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A Slow Maturation Process Renders Hepatitis B Virus Infectious

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A Slow Maturation Process Renders Hepatitis B Virus Infectious. / Seitz, Stefan; Iancu, Caroline; Volz, Tassilo; Mier, Walter; Dandri-Petersen, Maura; Urban, Stephan; Bartenschlager, Ralf.

In: CELL HOST MICROBE, Vol. 20, No. 1, 13.07.2016, p. 25-35.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Seitz, S, Iancu, C, Volz, T, Mier, W, Dandri-Petersen, M, Urban, S & Bartenschlager, R 2016, 'A Slow Maturation Process Renders Hepatitis B Virus Infectious', CELL HOST MICROBE, vol. 20, no. 1, pp. 25-35. https://doi.org/10.1016/j.chom.2016.05.013

APA

Seitz, S., Iancu, C., Volz, T., Mier, W., Dandri-Petersen, M., Urban, S., & Bartenschlager, R. (2016). A Slow Maturation Process Renders Hepatitis B Virus Infectious. CELL HOST MICROBE, 20(1), 25-35. https://doi.org/10.1016/j.chom.2016.05.013

Vancouver

Seitz S, Iancu C, Volz T, Mier W, Dandri-Petersen M, Urban S et al. A Slow Maturation Process Renders Hepatitis B Virus Infectious. CELL HOST MICROBE. 2016 Jul 13;20(1):25-35. https://doi.org/10.1016/j.chom.2016.05.013

Bibtex

@article{ba472503d4614a5b805564a92cf254f2,
title = "A Slow Maturation Process Renders Hepatitis B Virus Infectious",
abstract = "Hepatitis B virus (HBV) replication is strictly limited to the liver. Virions attach to hepatocytes through interactions of the viral PreS envelope protein domain with heparan sulfate proteoglycans (HSPGs). However, HSPG is ubiquitously present on many cell types, suggesting that HBV employs mechanisms to avoid attachment at extrahepatic sites. We demonstrate that HBV particles are released from cells in an inactive form with PreS hidden in the interior. These HSPG-non-binding (N-type) particles develop receptor binding competence by translocating PreS across the envelope onto their surface. Conversion into HSPG-binding (B-type) particles occurs spontaneously and renders HBV infectious. Low-dose inoculation of mice with human liver xenografts demonstrates superiority of N-type particles in establishing infections, while mature B-type virions, generated via N-type conversion, are profoundly impaired, correlating with non-selective accumulation in extrahepatic tissues. This dynamic topology switch represents a maturation process utilized by HBV to most likely avoid non-productive docking outside the liver.",
author = "Stefan Seitz and Caroline Iancu and Tassilo Volz and Walter Mier and Maura Dandri-Petersen and Stephan Urban and Ralf Bartenschlager",
note = "Copyright {\textcopyright} 2016 Elsevier Inc. All rights reserved.",
year = "2016",
month = jul,
day = "13",
doi = "10.1016/j.chom.2016.05.013",
language = "English",
volume = "20",
pages = "25--35",
journal = "CELL HOST MICROBE",
issn = "1931-3128",
publisher = "Cell Press",
number = "1",

}

RIS

TY - JOUR

T1 - A Slow Maturation Process Renders Hepatitis B Virus Infectious

AU - Seitz, Stefan

AU - Iancu, Caroline

AU - Volz, Tassilo

AU - Mier, Walter

AU - Dandri-Petersen, Maura

AU - Urban, Stephan

AU - Bartenschlager, Ralf

N1 - Copyright © 2016 Elsevier Inc. All rights reserved.

PY - 2016/7/13

Y1 - 2016/7/13

N2 - Hepatitis B virus (HBV) replication is strictly limited to the liver. Virions attach to hepatocytes through interactions of the viral PreS envelope protein domain with heparan sulfate proteoglycans (HSPGs). However, HSPG is ubiquitously present on many cell types, suggesting that HBV employs mechanisms to avoid attachment at extrahepatic sites. We demonstrate that HBV particles are released from cells in an inactive form with PreS hidden in the interior. These HSPG-non-binding (N-type) particles develop receptor binding competence by translocating PreS across the envelope onto their surface. Conversion into HSPG-binding (B-type) particles occurs spontaneously and renders HBV infectious. Low-dose inoculation of mice with human liver xenografts demonstrates superiority of N-type particles in establishing infections, while mature B-type virions, generated via N-type conversion, are profoundly impaired, correlating with non-selective accumulation in extrahepatic tissues. This dynamic topology switch represents a maturation process utilized by HBV to most likely avoid non-productive docking outside the liver.

AB - Hepatitis B virus (HBV) replication is strictly limited to the liver. Virions attach to hepatocytes through interactions of the viral PreS envelope protein domain with heparan sulfate proteoglycans (HSPGs). However, HSPG is ubiquitously present on many cell types, suggesting that HBV employs mechanisms to avoid attachment at extrahepatic sites. We demonstrate that HBV particles are released from cells in an inactive form with PreS hidden in the interior. These HSPG-non-binding (N-type) particles develop receptor binding competence by translocating PreS across the envelope onto their surface. Conversion into HSPG-binding (B-type) particles occurs spontaneously and renders HBV infectious. Low-dose inoculation of mice with human liver xenografts demonstrates superiority of N-type particles in establishing infections, while mature B-type virions, generated via N-type conversion, are profoundly impaired, correlating with non-selective accumulation in extrahepatic tissues. This dynamic topology switch represents a maturation process utilized by HBV to most likely avoid non-productive docking outside the liver.

U2 - 10.1016/j.chom.2016.05.013

DO - 10.1016/j.chom.2016.05.013

M3 - SCORING: Journal article

C2 - 27321908

VL - 20

SP - 25

EP - 35

JO - CELL HOST MICROBE

JF - CELL HOST MICROBE

SN - 1931-3128

IS - 1

ER -