A Slow Maturation Process Renders Hepatitis B Virus Infectious.Hepatitis B virus (HBV) replication is strictly limited to the liver.  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.  Conversion into HSPG-binding (B-type) particles occurs spontaneously and renders HBV infectious.  This dynamic topology switch represents a maturation process utilized by HBV to most likely avoid non-productive docking outside the liver.
HBV
A Slow Maturation Process Renders Hepatitis B Virus Infectious.Hepatitis B virus (HBV) replication is strictly limited to the liver.  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.  Conversion into HSPG-binding (B-type) particles occurs spontaneously and renders HBV infectious.  This dynamic topology switch represents a maturation process utilized by HBV to most likely avoid non-productive docking outside the liver.
HBV
A Slow Maturation Process Renders Hepatitis B Virus Infectious.Hepatitis B virus (HBV) replication is strictly limited to the liver.  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.  Conversion into HSPG-binding (B-type) particles occurs spontaneously and renders HBV infectious.  This dynamic topology switch represents a maturation process utilized by HBV to most likely avoid non-productive docking outside the liver.
HBV
A Slow Maturation Process Renders Hepatitis B Virus Infectious.Hepatitis B virus (HBV) replication is strictly limited to the liver.  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.  Conversion into HSPG-binding (B-type) particles occurs spontaneously and renders HBV infectious.  This dynamic topology switch represents a maturation process utilized by HBV to most likely avoid non-productive docking outside the liver.
HBV
A Slow Maturation Process Renders Hepatitis B Virus Infectious.Hepatitis B virus (HBV) replication is strictly limited to the liver.  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.  Conversion into HSPG-binding (B-type) particles occurs spontaneously and renders HBV infectious.  This dynamic topology switch represents a maturation process utilized by HBV to most likely avoid non-productive docking outside the liver.
HBV