Publications by authors named "Youssef M Eltalkhawy"
Article Synopsis
- HIV-1-infected individuals on antiretroviral therapy still face higher risks of non-AIDS-related health issues due to ongoing chronic inflammation, marked by specific changes in monocytes like increased CD16 subsets and elevated soluble markers sCD163 and sCD14.
- The study reveals that IL-10, an anti-inflammatory cytokine, can activate monocytes by increasing CD16 and other soluble markers through multiple signaling pathways, including Stat3 and AMPK.
- Additionally, the HIV-1 protein Nef promotes the production of IL-10 in macrophages, suggesting that IL-10 contributes to the persistent activated state of monocytes in individuals who have achieved viral suppression.
Despite effective antiretroviral therapy, HIV-1 persists in cells, including macrophages, which is an obstacle to cure. However, the precise role of macrophages in HIV-1 infection remains unclear because they reside in tissues that are not easily accessible. Monocyte-derived macrophages are widely used as a model in which peripheral blood monocytes are cultured and differentiated into macrophages.
View Article and Find Full Text PDFSince 1958 witnessed the detection of Monkeypox virus in monkeys, no human infection was encountered until 1970. Afterwards, zoonotic transmission was the rule near African rainforests, mainly in DRC. Most cases occurred in children who weren't immunized against smallpox.
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- The cytokine IL-32 is found at high levels in HIV-1-infected individuals, but its role is complex as it can both inhibit and stimulate HIV-1 production in different types of immune cells.
- IL-32 inhibits HIV-1 in monocyte-derived macrophages (MDMs) through the activation of SAMHD1, but this effect is lost when SAMHD1 is depleted, distinguishing its action from that in CD4 T cells.
- Additionally, IL-32 promotes immunosuppressive molecules and enhances MDM motility, suggesting that its overall impact may favor the progression of HIV-1 infection despite some inhibitory effects.
Article Synopsis
- Human T-cell leukemia virus type 1 (HTLV-1) primarily spreads between cells, and the protein M-Sec is crucial for this process.
- In HTLV-1 carriers, CD4+ T cells express M-Sec, which is induced by the viral protein Tax, while T cells from non-carriers do not show this expression.
- Reducing M-Sec levels leads to decreased viral infection and impacts cellular structures necessary for the virus, suggesting M-Sec enhances viral spread through promoting membrane protrusions and Gag protein clustering.