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Pathogenesis and Antiviral Treatment of Emerging and Reemerging Viral Infections

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 November 2025 | Viewed by 433

Special Issue Editor

Special Issue Information

Dear Colleagues,

Emerging and reemerging viruses represent a global public health concern, including those involving human infections resulting from zoonotic spillover events, for which pathogenesis remains poorly understood and effective therapeutic strategies are often unavailable. In recent decades, globalization, climate change, and increased mobility of people, animals, and products have contributed to a growing number of outbreaks and even pandemics. Moreover, continuous viral replication and dissemination frequently lead to genetic adaptation through the accumulation of mutations, recombination, and reassortment, facilitating the emergence of new viral variants. This Special Issue welcomes original and review articles focused on pathogenesis, clinical aspects, antiviral therapies, and prevention strategies, including the development or improvement of technologies targeting human and animal viruses. Our goal is to provide an updated and comprehensive overview of the molecular and clinical understanding of emerging viral infections while highlighting innovative approaches for their control.

This Special Issue is supervised by Dr. Luciana Barros de Arruda and assisted by our Guest Editor Assistant Dr. Sharton Vinicius Antunes Coelho (, Departamento de Virologia, Instituto de Microbiologia Paulo de Góes, Universidade Federal do Rio de Janeiro, Rio de Janeiro 21941-902, Brazil).

Dr. Luciana Barros de Arruda
Guest Editor

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Keywords

  • viral replication
  • antiviral
  • inflammation
  • vaccine
  • arbovirus
  • respiratory virus
  • hemorrhagic virus
  • neurotropic virus

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Published Papers (1 paper)

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Research

23 pages, 8153 KiB  
Article
SARS-Cov-2 Replication in a Blood–Brain Barrier Model Established with Human Brain Microvascular Endothelial Cells Induces Permeability and Disables ACE2-Dependent Regulation of Bradykinin B1 Receptor
by Sharton Vinicius Antunes Coelho, Gabriela Lisboa e Souza, Bruno Braz Bezerra, Luan Rocha Lima, Isadora Alonso Correa, Dalziza Victalina de Almeida, Rodrigo Pacheco da Silva-Aguiar, Ana Acácia S. Pinheiro, Pierre Sirois, Celso Caruso-Neves, Luciana Jesus da Costa, Julio Scharfstein and Luciana Barros de Arruda
Int. J. Mol. Sci. 2025, 26(12), 5540; https://doi.org/10.3390/ijms26125540 - 10 Jun 2025
Viewed by 375
Abstract
Endothelial dysfunction plays a central role in COVID-19 pathogenesis, by affecting vascular homeostasis and worsening thromboinflammation. This imbalance may contribute to blood–brain barrier (BBB) disruption, which has been reported in long COVID-19 patients with neurological sequelae. The kallikrein–kinin system (KKS) generates bradykinin (BK), [...] Read more.
Endothelial dysfunction plays a central role in COVID-19 pathogenesis, by affecting vascular homeostasis and worsening thromboinflammation. This imbalance may contribute to blood–brain barrier (BBB) disruption, which has been reported in long COVID-19 patients with neurological sequelae. The kallikrein–kinin system (KKS) generates bradykinin (BK), a proinflammatory peptide that induces microvascular leakage via B2R. Under inflammatory conditions, BK is converted to Des-Arg-BK (DABK), which activates B1R, a receptor upregulated in inflamed tissues. DABK is degraded by ACE2, the main SARS-CoV-2 receptor; thus, viral binding and ACE2 downregulation may lead to DABK/B1R imbalance. Here, we investigated these interactions using human brain microvascular endothelial cells (HBMECs), as a model of the BBB. Since endothelial cell lines express low levels of ACE2, HBMECs were modified with an ACE2-carrying pseudovirus. SARS-CoV-2 replication was confirmed by RNA, protein expression, and infectious particles release. Infection upregulated cytokines and endothelial permeability, enhancing viral and leukocyte transmigration. Additionally, viral replication impaired ACE2 function in HBMECs, amplifying the response to DABK, increasing nitric oxide (NO) production, and further disrupting endothelial integrity. Our findings reveal a mechanism by which SARS-CoV-2 impacts the BBB and highlights the ACE2/KKS/B1R axis as a potential contributor to long COVID-19 neurological symptoms. Full article
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