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Viruses
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Viruses and Endothelial Dysfunction
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Viruses and Endothelial Dysfunction

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Animal Viruses".

Deadline for manuscript submissions: closed (1 July 2023) | Viewed by 15888

Special Issue Editor

Dr. Francesca Caccuri

E-Mail Website
Guest Editor
Department of Molecular and Translational Medicine, Section of Microbiology, University of Brescia Medical School, Brescia, Italy
Interests: HIV; human respiratory viruses; vaccines; gene therapy; viral oncology; cell/host interaction; endothelial cell dysfunction; cancer microenvironment
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The aim of this Special Issue is to offer an opportunity to collect the newest contributions to the field of HIV Proteins and Endothelial Dysfunction.

The introduction of combined antiretroviral therapy (cART), has considerably decreased the viral burden and opportunistic infections, and increased the life expectancy in human immunodeficiency virus (HIV+)-infected people. Conversely, HIV+ individuals develop a greater vulnerability to non-AIDS (Acquired immunodeficiency syndrome)-related complications. In particular, HIV+ patients have a higher risk of developing endothelial dysfunction, which may occur in both the absence and presence of suppressive cART. HIV-1-encoded proteins are expressed in HIV+ individuals, even in the absence of viral replication, and are able to induce strong changes in endothelial cell (EC) physiology and morphology, to induce direct EC damage and to develop an inflammatory microenvironment. As a consequence, viral proteins may represent some of the essential factors involved in the development of endothelial disorders in AIDS. Understanding the key role of some HIV-1 protein in sustaining EC aberrant functioning may help in identifying new therapeutic approaches for combating and preventing HIV-1-related vascular diseases.

All researchers working in the field are cordially invited to contribute original research papers or propose reviews to feature in this Special Issue of Viruses.

Dr. Francesca Caccuri
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. Viruses 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 2600 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

  • HIV
  • HIV proteins
  • Endothelial cells
  • Vascular dysfunctions
  • Angiogenesis
  • Coagulation disorders
  • Cytokines
  • Inflammation

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Published Papers (4 papers)

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Research

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16 pages, 2495 KiB  
Article
The D405N Mutation in the Spike Protein of SARS-CoV-2 Omicron BA.5 Inhibits Spike/Integrins Interaction and Viral Infection of Human Lung Microvascular Endothelial Cells
by Antonella Bugatti, Federica Filippini, Serena Messali, Marta Giovanetti, Cosetta Ravelli, Alberto Zani, Massimo Ciccozzi, Arnaldo Caruso and Francesca Caccuri
Viruses 2023, 15(2), 332; https://doi.org/10.3390/v15020332 - 24 Jan 2023
Cited by 7 | Viewed by 2479
Abstract
Severe COVID-19 is characterized by angiogenic features, such as intussusceptive angiogenesis, endothelialitis, and activation of procoagulant pathways. This pathological state can be ascribed to a direct SARS-CoV-2 infection of human lung ECs. Recently, we showed the capability of SARS-CoV-2 to infect ACE2-negative primary [...] Read more.
Severe COVID-19 is characterized by angiogenic features, such as intussusceptive angiogenesis, endothelialitis, and activation of procoagulant pathways. This pathological state can be ascribed to a direct SARS-CoV-2 infection of human lung ECs. Recently, we showed the capability of SARS-CoV-2 to infect ACE2-negative primary human lung microvascular endothelial cells (HL-mECs). This occurred through the interaction of an Arg-Gly-Asp (RGD) motif, endowed on the Spike protein at position 403–405, with αvβ3 integrin expressed on HL-mECs. HL-mEC infection promoted the remodeling of cells toward a pro-inflammatory and pro-angiogenic phenotype. The RGD motif is distinctive of SARS-CoV-2 Spike proteins up to the Omicron BA.1 subvariant. Suddenly, a dominant D405N mutation was expressed on the Spike of the most recently emerged Omicron BA.2, BA.4, and BA.5 subvariants. Here we demonstrate that the D405N mutation inhibits Omicron BA.5 infection of HL-mECs and their dysfunction because of the lack of Spike/integrins interaction. The key role of ECs in SARS-CoV-2 pathogenesis has been definitively proven. Evidence of mutations retrieving the capability of SARS-CoV-2 to infect HL-mECs highlights a new scenario for patients infected with the newly emerged SARS-CoV-2 Omicron subvariants, suggesting that they may display less severe disease manifestations than those observed with previous variants. Full article
(This article belongs to the Special Issue Viruses and Endothelial Dysfunction)
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14 pages, 1889 KiB  
Article
Comparison of SARS-CoV-2 Receptors Expression in Primary Endothelial Cells and Retinoic Acid-Differentiated Human Neuronal Cells
by Francesca Benedetti, Giovannino Silvestri, Carla Mavian, Matthew Weichseldorfer, Arshi Munawwar, Melanie N. Cash, Melissa Dulcey, Amy Y. Vittor, Massimo Ciccozzi, Marco Salemi, Olga S. Latinovic and Davide Zella
Viruses 2021, 13(11), 2193; https://doi.org/10.3390/v13112193 - 30 Oct 2021
Cited by 11 | Viewed by 4192
Abstract
SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) is primarily responsible for coronavirus disease (COVID-19) and it is characterized by respiratory illness with fever and dyspnea. Severe vascular problems and several other manifestations, including neurological ones, have also been frequently reported, particularly in the [...] Read more.
SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) is primarily responsible for coronavirus disease (COVID-19) and it is characterized by respiratory illness with fever and dyspnea. Severe vascular problems and several other manifestations, including neurological ones, have also been frequently reported, particularly in the great majority of “long hauler” patients. SARS-CoV-2 infects and replicates in lung epithelial cells, while dysfunction of endothelial and neuronal brain cells has been observed in the absence of productive infection. It has been shown that the Spike protein can interact with specific cellular receptors, supporting both viral entry and cellular dysfunction. It is thus clear that understanding how and when these receptors are regulated, as well as how much they are expressed would help in unveiling the multifaceted aspects of this disease. Here, we show that SH-SY5Y neuroblastoma cells express three important cellular surface molecules that interact with the Spike protein, namely ACE2, TMPRSS2, and NRP1. Their levels increase when cells are treated with retinoic acid (RA), a commonly used agent known to promote differentiation. This increase matched the higher levels of receptors observed on HUVEC (primary human umbilical vein endothelial cells). We also show by confocal imaging that replication-defective pseudoviruses carrying the SARS-CoV-2 Spike protein can infect differentiated and undifferentiated SH-SY5Y, and HUVEC cells, although with different efficiencies. Neuronal cells and endothelial cells are potential targets for SARS-CoV-2 infection and the interaction of the Spike viral protein with these cells may cause their dysregulation. Characterizing RNA and protein expression tempo, mode, and levels of different SARS-CoV-2 receptors on both cell subpopulations may have clinical relevance for the diagnosis and treatment of COVID-19-infected subjects, including long hauler patients with neurological manifestations. Full article
(This article belongs to the Special Issue Viruses and Endothelial Dysfunction)
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18 pages, 6868 KiB  
Article
Vascular Inflammation Is Associated with Loss of Aquaporin 1 Expression on Endothelial Cells and Increased Fluid Leakage in SARS-CoV-2 Infected Golden Syrian Hamsters
by Lisa Allnoch, Georg Beythien, Eva Leitzen, Kathrin Becker, Franz-Josef Kaup, Stephanie Stanelle-Bertram, Berfin Schaumburg, Nancy Mounogou Kouassi, Sebastian Beck, Martin Zickler, Vanessa Herder, Gülsah Gabriel and Wolfgang Baumgärtner
Viruses 2021, 13(4), 639; https://doi.org/10.3390/v13040639 - 8 Apr 2021
Cited by 41 | Viewed by 4745
Abstract
Vascular changes represent a characteristic feature of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection leading to a breakdown of the vascular barrier and subsequent edema formation. The aim of this study was to provide a detailed characterization of the vascular alterations during SARS-CoV-2 [...] Read more.
Vascular changes represent a characteristic feature of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection leading to a breakdown of the vascular barrier and subsequent edema formation. The aim of this study was to provide a detailed characterization of the vascular alterations during SARS-CoV-2 infection and to evaluate the impaired vascular integrity. Groups of ten golden Syrian hamsters were infected intranasally with SARS-CoV-2 or phosphate-buffered saline (mock infection). Necropsies were performed at 1, 3, 6, and 14 days post-infection (dpi). Lung samples were investigated using hematoxylin and eosin, alcian blue, immunohistochemistry targeting aquaporin 1, CD3, CD204, CD31, laminin, myeloperoxidase, SARS-CoV-2 nucleoprotein, and transmission electron microscopy. SARS-CoV-2 infected animals showed endothelial hypertrophy, endothelialitis, and vasculitis. Inflammation mainly consisted of macrophages and lower numbers of T-lymphocytes and neutrophils/heterophils infiltrating the vascular walls as well as the perivascular region at 3 and 6 dpi. Affected vessels showed edema formation in association with loss of aquaporin 1 on endothelial cells. In addition, an ultrastructural investigation revealed disruption of the endothelium. Summarized, the presented findings indicate that loss of aquaporin 1 entails the loss of intercellular junctions resulting in paracellular leakage of edema as a key pathogenic mechanism in SARS-CoV-2 triggered pulmonary lesions. Full article
(This article belongs to the Special Issue Viruses and Endothelial Dysfunction)
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Review

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13 pages, 499 KiB  
Review
Viral Bad News Sent by EVAIL
by Matthias Clauss, Sarvesh Chelvanambi, Christine Cook, Rabab ElMergawy and Navneet Dhillon
Viruses 2021, 13(6), 1168; https://doi.org/10.3390/v13061168 - 18 Jun 2021
Cited by 6 | Viewed by 3511
Abstract
This article reviews the current knowledge on how viruses may utilize Extracellular Vesicle Assisted Inflammatory Load (EVAIL) to exert pathologic activities. Viruses are classically considered to exert their pathologic actions through acute or chronic infection followed by the host response. This host response [...] Read more.
This article reviews the current knowledge on how viruses may utilize Extracellular Vesicle Assisted Inflammatory Load (EVAIL) to exert pathologic activities. Viruses are classically considered to exert their pathologic actions through acute or chronic infection followed by the host response. This host response causes the release of cytokines leading to vascular endothelial cell dysfunction and cardiovascular complications. However, viruses may employ an alternative pathway to soluble cytokine-induced pathologies—by initiating the release of extracellular vesicles (EVs), including exosomes. The best-understood example of this alternative pathway is human immunodeficiency virus (HIV)-elicited EVs and their propensity to harm vascular endothelial cells. Specifically, an HIV-encoded accessory protein called the “negative factor” (Nef) was demonstrated in EVs from the body fluids of HIV patients on successful combined antiretroviral therapy (ART); it was also demonstrated to be sufficient in inducing endothelial and cardiovascular dysfunction. This review will highlight HIV-Nef as an example of how HIV can produce EVs loaded with proinflammatory cargo to disseminate cardiovascular pathologies. It will further discuss whether EV production can explain SARS-CoV-2-mediated pulmonary and cardiovascular pathologies. Full article
(This article belongs to the Special Issue Viruses and Endothelial Dysfunction)
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