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Viruses
Special Issues
Virology in Italy 2024
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Virology in Italy 2024

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

Deadline for manuscript submissions: 31 December 2024 | Viewed by 1920

Special Issue Editors

Prof. Dr. Enzo Tramontano

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Guest Editor
Chair, Department of Life and Environmental Sciences, University of Cagliari, Cittadella Universitaria di Monserrato SS554, Monserrato, 09042 Cagliari, Italy
Interests: virology; microbiology; antiviral drugs; drug development; endogenous retroviruses; innate immunity
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Arnaldo Caruso

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Guest Editor
Department of Molecular and Translational Medicine, University of Brescia, Viale Europa, 11–25123 Brescia, Italy
Interests: HIV; human respiratory viruses; vaccines; gene therapy; viral oncology; cell/host interaction; endothelial cell dysfunction; cancer microenvironment; clinical virology
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Massimiliano Galdiero

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Guest Editor
Department of Experimental Medicine, University of Campania “Luigi Vanvitelli”, 80138 Naples, Italy
Interests: viral entry; viral pathogenesis; peptides; anti-viral peptide; diagnostic virology
Special Issues, Collections and Topics in MDPI journals
Dr. Luisa Rubino

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Guest Editor
National Research Council, Institute for Sustainable Plant Protection, Via Amendola 165/A, 70126 Bari, Italy
Interests: plant virology; positive-strand RNA viruses; virus replication; virus taxonomy; Saccharomyces cerevisiae; electron microscopy
Special Issues, Collections and Topics in MDPI journals
Dr. Gabriele Vaccari

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Guest Editor
Department of Food Safety, Nutrition and Veterinary Public Health, Istituto Superiore di Sanità, 00161 Rome, Italy
Interests: emerging infectious diseases; zoonoses; prion disease; veterinary virology; genetic susceptibility to infectious disease; molecular diagnostics; epidemiology

Special Issue Information

Dear Colleagues,

This Special Issue is dedicated to the 8th Congress of the Italian Society for Virology (SIV-ISV (https://siv-isv.org), which will be held in Bologna, Italy, 7th–9th July 2024, and more generally to the research activities in the field of virology that are currently carried out in Italy.

The Special Issue will provide an important opportunity for Italian virologists across different disciplines (basic, clinical, epidemiological, veterinary, plant, etc.) to publish their research work in an internationally recognized scientific journal from a “One Health” perspective. Manuscripts will encompass a wide variety of virus-related topics, including emerging viruses, viral subversion of host cell processes, viruses of microbes, antivirals and vaccines, emerging methods in virology, RNA in virus infection, plant and animal virology, and antiviral innate immunity.

SIV-ISV Congress participants, as well as all other Italian virologists, are invited to contribute original research papers or reviews to this Special Issue of Viruses.

Prof. Dr. Enzo Tramontano
Prof. Dr. Arnaldo Caruso
Prof. Dr. Massimiliano Galdiero
Dr. Luisa Rubino
Dr. Gabriele Vaccari
Guest Editors

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

  • Italy
  • emerging viruses
  • viral subversion of host cell processes
  • viruses of microbes
  • antivirals
  • vaccines
  • emerging methods in virology
  • RNA in virus infection
  • plant viruses
  • antiviral innate immunity
  • animal viruses
  • mycoviruses

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Further information on MDPI's Special Issue polices can be found here.

Published Papers (2 papers)

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Research

14 pages, 5017 KiB  
Article
A Truncated Isoform of Cyclin T1 Could Contribute to the Non-Permissive HIV-1 Phenotype of U937 Promonocytic Cells
by Tiziana Alberio, Mariam Shallak, Amruth Kaleem Basha Shaik, Roberto Sergio Accolla and Greta Forlani
Viruses 2024, 16(8), 1176; https://doi.org/10.3390/v16081176 - 23 Jul 2024
Viewed by 763
Abstract
The different susceptibility to HIV-1 infection in U937 cells—permissive (Plus) or nonpermissive (Minus)—is linked to the expression in Minus cells of interferon (IFN)-γ inducible antiviral factors such as tripartite motif-containing protein 22 (TRIM22) and class II transactivator (CIITA). CIITA interacts with Cyclin T1, [...] Read more.
The different susceptibility to HIV-1 infection in U937 cells—permissive (Plus) or nonpermissive (Minus)—is linked to the expression in Minus cells of interferon (IFN)-γ inducible antiviral factors such as tripartite motif-containing protein 22 (TRIM22) and class II transactivator (CIITA). CIITA interacts with Cyclin T1, a key component of the Positive-Transcription Elongation Factor b (P-TEFb) complex needed for the efficient transcription of HIV-1 upon interaction with the viral transactivator Tat. TRIM22 interacts with CIITA, recruiting it into nuclear bodies together with Cyclin T1. A 50 kDa Cyclin T1 was found only in Minus cells, alongside the canonical 80 kDa protein. The expression of this truncated form remained unaffected by proteasome inhibitors but was reduced by IFNγ treatment. Unlike the nuclear full-length protein, truncated Cyclin T1 was also present in the cytoplasm, and this subcellular localization correlated with its capacity to inhibit Tat-mediated HIV-1 transcription. The 50 kDa Cyclin T1 in Minus cells likely contributes to their non-permissive phenotype by acting as a dominant negative factor, disrupting P-TEFb complex formation and function. Its reduction upon IFNγ treatment suggests a regulatory loop by which its inhibitory role on HIV-1 replication is then exerted by the IFNγ-induced CIITA, which binds to the canonical Cyclin T1, displacing it from the P-TEFb complex. Full article
(This article belongs to the Special Issue Virology in Italy 2024)
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19 pages, 5570 KiB  
Article
Molecular Mechanisms Involved in the B Cell Growth and Clonogenic Activity of HIV-1 Matrix Protein p17 Variants
by Pasqualina D’Ursi, Alessandro Rondina, Alberto Zani, Matteo Uggeri, Serena Messali, Arnaldo Caruso and Francesca Caccuri
Viruses 2024, 16(7), 1048; https://doi.org/10.3390/v16071048 - 28 Jun 2024
Viewed by 819
Abstract
The human immunodeficiency virus (HIV-1) matrix protein p17 (p17) is released from infected cells as a protein capable of deregulating the biological activity of different cells. P17 variants (vp17s), more frequently detected in the plasma of HIV-1+ patients with rather than without [...] Read more.
The human immunodeficiency virus (HIV-1) matrix protein p17 (p17) is released from infected cells as a protein capable of deregulating the biological activity of different cells. P17 variants (vp17s), more frequently detected in the plasma of HIV-1+ patients with rather than without lymphoma and characterized by amino acids insertions in their C-terminal region, were found to trigger B cell growth and clonogenicity. Vp17s endowed with B-cell-growth-promoting activity are drastically destabilized, whereas, in a properly folded state, reference p17 (refp17) does not exert any biological activity on B cell growth and clonogenicity. However, misfolding of refp17 is necessary to expose a masked functional epitope, interacting with the protease-activated receptor 1 (PAR-1), endowed with B cell clonogenicity. Indeed, it is worth noting that changes in the secondary structure can strongly impact the function of a protein. Here, we performed computational studies to show that the gain of function of vp17s is linked to dramatic conformational changes due to structural modification in the secondary-structure elements and in the rearrangement of the hydrogen bond (H-bond) network. In particular, all clonogenic vp17s showed the disengagement of two critical residues, namely Trp16 and Tyr29, from their hydrophobic core. Biological data showed that the mutation of Trp16 and Tyr29 to Ala in the refp17 backbone, alone or in combination, resulted in a protein endowed with B cell clonogenic activity. These data show the pivotal role of the hydrophobic component in maintaining refp17 stability and identify a novel potential therapeutic target to counteract vp17-driven lymphomagenesis in HIV-1+ patients. Full article
(This article belongs to the Special Issue Virology in Italy 2024)
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