T2 hyperintense signal in fetal brain MRI associated with positive cytomegalovirus infection has increased ADC values in the temporal and parietal lobes, suggestive of brain edema in these areas.
In this work we investigated the expression of soluble (s)HLA-G and beta-2 microglobulin (component of HLA) molecules in correlation with the risk of transmission and severity of congenital HCMV infection.
To our knowledge, our findings provide new insights into the roles of KLRG1 and CD57 expression in human T cells, forming the basis for a refined model of CD8<sup>+</sup> T cell differentiation during CMV infection.
Unlike cytomegalovirus (CMV) infection and aging, human immunodeficiency virus (HIV) decreases the proportion of CD28(-)CD8(+) T cells expressing CD57.
A population of Natural Killer (NK) cells expressing the activating receptor NKG2C and the maturation marker CD57 expands in response to human cytomegalovirus (HCMV) infection.
We extend previous observations of the impact of CMV on CD8<sup>+</sup> T cell functionality to the CD4<sup>+</sup> T cell compartment, revealing CD57 as a polyfunctionality marker of T cells which expands after CMV infection.
With a mediation analysis we demonstrated that cytomegalovirus (CMV) infection, which is an important driving force of immunosenescence, largely accounted for elevated CD57 expression observed in ELA.
As chronic cytomegalovirus (CMV) infection is probably one of the major driving forces of immunosenescence, and its persistent infection results in functional and phenotypic changes to the T-cell repertoire, the aim of this study was to analyze the effect of CMV-seropositivity and aging on the expression of CD300a and CD161 inhibitory receptors, along with the expression of CD57 marker on CD4<sup>+</sup>, CD8<sup>+</sup>, CD8<sup>+</sup>CD56<sup>+</sup> (NKT-Like) and CD4<sup>-</sup>CD8<sup>-</sup> (DN) T-cell subsets.
We here studied whether subclinical CD is associated with changes in blood CD57-expressing and Vδ1-expressing lymphocytes in children, and whether cytomegalovirus (CMV) infection modifies this association.
Whereas, FcRγ<sup>neg</sup> NK cells in CMV infection are reported to express increased levels of the maturation marker CD57, the FcRγ<sup>neg</sup> NK cells observed in our CMV-negative vaccine cohort express less CD57 than their FcRγ<sup>+</sup> counterparts.
In this article, we describe a case of transient monoclonal CD8+/CD57+ T-cell lymphocytosis with large granular lymphocyte (LGL) morphology occurring after primary CMV infection and review cases of virus-associated monoclonal CD8+ T-cell expansions reported in the literature.
Studies on dynamin function in CMV infection will help us understand the host-virus interaction pathways amenable to targeting by conventional small molecules, as well as by newer generation nucleotide-based therapeutics (e.g., small interfering RNA, CRISPR/CAS gRNA, etc.).
The blood ammonia levels of the children with infantile hepatitis syndrome induced by CMV infection were not correlated with the liver function indicators, such as total bilirubin, direct bilirubin, alanine aminotransferase, aspartate aminotransferase, γ-glutamyltransferase, total bile acid, and cholinesterase (P>0.05), but they were negatively correlated with blood albumin (ALB) (P<0.05).
CMV infection may activate the mitogen-activated protein kinase pathway, of which aberrant activation is frequently associated with BRAF mutation in papillary thyroid cancer.
It was indicated that miR-US25-1 level was upregulated in subjects or in endothelial cells with HCMV infection; and the miR-US25-1 downregulated the expression of BRCC 3 by targeting the 5' UTR of BRCC 3.
However, the involvement of type-I transmembrane glycoprotein CD147/EMMPRIN (extracellular matrix metalloproteinase inducer) in the antiviral response to HCMV infection is still unknown.
We report in this study on the expression of BTLA in human T cell subsets as well as its regulation on virus-specific T cells during primary human CMV infection.