Hepatitis B Virus infection initiates with a large surface protein-dependent binding to heparan sulfate proteoglycans

Schulze, Andreas; Seitz, Steven P.; Gripon, Philippe; Urban, S.

doi:10.1055/s-2008-1037636

Cited by 109 publications

(187 citation statements)

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“…Heparan sulfate (HS) acts as a coreceptor for the cellular entry of viruses including not only hepatitis B and C viruses (Barth H et al 2003;Schulze A et al 2007) but also many other viruses such as herpes simplex virus 1 (Shukla D et al). Viral uptake thus is particularly relevant to liver that is prone to many viral infections including hepatitis that often precedes the development of hepatocellular carcinoma.…”

Section: Discussionmentioning

confidence: 99%

SULF1/SULF2 reactivation during liver damage and tumour growth

Graham

Murphy

Dhoot

2016

Histochem Cell Biol

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Section: Discussionmentioning

confidence: 99%

SULF1/SULF2 reactivation during liver damage and tumour growth

Graham

Murphy

Dhoot

2016

Histochem Cell Biol

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“…HB virions can bind to the hepatocytes' membrane through a non-specific interaction with cell surface glycosaminoglycans (10). Then, a high-affinity interaction between the myristoylated N-terminal region of the preS1 domain and the sodium taurocholate co-transporting polypeptide (NTCP) triggers the virus uptake likely by endocytosis or by HBV envelope fusion with the plasma membrane (11,12).…”

Section: Hbv Replication Cyclementioning

confidence: 99%

Untitled

2017

Istanbul Med J

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Hepatitis B virus (HBV) is a small-enveloped DNA virus that belongs to the Hepadnaviridae family, representing the second greatest cause of chronic viral hepatitis worldwide (1). Despite decades of vaccination, HBV infection is still a major global burden, with 257 million persons chronically infected and approximately 880,000 deaths per year (2). Chronic hepatitis B (CHB) is the result of an acute, unresolved infection that induces an immune-mediated liver damage followed by fibrotic tissue deposition leading overtime to a complete alteration of the hepatic architecture toward cirrhosis and its complications, such as liver failure and hepatocellular carcinoma (HCC) (3, 4).Remarkable advances have been made in the setting of CHB treatment (5). In particular, the development of new molecular biology techniques in association with an ever deeper understanding of the different phases of HBV infection and primarily the introduction of nucleos(t)ide analogs (NAs) are the main features that may lead to the virological cure in the near term and the functional cure in the long-term follow-up (6).This review discusses the current available drugs and treatment guidelines for CHB therapy focusing on telbivudine (LtD), a thymidine analog that has demonstrated unique features that make the abovementioned drug still valid even in the era of new powerful anti-viral agents. HBV Virology and Replication CycleHBV structure Hepatitis B virus structure consists of an outer envelope made of three viral surface proteins named preS1 (large), preS2 (middle), and S (small), which correspond to the serologic HBsantigen (HBsAg), and an inner nucleocapsid formed by core proteins, which correspond to HBcore-antigen (HBcAg) (7). Within the nucleocapsid is present the full-length HBV genome as a partially double-stranded relaxed circular (rc) DNA linked to the viral polymerase protein by a phosphotyrosine bond (8). The genome has an extremely compact organization displaying four partially overlapped major open reading frames (ORFs): the preS/S that encodes the three viral surface proteins, the pre-core/core that encodes both the nucleocapsid core protein and the non-structural core protein known as the e-antigen (HBeAg); the polymerase ORF that encodes the viral polymerase; and the X ORF that encodes the regulatory X protein that is essential for viral replication (9). Chronic Hepatitis B Treatment: Current Perspectives on TelbivudineHepatitis B virus (HBV) is the primary cause of chronic viral hepatitis worldwide. Currently, there are 5 oral nucleos(t)ide analogs (NAs) approved for chronic hepatitis B (CHB) treatment and include lamivudine, adefovir, telbivudine (LtD), entecavir (ETV), and tenofovir disoproxil fumarate (TDF). ETV and TDF are those with higher anti-viral efficacy and lower resistance rates, whereas LtD shows similar efficacy but has a higher risk for viral resistance in long-term monotherapy. However, LtD carries several advantages that must be considered and are worthy of discussion. Compared to other NAs, LtD showed a poten...

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“…Studies have shown that heparin sulfate proteoglycans (HSPGs) provides an initial binding site to HBV on the surface of hepatocytes [57]. Studies have reported that the preS1 binds to HSPG through myristoylated N-terminal domain [57].…”

Section: Heparin Sulfatementioning

confidence: 99%

“…The primary target organ of HBV is hepatocytes, and all of receptors reported so far are not hepatocyte specific as P80 expresses not only in hepatocytes but also in all human tissues [56], HBV-BF is soluble receptor [8], IL6 also expresses on hepatic as well as on cells of non-hepatic origin [48], heparin sulfate is also not a specific hepatic receptor it expresses on many different cells [57], lipoprotein lipase is also not a liver specific receptor [10]. Although studies have reported that these receptors have binding motif for preS1 region of HBV but none of the study elaborating the post binding events.…”

Section: Why Many Receptors For Hbvmentioning

confidence: 99%

“…The same HepG2 cells were later reported to carry human squamous cell carcinoma antigen 1 [11], a membrane protein, interacting with the same infamous residues preS1 21-47 amino acids [47]. The list gets populated by past studies reporting immunoglobulin A receptor [54], asialoglycoprotein receptor [67], hepatitis B virus binding factor [5], Glyceraldehyde 3 phosphate dehydrogenase [52], P80 [56], nascent polypeptide-associated complex a polypeptide (NACA) [30], GRP75 [7], lipoprotein lipase [70], heparin sulfate [57] and sodium taurocholate cotransporting polypeptide (NTCP) (Fig. 1).…”

Section: Introductionmentioning

confidence: 99%

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Deciphering the mystery of hepatitis B virus receptors: A historical perspective

2015

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Hepatitis B virus is one of the major reasons of viral hepatitis with an estimated 350 million infected patients worldwide. Although, the virus was discovered and cloned more than three decades ago, its entry mechanism has still been in investigation. Numerous potential candidates have been proposed and investigated rigorously to reveal HBV entry mechanism and to unveil the first door of viral entry to hepatocytes. This review provides a short account of role of receptors for entry of HBV into hepatocytes. The viral preS1 region of large surface protein is involved in the attachment of HBV to hepatocytes. The putative attachment site of HBV is located at amino acids 21-47 of preS1. So far, several proteins have been proposed to interact with these different regions of the preS1 domain which includes human immunoglobulin A receptor, glyceraldehyde-3-phosphate dehydrogenase, interleukin-6, a 31-kDa protein, HBV binding factor, asialoglycoprotein receptor, nascent polypeptide-associated complex a polypeptide, lipoprotein lipase, hepatocyteassociated heparan sulfate proteoglycans, glucose-regulated protein 75. However, none of them have appeared to be generally accepted as a true receptor for the virus until recently when sodium taurocholate cotransporting polypeptide identified as HBV entry receptor. Current review provides scientific historical perspective of various candidates known to be interacting with preS1 of HBV for their possible role in viral entry.

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Hepatitis B Virus infection initiates with a large surface protein-dependent binding to heparan sulfate proteoglycans

Cited by 109 publications

References 0 publications

SULF1/SULF2 reactivation during liver damage and tumour growth

SULF1/SULF2 reactivation during liver damage and tumour growth

Untitled

Deciphering the mystery of hepatitis B virus receptors: A historical perspective

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