Rome, Italy
Interests: virus–host interaction; antiviral immunity; virus interferon resistance; flavivirus, HIV; respiratory infectious diseases

Special Issue Information

Dear Colleagues,

The 21st century has seen many serious outbreaks of viral infectious diseases, mainly caused by zoonotic viruses such as coronaviruses, influenza viruses, and arthropod-borne viruses. Emerging and re-emerging viral diseases have become increasingly frequent, often with no timely or effective countermeasures. Because disease severity results from complex virus–host interactions, understanding viral immunopathogenesis is critical to discover biomarkers and pave the way for novel antiviral targets. Viral genetic variability, tropism, molecular determinants, and host innate and adaptive immune responses all contribute to disease outcome. Symptoms result from direct viral damage—particularly through immune-evasion strategies—or from immune-mediated effects such as inflammation and immune cell activity.

This Special Issue explores the mechanisms underlying virus–host interactions, covering advances in the profiling of molecular events related to viral replication, immune signalling, cellular immune responses, and interaction networks, analysing various acute or chronic viral infections using in vitro and/or in vivo approaches. Insights into these processes will improve our understanding of viral disease outcomes and help to identify the determinants of severe disease and novel therapeutic viral or host targets.

Dr. Carolina Scagnolari
Dr. Federica Frasca
Guest Editors

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Keywords

  • virus–host interactions
  • viral immunopathogenesis
  • innate immunity
  • cellular immunity
  • viral genetic variability
  • inflammation
  • viral immune evasion strategies
  • antiviral responses
  • biomarker discovery
  • virulence determinants
  • immune signalling pathways
  • viral persistence

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Published Papers (1 paper)

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Review

36 pages, 1750 KB  
Review
Pattern Recognition Receptors (PRRs) Expression and Activation in COVID-19 and Long COVID: From SARS-CoV-2 Escape Mechanisms to Emerging PRR-Targeted Immunotherapies
by Luca Maddaloni, Ginevra Bugani, Matteo Fracella, Camilla Bitossi, Alessandra D’Auria, Francesca Aloisi, Abir Azri, Letizia Santinelli, Manel Ben M’Hadheb, Alessandra Pierangeli, Federica Frasca and Carolina Scagnolari
Microorganisms 2025, 13(9), 2176; https://doi.org/10.3390/microorganisms13092176 - 17 Sep 2025
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is recognized by pattern recognition receptors (PRRs), which play a vital role in triggering innate immune responses such as the production of type I and III interferons (IFNs). While modest PRR activation helps to defend against [...] Read more.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is recognized by pattern recognition receptors (PRRs), which play a vital role in triggering innate immune responses such as the production of type I and III interferons (IFNs). While modest PRR activation helps to defend against SARS-CoV-2, excessive or sustained activation can cause harmful inflammation and contribute to severe Coronavirus Disease 2019 (COVID-19). Altered expression of Toll-like receptors (TLRs), which are among the most important members of the PRR family members, particularly TLRs 2, 3, 4, 7, 8 and 9, has been strongly linked to COVID-19 severity. Furthermore, retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated protein 5 (MDA5), collectively known as RLRs (RIG-I-like receptors), act as sensors that detect SARS-CoV-2 RNA. The expression of these receptors, as well as that of different DNA sensors, varies in patients infected with SARS-CoV-2. Changes in PRR expression, particularly that of TLRs, cyclic GMP-AMP synthase (cGAS), and the stimulator of interferon genes (STING), have also been shown to play a role in the development and persistence of long COVID (LC). However, SARS-CoV-2 has evolved strategies to evade PRR recognition and subsequent signaling pathway activation, contributing to the IFN response dysregulation observed in SARS-CoV-2-infected patients. Nevertheless, PRR agonists and antagonists remain promising therapeutic targets for SARS-CoV-2 infection. This review aims to describe the PRRs involved in recognizing SARS-CoV-2, explore their expression during SARS-CoV-2 infection, and examine their role in determining the severity of both COVID-19 and long-term manifestations of the disease. It also describes the strategies developed by SARS-CoV-2 to evade PRR recognition and activation. Moreover, given the considerable interest in modulating PRR activity as a novel immunotherapy approach, this review will provide a description of PRR agonists and antagonists that have been investigated as antiviral strategies against SARS-CoV-2. This review aims to explore the complex interplay between PRRs and SARS-CoV-2 in depth, considering its implications for prognostic biomarkers, targeted therapeutic strategies and the mechanistic understanding of long LC. Additionally, it outlines future perspectives that could help to address knowledge gaps in PRR-mediated responses during SARS-CoV-2 infection. Full article
(This article belongs to the Special Issue Immunity and Viral Immune Evasion Strategies: Recent Insights)
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