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Cracking the cell access code for the deadly virus VEEV

The discovery that the receptor protein LDLRAD3 is essential for infection of human cells by Venezuelan equine encephalitis virus could inform strategies to combat this potentially lethal infection.
  1. James Zengel

    1. James Zengel is in the Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305, USA.

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  2. Jan E. Carette

    1. Jan E. Carette is in the Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305, USA.

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When viruses jump from animals to humans, disease outbreaks can follow. A striking example is Venezuelan equine encephalitis virus (VEEV). This virus causes sporadic disease outbreaks in horses in Latin America that frequently spill over into humans, resulting in often-deadly neurological disease1. Because of its pathogenicity in livestock and humans, VEEV has been studied as a biological weapon by several countries, including the United States2. Treatments for the disease are therefore highly desirable. It has been unknown how VEEV co-opts cellular pathways to establish infection in people — in particular, which host receptor protein allows VEEV to cross the cell membrane and initiate its replication cycle. Writing in Nature, Ma et al.3 describe the long-sought receptor for VEEV, and show that it is essential for viral replication in both human cells and mouse models.

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Nature 588, 223-224 (2020)

doi: https://doi.org/10.1038/d41586-020-03192-6

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