Special Issue "HIV and Host Interaction"

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 15 August 2019

Special Issue Editor

Guest Editor
Prof. Philippe Gallay

Department of Immunology and Microbiology, The Scripps Research Institute, 10550 North Torrey Pines Road (IMM9), La Jolla, CA 92037, USA
Website | E-Mail
Interests: HIV; HCV; cyclophilin; liver fibrosis; hepatocellular carcinoma; double membrane vesicles; HBV

Special Issue Information

Dear Colleagues,

One million people worldwide die of AIDS and two million are newly infected with HIV per year, while approximately forty million people are currently living with HIV. Both host and viral factors are thought to influence the natural course of HIV infection and disease progression. In the absence of a vaccine, a complete understanding of HIV–host interactions during the viral life cycle is central in order to develop new strategies to treat or even cure infected patients and prevent new infections. Although significant progress has been made in our knowledge of the interplay between HIV and its host, many of these interactions are multifaceted and remain to be further investigated to be fully understood.

This Special Issue “HIV and Host Interaction” welcomes original research articles and reviews covering topics regarding virus–host interactions during HIV infection and AIDS progression, which include host factors essential for viral infection and replication, host cellular restriction factors, host adaptive and innate immune factors, and viral and host genetic factors.

Prof. Philippe Gallay
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 papers will be 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. Cells 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 1800 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
  • host factors
  • restriction factors
  • adaptive and innate immune factors
  • viral and host genetic factors

Published Papers (2 papers)

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Research

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Open AccessArticle
Humoral Response to the HIV-1 Envelope V2 Region in a Thai Early Acute Infection Cohort
Received: 22 March 2019 / Revised: 11 April 2019 / Accepted: 15 April 2019 / Published: 19 April 2019
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Abstract
Reduced risk of HIV-1 infection correlated with antibody responses to the envelope variable 1 and 2 regions in the RV144 vaccine trial. To understand the relationship between antibody responses, V2 sequence, and structure, plasma samples (n = 16) from an early acute HIV-1 [...] Read more.
Reduced risk of HIV-1 infection correlated with antibody responses to the envelope variable 1 and 2 regions in the RV144 vaccine trial. To understand the relationship between antibody responses, V2 sequence, and structure, plasma samples (n = 16) from an early acute HIV-1 infection cohort from Thailand infected with CRF01_AE strain were analyzed for binding to V2 peptides by surface plasmon resonance. Five participants with a range of V2 binding responses at week 24 post-infection were further analyzed against a set of four overlapping V2 peptides that were designed based on envelope single-genome amplification. Antibody responses that were relatively consistent over the four segments of the V2 region or a focused response to the C-strand (residues 165–186) of the V2 region were observed. Viral escape in the V2 region resulted in significantly reduced antibody binding. Structural modeling indicated that the C-strand and the sites of viral variation were highly accessible in the open conformation of the HIV-1 Env trimer. V2 residues, 165–186 are preferentially targeted during acute infection. Residues 169–184 were also preferentially targeted by the protective immune response in the RV144 trial, thus emphasizing the importance of these residues for vaccine design. Full article
(This article belongs to the Special Issue HIV and Host Interaction)
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Open AccessCorrection
Correction: Trinh, H.V., et al. Humoral Response to the HIV-1 Envelope V2 Region in a Thai Early Acute Infection Cohort. Cells 2019, 8, 365
Received: 29 May 2019 / Accepted: 30 May 2019 / Published: 6 June 2019
PDF Full-text (196 KB)
Abstract
In the original version of our article [...] Full article
(This article belongs to the Special Issue HIV and Host Interaction)

Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: Protective effect of probiotic bacteria and estrogen in preventing HIV-1 mediated barrier breakdown in female genital tract epithelial cells
Authors: Sara Dizzell, Aisha Nazli, Gregor Reid and Charu Kaushic
Abstract: Approximately 40% of global HIV-1 transmission occurs in the female genital tract (FGT) through heterosexual transmission. Epithelial cells lining the FGT comprise the first barrier to HIV-1 entry. The functions of these cells are influenced by female sex hormones and the mucosal microbiota. Previous studies have suggested that certain hormonal contraceptives or a dysbiosis of the vaginal microbiota may enhanced HIV-1 acquisition in the FGT. We examined the effects of female sex hormones and lactobacilli on primary genital epithelial cell (GEC) barrier functions and innate immune responses. Two probiotic strains of Lactobacillus: L. reuteri (RC-14) and L. rhamnosus (GR-1), were tested in the presence or absence of the female sex hormones estrogen, progesterone, or hormonal contraceptive medroxyprogesterone acetate for their effects on confluent GEC monolayers in the presence or absence of HIV-1. Barrier integrity, cell viability and innate inflammatory factors were assessed in GEC monolayers after treatment. Our results demonstrate that probiotic lactobacilli enhance barrier function and reduce transepithelial leakage, regardless of hormone treatment in GEC monolayers and amiliorate HIV-1 mediated barrier disruption. GEC monolayers grown in presence of estrogen showed a reduction in HIV-1 mediated epithelial leakage and downregulated HIV-1 mediated induction of pro-inflammatory cytokines. Enhancement of barrier function and decrease in inflammation could enhance protection against HIV-1 infection. These studies provide an insight into how factors in the genital microenvironment can affect HIV-1 infection in the FGT.

Title: Interplay between intrinsic and innate immunity during infection
Author: Olivier Delelis
Abstract: Restriction factors are antiviral components of intrinsic immunity which constitute a first line of defense by blocking different steps of HIV replication cycle. In immune cells, HIV infection is also sensed by several pattern recognition receptors (PRRs), leading to type-I interferon (IFN-I) and inflammatory cytokines production that upregulate antiviral IFN-stimulated genes (ISGs). Several studies suggest a link between these two types of immunity. Indeed, restriction factors, that are generally interferon (IFN)-inducible, are able to modulate innate immune responses. This review highlights recent knowledge of the interplay between restriction factors and innate immune responses inducing antiviral defenses. Hijacking of this intrinsic and innate immunity by HIV viral proteins will also be discussed.

Title: Dissecting ERAP2 genetic variant role in HIV-1 infection
Author: Mara Biasin

Title: Plasma membrane-associated restriction factors and their counteraction by HIV accessory proteins
Author: John Guatelli

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