Measles virus breaks through epithelial cell barriers to achieve transmission
Makoto Takeda
Makoto Takeda
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Commentary

Measles virus breaks through epithelial cell barriers to achieve transmission

Abstract

Measles is a highly contagious disease that causes immunosuppression in patients. Measles virus infection has been thought to begin in the respiratory epithelium and then spread to lymphoid tissue. In this issue of the JCI, Leonard et al. provide data to suggest an alternative model of measles virus pathogenesis (see the related article beginning on page 2448). In human primary epithelial cells and rhesus monkeys in vivo, the authors show that initial infection of respiratory epithelium is not necessary for the virus to enter the host but that viral entry into epithelial cells via interaction of the virus with a receptor located on the basolateral side of the epithelium is required for viral shedding into the airway and subsequent transmission.

Authors

Makoto Takeda

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Figure 1

Schema of the MV particle and its receptor-binding H protein.

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Schema of the MV particle and its receptor-binding H protein. MV is an e...
MV is an enveloped virus and possesses 2 types of glycoprotein spikes, designated H and F proteins. The F protein mediates membrane fusion between the viral envelope and the host cell plasma membrane, while the H protein that forms homodimers on the viral envelope is responsible for binding of virus to receptors on target cells. The head domain of the H protein exhibits a six-bladed β-propeller fold. Residues important for using SLAM as a receptor map to a localized area of the β5 sheet, forming a putative SLAM-binding site (shown in blue). On the other hand, relevant residues for epithelial cell infection map to a small area in the β5 and β4 sheets, forming another putative receptor-binding site (yellow) that is essentially distinct from the SLAM-binding site.