HCV infection may induce thyroid dysfunction by different mechanisms including direct infection of thyrocytes leading to activation of inflammatory pathways and upregulation of miR-122.
Depletion results from both direct infection and bystander loss of memory CD4<sup>+</sup> T cells in part attributed to dysregulated IL-7/IL-7R signaling.
Depletion results from both direct infection and bystander loss of memory CD4<sup>+</sup> T cells in part attributed to dysregulated IL-7/IL-7R signaling.
The percentage of T cell receptor (TCR) iVα7.2<sup>+</sup> CD161<sup>+</sup> MAIT cells did not correlate with HBV viral load but inversely with HLA-DR on CD4<sup>+</sup> T cells and MAIT cells and with CD57 on CD8<sup>+</sup> T cells suggesting that decrease of MAIT cells may not be attributed to direct infection by HBV but driven by HBV-induced chronic immune activation.
HBD1 expression in monocytes can be induced by HIV-1 in vitro, although direct infection may not entirely account for the increase in HBD1 during acute infection.
Here we used CNS and PNS myelinating cultures from wild type and Ifnar1 knockout mice to examine neuronal and glial tropism and short-term consequences of direct infection with a Brazilian variant of ZIKV.
Analysis of all of the MMPs demonstrated that conditioned medium from Mycobacterium tuberculosis-infected human monocytes (CoMTb) stimulated greater MMP-1, -3, and -9 gene expression in human microglial cells than direct infection.
These data suggest that both direct infection by HIV-1 and tissue redistribution are possible explanations for declining FoxP3(+) Tregs in progressive HIV-1 infection.
In this first report of SLPI regulation by HIV-1, we show that the expression and production of the antimicrobial and anti-inflammatory protein can be stimulated in oral epithelial cells by the virus through interactions with gp120 in the absence of direct infection.
In this first report of SLPI regulation by HIV-1, we show that the expression and production of the antimicrobial and anti-inflammatory protein can be stimulated in oral epithelial cells by the virus through interactions with gp120 in the absence of direct infection.
Taken together, the results suggest that in HSV1-infection of the CNS, enhancement of IL-6 production in glial cells is mediated not by direct infection to glial cells but rather by IL-1beta released from HSV1-stimulated MNC.
Our results indicate that HIV-1 infection alone leads to hematopoietic inhibition in vivo; however, this effect is due to indirect mechanisms rather than to direct infection of CD34(+) cells in vivo.