FIGURE 39.5. Mechanisms of viral entry into host cells.

FIGURE 39.5

Correction

The major gp120 receptor is CD4 and CXCR4, not CCR4 as indicated in the original figure.

Mechanisms of viral entry into host cells. (a) Influenza virus initiates host cell contact and entry by binding to cell-surface sialic acid receptors through its surface glycoprotein hemagglutinin. After intracellular replication, a cell-surface neuraminidase cleaves sialic acid from the cell membrane allowing viral escape. (b) Herpes simplex virus (HSV) engages host cells first through a low-affinity engagement of heparan sulfate proteoglycans via its surface glycoproteins gB and gC. Subsequently, a higher-affinity binding of viral protein gD to a member of the tumor necrosis factor–nerve growth factor (TNF/NGF) receptor family promotes membrane fusion. (c) Human immunodeficiency virus (HIV) surface glycoprotein gp120 binds sequentially to the CD4 receptor on T cells and then to a coreceptor such as chemokine receptor CCR4. The latter interaction triggers a conformational change in gp120, which exposes gp41, the HIV factor capable of initiating membrane fusion.

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From: Chapter 39, Bacterial and Viral Infections

Cover of Essentials of Glycobiology
Essentials of Glycobiology. 2nd edition.
Varki A, Cummings RD, Esko JD, et al., editors.
Cold Spring Harbor (NY): Cold Spring Harbor Laboratory Press; 2009.
Copyright © 2009, The Consortium of Glycobiology Editors, La Jolla, California.

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