from Part II - Basic virology and viral gene effects on host cell functions: betaherpesviruses
Published online by Cambridge University Press: 24 December 2009
Introduction
All viruses must deliver their genomes to host cells to initiate infection. The plasma membrane together with cell surface constituents serve as initial barriers to entry as well as the mediators that facilitate the process. This chapter will summarize what is known about the entry pathway of human cytomegalovirus, noting certain parallels and commonalities between human cytomegalovirus (HCMV) and other betaherpesviruses (see Chapter 46 for specific pathways of HHV-6 and HHV-7 entry). The roles of HCMV envelope glycoproteins and cellular receptors that control virion attachment and membrane fusion will be summarized. This chapter will also discuss the emerging role of signaling pathways in the early events in infection and examine how virus entry and innate immune activation may be coordinated.
In the simplest context, entry requires that enveloped viruses, including HCMV, HHV-6A or B and HHV-7, use virion envelope proteins to facilitate adherence to the cell surface and fusion between the virus envelope and a cellular membrane that results in the deposition of virion components into the cytoplasm. Following delivery to the cytoplasm, capsid or tegument proteins facilitate transport through the cytoplasm to and delivery of the viral genome to the nucleus in a process known as uncoating. Tegument proteins also translocate independent of the capsid to cytoplasmic or nuclear sites. For structurally complex viruses whose envelopes contain as many as 20 proteins and glycoproteins, attachment is a multi-step process typically involving more than one envelope glycoprotein interacting with a series of cell surface receptors that serve as primary receptors and coreceptors.
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