Publications by authors named "C A Pise-Masison"
The transient depletion of monocytes alone prior to exposure of macaques to HTLV-1 enhances both HTLV-1 (wild type) and HTLV-1 (Orf-1 knockout) infectivity, but seroconversion to either virus is not sustained over time, suggesting a progressive decrease in virus expression. These results raise the hypotheses that either HTLV-1 persistence depends on a monocyte reservoir or monocyte depletion provides a transient immune evasion benefit. To test these hypotheses, we simultaneously depleted NK cells, CD8 T cells, and monocytes (triple depletion) prior to exposure to HTLV-1 or HTLV-1.
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- HTLV-1 infection is prevalent in Brazil and is associated with serious inflammatory conditions like HAM/TSP, a debilitating neuroinflammatory disease that leads to loss of motor function.
- The study examined how HTLV-1 impacts cellular prion protein (PrP) levels in immune cells using flow cytometry and western blot assays.
- Results showed that HTLV-1 infection reduces PrP expression and CD4 T cells in infected individuals, suggesting that this downregulation may contribute to the disease's progression.
Human T-cell Leukemia virus type-1 (HTLV-1) causes adult T-cell leukemia/lymphoma (ATLL), HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and other inflammatory diseases. High viral DNA burden (VL) in peripheral blood mononuclear cells is a documented risk factor for ATLL and HAM/TSP, and patients with HAM/TSP have a higher VL in cerebrospinal fluid than in peripheral blood. VL alone is not sufficient to differentiate symptomatic patients from healthy carriers, suggesting the importance of other factors, including host immune response.
View Article and Find Full Text PDFHuman T cell leukemia virus type 1 (HTLV-1) persists in the host despite a vigorous immune response that includes cytotoxic T cells (CTL) and natural killer (NK) cells, suggesting the virus has developed effective mechanisms to counteract host immune surveillance. We recently showed that treatment of HTLV-1-infected cells with the drug pomalidomide (Pom) increases surface expression of MHC-I, ICAM-1, and B7-2, and significantly increases the susceptibility of HTLV-1-infected cells to NK and CTL killing, which is dependent on viral expression. We reasoned that by restoring cell surface expression of these molecules, Pom treatment has the potential to reduce virus burden by rendering infected cells susceptible to NK and CTL killing.
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- The study examined how specific immune cells (monocytes, NK cells, and CD8+ T-cells) influence the infection process of HTLV-1 in macaques by using two strains of the virus: the wild type and a mutant that is less infectious.
- Results showed that depleting NK cells or CD8+ T-cells accelerated the immune response in animals exposed to the wild type virus, highlighting the protective role of NK cells during infection.
- Additionally, the research revealed that the orf-I protein produced by the virus helps infected cells evade destruction, suggesting it plays a crucial role in both facilitating viral transmission and potentially contributing to chronic inflammation during HTLV-1 infection.