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Viruses
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Chemokines and Chemokine Receptors in Viral Infection 2024
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Chemokines and Chemokine Receptors in Viral Infection 2024

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Viral Immunology, Vaccines, and Antivirals".

Deadline for manuscript submissions: 31 December 2024 | Viewed by 6413

Special Issue Editor

Dr. Philippe Colin

E-Mail Website
Guest Editor
Infinity-Toulouse Institute for Infectious and Inflammatory Diseases, INSERM U1291, 31024 Toulouse, France
Interests: HIV; AIDS; HIV entry; chemokine receptors; viral tropism; bNAbs; immunogen design

Special Issue Information

Dear Colleagues,

Chemokines and their receptors play a critical role in the development, homeostasis, and diverse functions of the immune system. In particular, they are involved in the defense against viruses by mobilizing innate and adaptive immune cells to sites of infection. As with other members of the G protein-coupled receptors, chemokine receptors exist in different conformational forms, varying between cell types, and this structural plasticity allows the triggering of different physiological outcomes from chemokines, a phenomenon known as functional selectivity.

However, some viruses are able to bypass the chemokine system by producing viral proteins mimicking the molecules (Herpesviruses) and disrupting the immune response; to use the chemokine system to favor their viral entry (HIV); or to overstimulate the chemokine system and lead to hyperinflammation and tissue damage (Coronaviruses).

This Special Issue is devoted to studies regarding a better understanding of the chemokine/chemokine receptor system in viral infection, such as research on the immune response developed by chemokines towards viruses, or studies on the structural plasticity of chemokine receptors and its importance in viral escape from the immune system, and on mechanisms used by viruses to modulate chemokine activities.

Findings dealing with the development of chemokine analogs or drugs targeting chemokine receptors are also welcomed.

Dr. Philippe Colin
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

  • chemokine
  • chemokine receptor
  • immune therapy
  • viral escape
  • tropism

Published Papers (3 papers)

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Research

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11 pages, 1319 KiB  
Article
Rational Engineering of a Sub-Picomolar HIV-1 Blocker
by Massimiliano Secchi and Luca Vangelista
Viruses 2022, 14(11), 2415; https://doi.org/10.3390/v14112415 - 31 Oct 2022
Cited by 1 | Viewed by 1323
Abstract
With the aim of rationally devising a refined and potent HIV-1 blocker, the cDNA of CCL5 5p12 5m, an extremely potent CCR5 antagonist, was fused to that of C37, a gp41-targeted fusion inhibitor. The resulting CCL5 5p12 5m-C37 fusion protein was expressed in [...] Read more.
With the aim of rationally devising a refined and potent HIV-1 blocker, the cDNA of CCL5 5p12 5m, an extremely potent CCR5 antagonist, was fused to that of C37, a gp41-targeted fusion inhibitor. The resulting CCL5 5p12 5m-C37 fusion protein was expressed in E. coli and proved to be capable of inhibiting R5 HIV-1 strains with low to sub-picomolar IC50, maintaining its antagonism toward CCR5. In addition, CCL5 5p12 5m-C37 inhibits R5/X4 and X4 HIV-1 strains in the picomolar concentration range. The combination of CCL5 5p12 5m-C37 with tenofovir (TDF) exhibited a synergic effect, promoting this antiviral cocktail. Interestingly, a CCR5-targeted combination of maraviroc (MVC) with CCL5 5p12 5m-C37 led to a synergic effect that could be explained by an extensive engagement of different CCR5 conformational populations. Within the mechanism of HIV-1 entry, the CCL5 5p12 5m-C37 chimera may fit as a powerful blocker in several instances. In its possible consideration for systemic therapy or pre-exposure prophylaxis, this protein design represents an interesting lead in the combat of HIV-1 infection. Full article
(This article belongs to the Special Issue Chemokines and Chemokine Receptors in Viral Infection 2024)
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20 pages, 3454 KiB  
Article
Macrophage Migration Inhibitory Factor (MIF) Promotes Increased Proportions of the Highly Permissive Th17-like Cell Profile during HIV Infection
by César Trifone, Lucía Baquero, Alejandro Czernikier, Paula Benencio, Lin Leng, Natalia Laufer, María Florencia Quiroga, Richard Bucala, Yanina Ghiglione and Gabriela Turk
Viruses 2022, 14(10), 2218; https://doi.org/10.3390/v14102218 - 09 Oct 2022
Cited by 1 | Viewed by 1767
Abstract
In this study, we evaluate the role of the MIF/CD74 axis in the functionality of CD4+ T lymphocytes (CD4TL) during HIV infection. MDMs from healthy donors were infected with a R5-tropic or Transmitted/Founder (T/F) HIV strain. At day 11 post-MDM infection, allogeneic [...] Read more.
In this study, we evaluate the role of the MIF/CD74 axis in the functionality of CD4+ T lymphocytes (CD4TL) during HIV infection. MDMs from healthy donors were infected with a R5-tropic or Transmitted/Founder (T/F) HIV strain. At day 11 post-MDM infection, allogeneic co-cultures with uninfected CD4TLs plus MIF stimulus were performed. Cytokine production was evaluated by ELISA. MIF plasma levels of people with HIV (PWH) were evaluated by ELISA. The phenotype and infection rate of CD4TLs from PWH were analyzed after MIF stimulus. Intracellular cytokines and transcription factors were evaluated by flow cytometry. Data were analyzed by parametric or non-parametric methods. The MIF stimulation of HIV-infected MDMs induced an increased expression of IL-6, IL-1β and IL-8. In CD4TL/MDM co-cultures, the MIF treatment increased IL-17A/RORγt-expressing CD4TLs. Higher concentrations of IL-17A in supernatants were also observed. These results were recapitulated using transmitted/founder (T/F) HIV-1 strains. The MIF treatment appeared to affect memory CD4TLs more than naïve CD4TLs. MIF blocking showed a negative impact on IL17A+CD4TL proportions. Higher MIF concentrations in PWH-derived plasma were correlated with higher IL-17A+CD4TL percentages. Finally, MIF stimulation in PWH-derived PBMCs led to an increase in Th17-like population. MIF may contribute to viral pathogenesis by generating a microenvironment enriched in activating mediators and Th17-like CD4TLs, which are known to be highly susceptible to HIV-1 infection and relevant to viral persistence. These observations establish a basis for considering MIF as a possible therapeutic target. Full article
(This article belongs to the Special Issue Chemokines and Chemokine Receptors in Viral Infection 2024)
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Review

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17 pages, 969 KiB  
Review
CXCL10 Chemokine: A Critical Player in RNA and DNA Viral Infections
by Noha Mousaad Elemam, Iman Mamdouh Talaat and Azzam A. Maghazachi
Viruses 2022, 14(11), 2445; https://doi.org/10.3390/v14112445 - 03 Nov 2022
Cited by 11 | Viewed by 3087
Abstract
Chemokines constitute a group of small, secreted proteins that regulate leukocyte migration and contribute to their activation. Chemokines are crucial inflammatory mediators that play a key role in managing viral infections, during which the profile of chemokine expression helps shape the immune response [...] Read more.
Chemokines constitute a group of small, secreted proteins that regulate leukocyte migration and contribute to their activation. Chemokines are crucial inflammatory mediators that play a key role in managing viral infections, during which the profile of chemokine expression helps shape the immune response and regulate viral clearance, improving clinical outcome. In particular, the chemokine ligand CXCL10 and its receptor CXCR3 were explored in a plethora of RNA and DNA viral infections. In this review, we highlight the expression profile and role of the CXCL10/CXCR3 axis in the host defense against a variety of RNA and DNA viral infections. We also discuss the interactions among viruses and host cells that trigger CXCL10 expression, as well as the signaling cascades induced in CXCR3 positive cells. Full article
(This article belongs to the Special Issue Chemokines and Chemokine Receptors in Viral Infection 2024)
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