Special Issue "HIV-1 Infection and Immunometabolism: Relevance to HIV Pathogenesis and Persistence"

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

Deadline for manuscript submissions: 15 December 2021.

Special Issue Editor

Dr. Sonia Moretti
E-Mail Website
Guest Editor
National HIV/AIDS Research Center, Istituto Superiore Di Sanità, Rome, Italy
Interests: infectious diseases; clinical virology; HIV infection; HIV persistence; immune responses to viral infections

Special Issue Information

Dear Colleagues,

Despite the significant success of HIV treatments in blocking HIV-1 replication and in reducing AIDS-associated morbidity and mortality, these treatments do not fully inhibit HIV-1-related inflammation and chronic immune activation, and viral reservoirs persist for life. Recently, growing evidence has emphasized the interplay between immunometabolism, HIV-1 pathogenesis and viral persistence. Since metabolism control depends on signals that are deregulated during HIV-1 infection, people living with HIV, even under ART, show an increased rate of metabolic abnormalities that negatively impact the immune functions and contribute to viral pathogenesis and persistence. In fact, studies suggest that the metabolic pathways of CD4+ T cells and macrophages determine their susceptibility to HIV-1 infection, the persistence of infected cells and the establishment of latency. Moreover, metabolic abnormalities may further contribute to the development of non-AIDS-associated complications and comorbidities, such as cardiovascular disease, ageing, liver and kidney disease, neurocognitive impairment and non-AIDS malignancies. Thus, targeting metabolism may become a promising approach to modulate immune system and may lead to new therapeutic strategies against HIV and related complications.

For this Special Issue, research articles and review articles, as well as short communications, are welcome in order to provide new insights aimed at dissecting the role of immunometabolism in HIV pathogenesis and latency.

Dr. Sonia Moretti
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. 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 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

  • immunometabolism
  • HIV-1
  • inflammation
  • immune activation
  • HIV pathogenesis
  • HIV latency
  • metabolic diseases
  • non-AIDS-associated comorbidities

Published Papers (1 paper)

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Research

Article
Impact of HCV Eradication on Lipid Metabolism in HIV/HCV Coinfected Patients: Data from ICONA and HepaICONA Foundation Cohort Study
Viruses 2021, 13(7), 1402; https://doi.org/10.3390/v13071402 - 19 Jul 2021
Viewed by 450
Abstract
Objectives: HCV shows complex interactions with lipid metabolism. Our aim was to examine total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) changes in HIV/HCV coinfected patients, after achieving sustained virological response (SVR), according to different HCV genotypes and specific antiretroviral use. Methods: HIV/HCV [...] Read more.
Objectives: HCV shows complex interactions with lipid metabolism. Our aim was to examine total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) changes in HIV/HCV coinfected patients, after achieving sustained virological response (SVR), according to different HCV genotypes and specific antiretroviral use. Methods: HIV/HCV coinfected patients, enrolled in the ICONA and HepaICONA cohorts, who achieved DAA-driven SVR were included. Paired t-tests were used to examine whether the pre- and post-SVR laboratory value variations were significantly different from zero. ANCOVA regression models were employed to estimate the causal effect of SVR and of PI/r use on lipid changes. The interaction between the effect of eradication and HCV genotype was formally tested. Results: six hundred and ninety-nine HIV/HCV coinfected patients were enrolled. After HCV eradication, a significant improvement in liver function occurred, with a significant decrease in AST, ALT, GGT, and total plasmatic bilirubin. TC and LDL-C significantly increased by 21.4 mg/dL and 22.4 mg/dL, respectively (p < 0.001), after SVR, whereas there was no evidence for a change in HDL-C (p = 0.45) and triglycerides (p = 0.49). Notably, the TC and LDL-C increase was higher for participants who were receiving darunavir/ritonavir, and the TC showed a more pronounced increase among HCV genotype 3 patients (interaction-p value = 0.002). Conclusions: complex and rapid changes in TC and LDL-C levels, modulated by HCV genotype and PI/r-based ART combinations, occurred in HIV/HCV coinfected patients after SVR. Further studies are needed to evaluate the clinical impact of these changes on the long-term risk of cardiovascular disease. Full article
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