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Mechanisms of human cytomegalovirus infection with a focus on epidermal growth factor receptor interactions
Author(s) -
Falcão Aline Semblano Carreira,
Costa Vasconcelos Pedro Fernando,
Lobato da Silva Dorotéa de Fátima,
Viana Pinheiro João de Jesus,
Falcão Luiz Fábio Magno,
Quaresma Juarez Antonio Simões
Publication year - 2017
Publication title -
reviews in medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.06
H-Index - 90
eISSN - 1099-1654
pISSN - 1052-9276
DOI - 10.1002/rmv.1955
Subject(s) - human cytomegalovirus , biology , cytomegalovirus , receptor , immunology , viral entry , epidermal growth factor receptor , tropism , epidermal growth factor , virology , tyrosine kinase , cell type , signal transduction , cell , virus , herpesviridae , viral replication , microbiology and biotechnology , viral disease , genetics
Summary Human cytomegalovirus (HCMV) is a widespread opportunistic herpesvirus that causes severe diseases in immunocompromised individuals. It has a high prevalence worldwide that is linked with socioeconomic factors. Similar to other herpesviruses, HCMV has the ability to establish lifelong persistence and latent infection following primary exposure. HCMV infects a broad range of cell types. This broad tropism suggests that it may use multiple receptors for host cell entry. The identification of receptors used by HCMV is essential for understanding viral pathogenesis, because these receptors mediate the early events necessary for infection. Many cell surface components have been identified as virus receptors, such as epidermal growth factor receptor (EGFR), which is characterized by tyrosine kinase activity and plays a crucial role in the control of key cellular transduction pathways. EGFR is essential for HCMV binding, signaling, and host cell entry. This review focuses on HCMV infection via EGFR on different cell types and its implications for the cellular environment, viral persistence, and infection.