Publications by authors named "Greta A Beckerle"

Introduction: Around 1.7 million children are estimated to live with HIV-1 worldwide, and about 160,000 infants are newly infected every year. Since adaptive immunity takes time to mature and develop in infants, and maternal antibodies provide limited antiviral activity, innate and intrinsic immunity against HIV-1 in the young is of critical importance.

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Article Synopsis
  • Chronic inflammation in people living with HIV not only promotes the onset and growth of cancer but also hampers immune response, potentially exacerbated by increased expression of Human Endogenous Retroviruses (HERVs).
  • A study analyzed RNA from breast cancer samples of both HIV-positive and HIV-negative women, revealing 185 genes with different expression levels—181 being host genes and 4 being HERV transcripts in HIV-positive samples.
  • The results suggest that HERV expression could influence breast cancer-related genes and immune signaling pathways in individuals with HIV, indicating the virus may indirectly alter the breast cancer microenvironment.
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Much has been learnt from the functions of host restriction factors during acute and chronic HIV-1 infection, but far less is known about their role in HIV-1-infected individuals in which viral load is stably suppressed with antiretroviral therapy (ART). In this study transcriptional expression of 42 host restriction factors was determined for memory CD4+ T cells sorted from 10 uninfected and 21 HIV-1-infected individuals, treated with suppressive ART and for which the viral reservoir was quantified. No significant associations were observed between restriction factor expression and HIV-1 reservoir size, quantified by measurement of HIV-1 Gag DNA using droplet digital polymerase chain reaction, and by measurement of replication-competent inducible virus using quantitative viral outgrowth assays.

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HIV-1 persistence in latent reservoirs during antiretroviral therapy (ART) is the main obstacle to virus eradication. To date, there is no marker that adequately identifies latently infected CD4 T cells in vivo. Using a well-established ex vivo model, we generated latently infected CD4 T cells and identified interferon-induced transmembrane protein 1 (IFITM1), a transmembrane antiviral factor, as being overexpressed in latently infected cells.

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