There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.
ABSTRACT
Hepatitis E virus (HEV) poses a global threat, which currently remains understudied
in terms of host interactions. Epidermal growth factor receptor (EGFR) plays multifaceted
roles in viral pathogenesis, impacting host-cell entry, viral replication, and host-defense
modulation. On the one hand, EGFR signaling emerged as a major driver in innate immunity;
on the other hand, a crosstalk between HEV and EGFR requires deeper analysis. We therefore
aimed to dissect the receptor’s involvement in the HEV life cycle. In persistently
HEV-infected cells, the EGFR amount is decreased alongside with enhanced receptor
internalization. As compared with the control ligand-induced EGFR, activation revealed
an early receptor internalization and degradation in HEV-replicating cells, resulting
in a notable EGFR signaling delay. Interestingly, inhibition or silencing of EGFR
increased viral replication, extracellular and intracellular viral transcripts, and
released infectious particles. The pro-viral impact of EGFR inhibition was attributed
to (i) impaired expression of interferon-stimulated genes, (ii) activation of the
autophagosomal system, (iii) virus-induced inhibition of lysosomal acidification,
and (iv) a decrease of the cellular cholesterol level.
IMPORTANCE
This study identifies epidermal growth factor receptor (EGFR) as a novel host factor
affecting hepatitis E virus (HEV): EGFR downregulation promotes viral replication,
release, and evasion from the innate immune response. The discovery that EGFR inhibition
favors viral spread is particularly concerning for HEV patients undergoing EGFR inhibitor
treatment.
The two most commonly used methods to analyze data from real-time, quantitative PCR experiments are absolute quantification and relative quantification. Absolute quantification determines the input copy number, usually by relating the PCR signal to a standard curve. Relative quantification relates the PCR signal of the target transcript in a treatment group to that of another sample such as an untreated control. The 2(-Delta Delta C(T)) method is a convenient way to analyze the relative changes in gene expression from real-time quantitative PCR experiments. The purpose of this report is to present the derivation, assumptions, and applications of the 2(-Delta Delta C(T)) method. In addition, we present the derivation and applications of two variations of the 2(-Delta Delta C(T)) method that may be useful in the analysis of real-time, quantitative PCR data. Copyright 2001 Elsevier Science (USA).
Fiji is a distribution of the popular open-source software ImageJ focused on biological-image analysis. Fiji uses modern software engineering practices to combine powerful software libraries with a broad range of scripting languages to enable rapid prototyping of image-processing algorithms. Fiji facilitates the transformation of new algorithms into ImageJ plugins that can be shared with end users through an integrated update system. We propose Fiji as a platform for productive collaboration between computer science and biology research communities.
scite shows how a scientific paper has been cited by providing the context of the citation, a classification describing whether it supports, mentions, or contrasts the cited claim, and a label indicating in which section the citation was made.
Smart Citations