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Virus entry is a multistep process that triggers a variety of cellularpathways interconnecting into a complex network, yet the molecular complexityof this network remains largely unsolved. Here, by employing systems biologyapproach, we reveal a systemic virus-entry network initiated by humancytomegalovirus (HCMV), a widespread opportunistic pathogen. This networkcontains all known interactions and functional modules (i.e. groups ofproteins) coordinately responding to HCMV entry. The number of both genes andfunctional modules activated in this network dramatically declines shortly,within 25 min post-infection. While modules annotated as receptor system, iontransport, and immune response are continuously activated during the entireprocess of HCMV entry, those for cell adhesion and skeletal movement arespecifically activated during viral early attachment, and those for immuneresponse during virus entry. HCMV entry requires a complex receptor networkinvolving different cellular components, comprising not only cell surfacereceptors, but also pathway components in signal transduction, skeletaldevelopment, immune response, endocytosis, ion transport, macromoleculemetabolism and chromatin remodeling. Interestingly, genes that function inchromatin remodeling are the most abundant in this receptor system, suggestingthat global modulation of transcriptions is one of the most important events inHCMV entry. Results of in silico knock out further reveal that this entirereceptor network is primarily controlled by multiple elements, such as EGFR(Epidermal Growth Factor) and SLC10A1 (sodium/bile acid cotransporter family,member 1). Thus, our results demonstrate that a complex systemic network, inwhich components coordinating efficiently in time and space contributes tovirus entry.

A Systemic Receptor Network Triggered by Human cytomegalovirus Entry