A pathogenic picornavirus acquires an envelope by hijacking cellular membranes View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2013-03-31

AUTHORS

Zongdi Feng, Lucinda Hensley, Kevin L. McKnight, Fengyu Hu, Victoria Madden, LiFang Ping, Sook-Hyang Jeong, Christopher Walker, Robert E. Lanford, Stanley M. Lemon

ABSTRACT

Animal viruses are broadly categorized structurally by the presence or absence of an envelope composed of a lipid-bilayer membrane, attributes that profoundly affect stability, transmission and immune recognition. Among those lacking an envelope, the Picornaviridae are a large and diverse family of positive-strand RNA viruses that includes hepatitis A virus (HAV), an ancient human pathogen that remains a common cause of enterically transmitted hepatitis. HAV infects in a stealth-like manner and replicates efficiently in the liver. Virus-specific antibodies appear only after 3-4 weeks of infection, and typically herald its resolution. Although unexplained mechanistically, both anti-HAV antibody and inactivated whole-virus vaccines prevent disease when administered as late as 2 weeks after exposure, when virus replication is well established in the liver. Here we show that HAV released from cells is cloaked in host-derived membranes, thereby protecting the virion from antibody-mediated neutralization. These enveloped viruses ('eHAV') resemble exosomes, small vesicles that are increasingly recognized to be important in intercellular communications. They are fully infectious, sensitive to extraction with chloroform, and circulate in the blood of infected humans. Their biogenesis is dependent on host proteins associated with endosomal-sorting complexes required for transport (ESCRT), namely VPS4B and ALIX. Whereas the hijacking of membranes by HAV facilitates escape from neutralizing antibodies and probably promotes virus spread within the liver, anti-capsid antibodies restrict replication after infection with eHAV, suggesting a possible explanation for prophylaxis after exposure. Membrane hijacking by HAV blurs the classic distinction between 'enveloped' and 'non-enveloped' viruses and has broad implications for mechanisms of viral egress from infected cells as well as host immune responses. More... »

PAGES

367-371

References to SciGraph publications

  • 2007-12. Beyond Tsg101: the role of Alix in 'ESCRTing' HIV-1 in NATURE REVIEWS MICROBIOLOGY
  • 2012-06-03. Syndecan–syntenin–ALIX regulates the biogenesis of exosomes in NATURE CELL BIOLOGY
  • 2002. The Molecular Biology of Hepatitis A Virus in HEPATITIS VIRUSES
  • Journal

    TITLE

    Nature

    ISSUE

    7445

    VOLUME

    496

    Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nature12029

    DOI

    http://dx.doi.org/10.1038/nature12029

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1050823567

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/23542590


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    99 prophylaxis
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    103 resolution
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