Molecular and Cellular Mechanisms of Diseases: HIV

Topic Information

Dear Colleagues,

HIV and human defense mechanisms have coevolved to neutralize each other. In the course of infection, HIV exploits the cellular equipment and inhibits the action of antiviral proteins (termed restriction factors). Not everyone exposed to the virus becomes infected and there is considerable heterogeneity in the clinical course of HIV infection, with some people progressing rapidly to disease and death while others show no signs of immunodeficiency for decades. These individuals exhibit immunological and genetic features that confer upon them a natural resistance to infection and/or disease progression. The study of these correlates of protection is valuable because the reasons for the devastating immune-deficiency caused by HIV-1 infection are not entirely known, nor are we aware of why the potent antiviral immune response eventually fails to control viral replication. Despite HIV’s ability to evade host restriction factors, detecting these determinants and understanding how they interact with viral accessory proteins could provide remarkable insight into the potential mechanisms involved in the pathogenesis of HIV-1 infection. The discovery of molecular profiles and mechanisms that are distinctive of these individuals could also provide new insights to control HIV infection and contribute to the development of new antivirals and, hopefully, vaccines against AIDS.

Dr. Mara Biasin
Prof. Dr. Daria Lucia Trabattoni
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Biomolecules biomolecules	4.8	9.4	2011	16.3 Days	CHF 2700
Cells cells	5.1	9.9	2012	17.5 Days	CHF 2700
Journal of Molecular Pathology jmp	-	-	2020	25.4 Days	CHF 1000
Pathogens pathogens	3.3	6.4	2012	16.3 Days	CHF 2200
Viruses viruses	3.8	7.3	2009	16.1 Days	CHF 2600

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Published Papers (3 papers)

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All Biomolecules Cells JMP Pathogens Viruses

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Open AccessArticle

Determination of Binding Affinity of Antibodies to HIV-1 Recombinant Envelope Glycoproteins, Pseudoviruses, Infectious Molecular Clones, and Cell-Expressed Trimeric gp160 Using Microscale Thermophoresis

by Shraddha Basu, Neelakshi Gohain, Jiae Kim, Hung V. Trinh, Misook Choe, M. Gordon Joyce and Mangala Rao

Cells 2024, 13(1), 33; https://doi.org/10.3390/cells13010033 - 22 Dec 2023

Viewed by 2345

Abstract

Developing a preventative vaccine for HIV-1 has been a global priority. The elicitation of broadly neutralizing antibodies (bNAbs) against a broad range of HIV-1 envelopes (Envs) from various strains appears to be a critical requirement for an efficacious HIV-1 vaccine. To understand their [...] Read more.

Developing a preventative vaccine for HIV-1 has been a global priority. The elicitation of broadly neutralizing antibodies (bNAbs) against a broad range of HIV-1 envelopes (Envs) from various strains appears to be a critical requirement for an efficacious HIV-1 vaccine. To understand their ability to neutralize HIV-1, it is important to characterize the binding characteristics of bNAbs. Our work is the first to utilize microscale thermophoresis (MST), a rapid, economical, and flexible in-solution temperature gradient method to quantitatively determine the binding affinities of bNAbs and non-neutralizing monoclonal antibodies (mAbs) to HIV-1 recombinant envelope monomer and trimer proteins of different subtypes, pseudoviruses (PVs), infectious molecular clones (IMCs), and cells expressing the trimer. Our results demonstrate that the binding affinities were subtype-dependent. The bNAbs exhibited a higher affinity to IMCs compared to PVs and recombinant proteins. The bNAbs and mAbs bound with high affinity to native-like gp160 trimers expressed on the surface of CEM cells compared to soluble recombinant proteins. Interesting differences were seen with V2-specific mAbs. Although they recognize linear epitopes, one of the antibodies also bound to the Envs on PVs, IMCs, and a recombinant trimer protein, suggesting that the epitope was not occluded. The identification of epitopes on the envelope surface that can bind to high affinity mAbs could be useful for designing HIV-1 vaccines and for down-selecting vaccine candidates that can induce high affinity antibodies to the HIV-1 envelope in their native conformation. Full article

(This article belongs to the Topic Molecular and Cellular Mechanisms of Diseases: HIV)

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Open AccessArticle

Cell-to-Cell Transmission of HIV-1 and HIV-2 from Infected Macrophages and Dendritic Cells to CD4+ T Lymphocytes

by Marta Calado, David Pires, Carolina Conceição, Rita Ferreira, Quirina Santos-Costa, Elsa Anes and José Miguel Azevedo-Pereira

Viruses 2023, 15(5), 1030; https://doi.org/10.3390/v15051030 - 22 Apr 2023

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Abstract

Macrophages (Mø) and dendritic cells (DCs) are key players in human immunodeficiency virus (HIV) infection and pathogenesis. They are essential for the spread of HIV to CD4+ T lymphocytes (TCD4+) during acute infection. In addition, they constitute a persistently infected reservoir in which [...] Read more.

Macrophages (Mø) and dendritic cells (DCs) are key players in human immunodeficiency virus (HIV) infection and pathogenesis. They are essential for the spread of HIV to CD4+ T lymphocytes (TCD4+) during acute infection. In addition, they constitute a persistently infected reservoir in which viral production is maintained for long periods of time during chronic infection. Defining how HIV interacts with these cells remains a critical area of research to elucidate the pathogenic mechanisms of acute spread and sustained chronic infection and transmission. To address this issue, we analyzed a panel of phenotypically distinct HIV-1 and HIV-2 primary isolates for the efficiency with which they are transferred from infected DCs or Mø to TCD4+. Our results show that infected Mø and DCs spread the virus to TCD4+ via cell-free viral particles in addition to other alternative pathways. We demonstrate that the production of infectious viral particles is induced by the co-culture of different cell populations, indicating that the contribution of cell signaling driven by cell-to-cell contact is a trigger for viral replication. The results obtained do not correlate with the phenotypic characteristics of the HIV isolates, namely their co-receptor usage, nor do we find significant differences between HIV-1 and HIV-2 in terms of cis- or trans-infection. The data presented here may help to further elucidate the cell-to-cell spread of HIV and its importance in HIV pathogenesis. Ultimately, this knowledge is critical for new therapeutic and vaccine approaches. Full article

(This article belongs to the Topic Molecular and Cellular Mechanisms of Diseases: HIV)

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Open AccessArticle

17⍺-Estradiol Protects against HIV-1 Tat-Induced Endolysosome Dysfunction and Dendritic Impairments in Neurons

by Gaurav Datta, Nicole M. Miller and Xuesong Chen

Cells 2023, 12(5), 813; https://doi.org/10.3390/cells12050813 - 6 Mar 2023

Cited by 1 | Viewed by 1801

Abstract

HIV-1 Tat continues to play an important role in the development of HIV-associated neurocognitive disorders (HAND), which persist in 15–55% of people living with HIV even with virological control. In the brain, Tat is present on neurons, where Tat exerts direct neuronal damaging [...] Read more.

HIV-1 Tat continues to play an important role in the development of HIV-associated neurocognitive disorders (HAND), which persist in 15–55% of people living with HIV even with virological control. In the brain, Tat is present on neurons, where Tat exerts direct neuronal damaging effects by, at least in part, disrupting endolysosome functions, a pathological feature present in HAND. In this study, we determined the protective effects of 17α-estradiol (17αE2), the predominant form of estrogen in the brain, against Tat-induced endolysosome dysfunction and dendritic impairment in primary cultured hippocampal neurons. We demonstrated that pre-treatment with 17αE2 protected against Tat-induced endolysosome dysfunction and reduction in dendritic spine density. Estrogen receptor alpha (ERα) knockdown impairs the ability of 17αE2 to protect against Tat-induced endolysosome dysfunction and reduction in dendritic spine density. Furthermore, over-expressing an ERα mutant that fails to localize on endolysosomes impairs 17αE2′s protective effects against Tat-induced endolysosome dysfunction and reduction in dendritic spine density. Our findings demonstrate that 17αE2 protects against Tat-induced neuronal injury via a novel ERα-mediated and endolysosome-dependent pathway, and such a finding might lead to the development of novel adjunct therapeutics against HAND. Full article

(This article belongs to the Topic Molecular and Cellular Mechanisms of Diseases: HIV)

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