PubMed · 8050285
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G W Both, A R Bellamy, D B Mitchell. 1994. Rotavirus protein structure and function.. https://doi.org/10.1007/978-3-642-78256-5_4
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Delayed elimination of human cytomegalovirus (HCMV)-infected cells by the host immune system may contribute to viral dissemination and pathogenesis of HCMV infection. The mRNA expression dynamics of HCMV-encoded immune evasion genes US3, US6, and US11 expressed after active HCMV infection were analyzed in blood samples of lung transplant recipients by means of quantitative nucleic acid sequence-based amplification. The results were compared with the expression dynamics of IE1 mRNA and pp67 late mRNA, levels of pp65 antigenemia, and antiviral treatment. During acute infection, high levels of US3 and US6 RNA were detected before antigenemia, which were detected simultaneously with IE1 RNA. US11 RNA was detected simultaneously with antigenemia but before late pp67 RNA. These data suggest an active role of viral immune evasion during HCMV infection in vivo. Interestingly, immune evasion RNA remained detectable after clinical recovery, often independently of IE1 RNA expression, indicating persistent viral activity, which may have implications for long-term control of HCMV.
H-Cys-Leu-Gly-Gly-Leu-Leu-Thr-Met-Val-OH (CLG) peptide is an EBV subdominant epitope that represents the target of HLA-A2 restricted CTL responses. The CLG peptide has low affinity for HLA-A2 and does not produce stable complexes, both factors that determine weak CTL responses. In contrast, the [Tyr(1), Ala(3)]CLG (YLA) analogue showed high affinity for HLA-A2 molecules and efficiently stimulated CLG-specific CTL precursors. Nevertheless, this modified epitope showed low enzymatic stability. To further improve the immunotherapeutical potential of this "improved epitope", we have synthesized and tested YLA analogues containing different modifications next to the scissile peptide bond. Among the analogues we found three peptides, with higher enzymatic resistance, that efficiently stimulate CTL responses. These peptides may be used for EBV-specific immunotherapies.
We previously reported that major immediate-early promoter (MIEP) activity was regulated by intercellular zinc levels. In this report, we elucidate the mechanisms involved in this phenomenon. In luciferase reporter assays, zinc-induced activation of MIEP (-735/+62) was decreased with deletion of the promoter in stages, and MIEP (-117/+62) did not respond to zinc. The time course of the activity of MIEP responding to diethylenetriamine pentaacetic acid and zinc was not parallel with metallothionein (MT) promoter, which contains metal responsive elements. SV40 promoter that contains AP-1 binding sites, a candidate for the zinc-responsive motif in the MIEP, was not affected by zinc under our conditions. The activation of MIEP (-735/+62) by zinc was prevented with NF-kappaB decoy. When three kappaB motifs from the enhancer in the MIEP were inserted in the front of the zinc-nonresponsive MIEP (-117/+62), it became responsive to zinc. Moreover, overexpression of MT up-regulates the DNA binding of NF-kappaB and NF-kappaB-induced activation of transcription. These findings strongly suggest that MT and NF-kappaB act as mediator/regulator in zinc-induced activation of MIEP.