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Pathogens
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Pathogenesis, Molecular Epidemiology, and Immune Response to Lentiviral Infections
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Pathogenesis, Molecular Epidemiology, and Immune Response to Lentiviral Infections

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Viral Pathogens".

Deadline for manuscript submissions: closed (15 September 2021) | Viewed by 22656

Special Issue Editors

Dr. Alessandra Borsetti

E-Mail Website
Guest Editor
National HIV/AIDS Research Center (CNAIDS), Istituto Superiore di Sanità, Rome, Italy
Interests: infectious disease; lentiviruses; HIV-1; SIV; animal model; primate; host–virus interactions; viral pathogenesis; molecular epidemiology; immune response to viral infections
Prof. Dr. Cristina Parolin

E-Mail Website
Guest Editor
Department of Molecular Medicine, University of Padova, Padova, Italy
Interests: infectious disease; lentiviruses; HIV-1; FIV; host–virus interactions; viral pathogenesis; antiviral drugs; genetic treatment of HIV-1 infection

Special Issue Information

Dear Colleagues,

Lentiviruses are a genus of the Retroviridae family that encompass bovine (BIV), small ruminant (SRLV), equine (EIAV), feline (FIV), and human/non-human primate immunodeficiency viruses (HIV/SIV), characterized by long incubation periods and a variety of progressively degenerative pathologies, including immunodeficiencies, which lead inexorably to death of the host. Lentiviruses infect both dividing and non-dividing cells, in general immune cells, integrate the viral genome into the host DNA, and persist indefinitely in the infected animal, replicating continuously and eluding the immune system. High genetic variation is a hallmark of lentiviral infections. The consequences of virus variability are mutations of surface antigens that allow virus escape from immune control of T-cell or antibody-mediated responses, resulting in a defeat of the immune system in controlling infection, thus hindering the development of effective vaccines. The best known lentivirus is the human immunodeficiency virus type 1 (HIV-1) that establishes a persistent infection characterized by high genetic diversity and mutation rates, which represent one of the major obstacles to virus eradication. Molecular epidemiology studies of globally circulating HIV-1 strains and recombinant forms are a powerful tool for tracking the spread and evolution of the epidemic over time.

Although major progresses have been made in our knowledge of the interplay between lentivirus and the host, even more remains to be revealed.

The goal of this Special Issue is to provide an overview of the recent advances in the research of lentiviral infections including virus–host interactions, viral pathogenesis, and their consequences for the immune system. Studies on molecular epidemiology are encouraged to be submitted. Any original research article and review covering topics regarding “Pathogenesis, Molecular Epidemiology, and Immune Response to Lentiviral Infections” is very welcome.

Dr. Alessandra Borsetti
Prof. Dr. Cristina Parolin
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. Pathogens 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 2200 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

  • virus–host interaction
  • persistent infection
  • immune response
  • host factors
  • virus evolution
  • phylogenetic analysis
  • SRLV
  • EIAV
  • FIV
  • BIV
  • SIV
  • HIV-1
  • HIV-2

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Published Papers (6 papers)

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Research

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12 pages, 1382 KiB  
Article
Decreased MIP-3α Production from Antigen-Activated PBMCs in Symptomatic HIV-Infected Subjects
by Fuchun Zhang, Lingling Sun, Mark K. Lafferty, Joseph B. Margolick and Alfredo Garzino-Demo
Pathogens 2022, 11(1), 7; https://doi.org/10.3390/pathogens11010007 - 22 Dec 2021
Viewed by 2781
Abstract
CD4+ CCR6+ T cells are highly susceptible to HIV infection, and a high cytokine producing CCR6+ T cell subset is selectively lost during HIV infection. The CCR6 chemokine MIP-3α (CCL20) is produced at sites of infection in SIV animal models. [...] Read more.
CD4+ CCR6+ T cells are highly susceptible to HIV infection, and a high cytokine producing CCR6+ T cell subset is selectively lost during HIV infection. The CCR6 chemokine MIP-3α (CCL20) is produced at sites of infection in SIV animal models. Recently, we have shown that MIP-3α inhibits HIV replication. This inhibition of HIV infection is mediated by CCR6 signaling and eventuates in increased APOBEC3G expression. Since there are few existing reports on the role of MIP-3α in health or disease, we studied its production by PBMCs from HIV-seronegative and HIV+ subjects. We evaluated the ability of PBMCs to produce MIP-3α in response to antigen stimulation using cells obtained from two groups: one composed of HIV-seronegative subjects (n = 16) and the other composed of HIV+ subjects (n = 58), some asymptomatic and some with clinically defined AIDS. Antigens included fragment C of the tetanus toxin, Candida albicans, whole-inactivated HIV, and HIV p24. MIP-3α was detected by ELISA in tissue culture supernatants of antigen-stimulated PBMCs. MIP-3α production by antigen-stimulated PBMCs was readily measured for HIV-negative subjects and for HIV-seropositive asymptomatic subjects, but not for patients with AIDS. These results suggest that subversion of the MIP-3α-CCR6 axis by HIV during the course of infection contributes to the loss of immune function that eventually leads to AIDS. Full article
(This article belongs to the Special Issue Pathogenesis, Molecular Epidemiology, and Immune Response to Lentiviral Infections)
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11 pages, 1447 KiB  
Article
Serum Samples from Co-Infected and Domestic Cat Field Isolates Nonspecifically Bind FIV and Other Antigens in Enzyme-Linked Immunosorbent Assays
by Alex Moskaluk, Mary Nehring and Sue VandeWoude
Pathogens 2021, 10(6), 665; https://doi.org/10.3390/pathogens10060665 - 28 May 2021
Cited by 3 | Viewed by 2568
Abstract
We evaluated enzyme-linked immunosorbent assay (ELISA) specificity for measuring seroantibody responses to two types of retroviral infections in domestic cats: feline immunodeficiency virus (FIV) and feline foamy virus (FFV). We compared the seroreactivity of specific pathogen-free (SPF) cat sera, sera from SPF cats [...] Read more.
We evaluated enzyme-linked immunosorbent assay (ELISA) specificity for measuring seroantibody responses to two types of retroviral infections in domestic cats: feline immunodeficiency virus (FIV) and feline foamy virus (FFV). We compared the seroreactivity of specific pathogen-free (SPF) cat sera, sera from SPF cats inoculated with either FIV or FFV, and field isolates (e.g., shelter or privately owned cats). Sera from SPF cats experimentally infected with the cognate virus had significantly lower background in both FIV and FFV ELISAs compared to sera from negative field isolates. ELISA values for SPF cats exposed to either FIV or FFV tended to have higher OD values on the opposite ELISA antigen plate. FIV nonspecific background absorbance was greater than that of FFV, and 10 of 15 sera samples from FIV seronegative field samples were measured in the indeterminant range. These findings highlight that exposure to off-target pathogens elicit antibodies that may nonspecifically bind to antigens used in binding assays; therefore, validation using sera from SPF animals exposed during controlled infection results in the setting of a cutoff value that may be inappropriately low when applied to field samples. Our work also suggests that infection of domestic cats with pathogens other than FIV results in antibodies that cross-react with the FIV Gag antigen. Full article
(This article belongs to the Special Issue Pathogenesis, Molecular Epidemiology, and Immune Response to Lentiviral Infections)
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Review

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26 pages, 1974 KiB  
Review
Fighting HIV-1 Persistence: At the Crossroads of “Shoc-K and B-Lock”
by Chiara Acchioni, Enrico Palermo, Silvia Sandini, Marta Acchioni, John Hiscott and Marco Sgarbanti
Pathogens 2021, 10(11), 1517; https://doi.org/10.3390/pathogens10111517 - 20 Nov 2021
Cited by 12 | Viewed by 4545
Abstract
Despite the success of highly active antiretroviral therapy (HAART), integrated HIV-1 proviral DNA cannot be eradicated from an infected individual. HAART is not able to eliminate latently infected cells that remain invisible to the immune system. Viral sanctuaries in specific tissues and immune-privileged [...] Read more.
Despite the success of highly active antiretroviral therapy (HAART), integrated HIV-1 proviral DNA cannot be eradicated from an infected individual. HAART is not able to eliminate latently infected cells that remain invisible to the immune system. Viral sanctuaries in specific tissues and immune-privileged sites may cause residual viral replication that contributes to HIV-1 persistence. The “Shock or Kick, and Kill” approach uses latency reversing agents (LRAs) in the presence of HAART, followed by cell-killing due to viral cytopathic effects and immune-mediated clearance. Different LRAs may be required for the in vivo reactivation of HIV-1 in different CD4+ T cell reservoirs, leading to the activation of cellular transcription factors acting on the integrated proviral HIV-1 LTR. An important requirement for LRA drugs is the reactivation of viral transcription and replication without causing a generalized immune activation. Toll-like receptors, RIG-I like receptors, and STING agonists have emerged recently as a new class of LRAs that augment selective apoptosis in reactivated T lymphocytes. The challenge is to extend in vitro observations to HIV-1 positive patients. Further studies are also needed to overcome the mechanisms that protect latently infected cells from reactivation and/or elimination by the immune system. The Block and Lock alternative strategy aims at using latency promoting/inducing agents (LPAs/LIAs) to block the ability of latent proviruses to reactivate transcription in order to achieve a long term lock down of potential residual virus replication. The Shock and Kill and the Block and Lock approaches may not be only alternative to each other, but, if combined together (one after the other), or given all at once [namely “Shoc-K(kill) and B(block)-Lock”], they may represent a better approach to a functional cure. Full article
(This article belongs to the Special Issue Pathogenesis, Molecular Epidemiology, and Immune Response to Lentiviral Infections)
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13 pages, 1069 KiB  
Review
Human Immunodeficiency Virus Type 2: The Neglected Threat
by Giancarlo Ceccarelli, Marta Giovanetti, Caterina Sagnelli, Alessandra Ciccozzi, Gabriella d’Ettorre, Silvia Angeletti, Alessandra Borsetti and Massimo Ciccozzi
Pathogens 2021, 10(11), 1377; https://doi.org/10.3390/pathogens10111377 - 25 Oct 2021
Cited by 16 | Viewed by 3170
Abstract
West Africa has the highest prevalence of human immunodeficiency virus (HIV)-2 infection in the world, but a high number of cases has been recognized in Europe, India, and the United States. The virus is less transmissible than HIV-1, with sexual contacts being the [...] Read more.
West Africa has the highest prevalence of human immunodeficiency virus (HIV)-2 infection in the world, but a high number of cases has been recognized in Europe, India, and the United States. The virus is less transmissible than HIV-1, with sexual contacts being the most frequent route of acquisition. In the absence of specific antiretroviral therapy, most HIV-2 carriers will develop AIDS. Although, it requires more time than HIV-1 infection, CD4+ T cell decline occurs more slowly in HIV-2 than in HIV-1 patients. HIV-2 is resistant to non-nucleoside reverse transcriptase inhibitors (NNRTIs) and some protease inhibitors. Misdiagnosis of HIV-2 in patients mistakenly considered HIV-1-positive or in those with dual infections can cause treatment failures with undetectable HIV-1 RNA. In this era of global integration, clinicians must be aware of when to consider the diagnosis of HIV-2 infection and how to test for this virus. Although there is debate regarding when therapy should be initiated and which regimen should be chosen, recent trials have provided important information on treatment options for HIV-2 infection. In this review, we focus mainly on data available and on the insight they offer about molecular epidemiology, clinical presentation, antiretroviral therapy, and diagnostic tests of HIV-2 infection. Full article
(This article belongs to the Special Issue Pathogenesis, Molecular Epidemiology, and Immune Response to Lentiviral Infections)
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17 pages, 1685 KiB  
Review
Targeting and Understanding HIV Latency: The CRISPR System against the Provirus
by Gloria Magro, Arianna Calistri and Cristina Parolin
Pathogens 2021, 10(10), 1257; https://doi.org/10.3390/pathogens10101257 - 28 Sep 2021
Cited by 7 | Viewed by 3858
Abstract
The presence of latently infected cells and reservoirs in HIV-1 infected patients constitutes a significant obstacle to achieve a definitive cure. Despite the efforts dedicated to solve these issues, the mechanisms underlying viral latency are still under study. Thus, on the one hand, [...] Read more.
The presence of latently infected cells and reservoirs in HIV-1 infected patients constitutes a significant obstacle to achieve a definitive cure. Despite the efforts dedicated to solve these issues, the mechanisms underlying viral latency are still under study. Thus, on the one hand, new strategies are needed to elucidate which factors are involved in latency establishment and maintenance. On the other hand, innovative therapeutic approaches aimed at eradicating HIV infection are explored. In this context, advances of the versatile CRISPR-Cas gene editing technology are extremely promising, by providing, among other advantages, the possibility to target the HIV-1 genome once integrated into cellular DNA (provirus) and/or host-specific genes involved in virus infection/latency. This system, up to now, has been employed with success in numerous in vitro and in vivo studies, highlighting its increasing significance in the field. In this review, we focus on the progresses made in the use of different CRISPR-Cas strategies to target the HIV-1 provirus, and we then discuss recent advancements in the use of CRISPR screens to elucidate the role of host-specific factors in viral latency. Full article
(This article belongs to the Special Issue Pathogenesis, Molecular Epidemiology, and Immune Response to Lentiviral Infections)
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19 pages, 1070 KiB  
Review
Advances in SIV/SHIV Non-Human Primate Models of NeuroAIDS
by Sonia Moretti, Sara Virtuoso, Leonardo Sernicola, Stefania Farcomeni, Maria Teresa Maggiorella and Alessandra Borsetti
Pathogens 2021, 10(8), 1018; https://doi.org/10.3390/pathogens10081018 - 12 Aug 2021
Cited by 15 | Viewed by 4262
Abstract
Non-human primates (NHPs) are the most relevant model of Acquired Immunodeficiency Syndrome (AIDS) and neuroAIDS, being of great importance in explaining the pathogenesis of HIV-induced nervous system damage. Simian Immunodeficiency Virus (SIV)/ Simian-Human Immunodeficiency Virus (SHIV)-infected monkeys have provided evidence of complex interactions [...] Read more.
Non-human primates (NHPs) are the most relevant model of Acquired Immunodeficiency Syndrome (AIDS) and neuroAIDS, being of great importance in explaining the pathogenesis of HIV-induced nervous system damage. Simian Immunodeficiency Virus (SIV)/ Simian-Human Immunodeficiency Virus (SHIV)-infected monkeys have provided evidence of complex interactions between the virus and host that include host immune response, viral genetic diversity, and genetic susceptibility, which may explain virus-associated central nervous system (CNS) pathology and HIV-associated neurocognitive disorders (HAND). In this article, we review the recent progress contributions obtained using monkey models of HIV infection of the CNS, neuropathogenesis and SIV encephalitis (SIVE), with an emphasis on pharmacologic therapies and dependable markers that predict development of CNS AIDS. Full article
(This article belongs to the Special Issue Pathogenesis, Molecular Epidemiology, and Immune Response to Lentiviral Infections)
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