The CD4 molecule was reconstituted into the bilayers of large liposomes. Fluorescence microscopy and electron microscopy showed that these liposomes interact with HIV-infected H9-HT cells, delivering their contents to the cell interior. Liposomes bearing CD4 did not interact in this way with noninfected H9-HT cells nor did liposomes without CD4 interact significantly with HIV-infected cells. From electron micrographs, it appeared that HIV binds to liposomes bearing CD4; no attachment of virions to liposomes without CD4 was observed.
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EBioMedicine
January 2025
State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, NHC Key Laboratory of AIDS Prevention and Treatment, National Clinical Research Center for Laboratory Medicine, The First Hospital of China Medical University, China Medical University, Shenyang, 110001, China; Key Laboratory of AIDS Immunology, Chinese Academy of Medical Sciences, Shenyang, 110001, China; Key Laboratory of AIDS Immunology of Liaoning Province, Shenyang, 110001, China. Electronic address:
Background: Although antiretroviral therapy (ART) effectively inhibits viral replication, it does not fully mitigate the immunosenescence instigated by HIV infection. Cellular metabolism regulates cellular differentiation, survival, and senescence. Serine hydroxymethyltransferase 2 (SHMT2) is the first key enzyme for the entry of serine into the mitochondria from the de novo synthesis pathway that orchestrates its conversion glutathione (GSH), a key molecule in neutralising ROS and ensuring the stability of the immune system.
View Article and Find Full Text PDFNPJ Vaccines
January 2025
Department of Microbial Infection and Immunity, College of Medicine, The Ohio State University, Columbus, OH, USA.
Natural killer (NK) cell-driven effector mechanisms, such as antibody-dependent cell-mediated cytotoxicity, emerged as a secondary correlate of protection in the RV144 HIV vaccine clinical trial, the only vaccine thus far demonstrating some efficacy in human trials. Therefore, leveraging NK cells with enhanced cytotoxic effector responses may bolster vaccine-induced protection against HIV. Here, we investigated the effect of orally administering indole-3-carbinol (I3C), an aryl hydrocarbon receptor (AHR) agonist, as an adjuvant to an RV144-like vaccine platform in a mouse model.
View Article and Find Full Text PDFMed Mycol
December 2024
Division of Infectious Diseases, Department of Medicine, University of Minnesota, Minneapolis, Minnesota, USA.
Given extensive improvements in access to antiretroviral therapy (ART) over the past 12 years, the HIV and cryptococcal meningitis landscapes have dramatically changed since 2010. We sought to evaluate changes in clinical presentation and clinical outcomes of people presenting with HIV-associated cryptococcal meningitis between 2010 and 2022 in Uganda. We analyzed three prospective cohorts of HIV-infected Ugandans with cryptococcal meningitis during 2010-2012, 2013-2017, and 2018-2022.
View Article and Find Full Text PDFBMC Res Notes
January 2025
Ragon Institute of MGH, MIT, and Harvard, 600 Main Street, Cambridge, MA, 02139, USA.
Background: Immune reconstitution following the initiation of combination antiretroviral therapy (cART) significantly impacts the prognosis of individuals infected with human immunodeficiency virus (HIV). Our previous studies have indicated that the baseline CD4 T cells count and percentage before cART initiation are predictors of immune recovery in TB-negative children infected with HIV, with TB co-infection potentially causing a delay in immune recovery. However, it remains unclear whether these predictors consistently impact immune reconstitution during long-term intensive cART treatment in TB-negative/positive children infected with HIV.
View Article and Find Full Text PDFCytotoxic T-lymphocytes (CTL) exert sustained pressure on reservoirs of HIV-infected cells that persist through years of antiretroviral therapy (ART). This selects for latently infected cells, but also potentially for cells that express HIV but possess intrinsic CTL resistance. We demonstrate that such resistance exists in HIV-infected CD4 T-cells that survive rigorous CTL attack and map CTL susceptibility to cell identities and states defined by single-cell multi-omics and functional metabolic profiling.
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