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Early diagnosis of the infection caused by human immunodeficiency virus type-1 (HIV-1) is vital to achieve efficient therapeutic treatment and limit the disease spreading when the viremia is at its highest level. To this end, a point-of-care HIV-1 detection carried out with label-free, low-cost, and ultra-sensitive screening technologies would be of great relevance. Herein, a label-free single molecule detection of HIV-1 p24 capsid protein with a large (wide-field) single-molecule transistor (SiMoT) sensor is proposed. The system is based on an electrolyte-gated field-effect transistor whose gate is bio-functionalized with the antibody against the HIV-1 p24 capsid protein. The device exhibits a limit of detection of a single protein and a limit of quantification in the 10 molecule range. This study paves the way for a low-cost technology that can quantify, with single-molecule precision, the transition of a biological organism from being "healthy" to being "diseased" by tracking a target biomarker. This can open to the possibility of performing the earliest possible diagnosis.
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http://dx.doi.org/10.1007/s00216-019-02319-7 | DOI Listing |
Diagn Microbiol Infect Dis
August 2025
Blood Center of Zhejiang Province, Hangzhou 310006, China.
This study analyzed the correlation between false-positive HIV ELISA results (using Bio-Rad reagents) and SARS-COV-2 antibody levels in 301 unpaid apheresis platelet donors with prior infection or vaccination, enrolled from Zhejiang Blood Center between February 1 and May 31, 2023. Trends in both the HIV ELISA false-positive rate and SARS-COV-2 antibody levels were assessed. The false-positive rate rose in early 2023, peaking at 0.
View Article and Find Full Text PDFAntimicrob Agents Chemother
September 2025
Discovery Biology, ViiV Healthcare, Branford, Connecticut, USA.
With its high degree of conservation and critical role in multiple steps of the HIV-1 life cycle, the HIV-1 capsid protein presents an attractive therapeutic target. Herein, the virologic properties of the HIV-1 capsid inhibitors VH4004280 (VH-280) and VH4011499 (VH-499), including potency, mechanisms of action, and resistance profiles, are described. VH-280 and VH-499 inhibited panels of HIV-1 laboratory strains and viruses containing capsid sequences from clinical isolates with half-maximal effective concentrations in the picomolar range.
View Article and Find Full Text PDFJ Virus Erad
September 2025
Center of Excellence for Inflammation, Infectious Disease and Immunity, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, 37614, USA.
Evaluation of CD4 T cell status in early HIV infection is critical for developing strategies targeting HIV replication. In this study, we infected CD4 T cells with HIV-1 and investigated the cell survival mechanisms in HIV-infected versus uninfected cells during early HIV infection. Notably, HIV-infected CD4 T cells exhibited elevated levels of phosphorylated eukaryotic translation initiation factor 2-alpha (p-eIF2α) compared to uninfected cells.
View Article and Find Full Text PDFFront Pharmacol
July 2025
Traditional Medicine Laboratory, School of Nursing and Public Health, Howard College, University of KwaZulu-Natal, Durban, South Africa.
Background: While antiretroviral therapy (ART) has transformed HIV-1 into a manageable chronic illness, its long-term affordability and accessibility remain major challenges in resource-limited settings. Additionally, adverse side effects can compromise treatment adherence and effectiveness. These limitations highlight the need for novel, affordable therapeutic alternatives.
View Article and Find Full Text PDFbioRxiv
July 2025
Department of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, PA 19102.
Infection with human immunodeficiency virus (HIV-1) remains a global health issue and still drives the development of significant pathology and various comorbidities. Antiretroviral therapy (ART) can effectively suppress viral replication but is often initiated months or years after initial infection, leaving a substantial period in which viral replication progresses unchecked. While ART suppresses HIV-1 replication, it does not prohibit the development of HIV-1-associated comorbidities, highlighting a lack of understanding in the connection between replication and HIV-1-associated pathogeneses.
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