1984
DOI: 10.1016/0166-0934(84)90071-5
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Virus-binding activity of fibronectin: Masking of hepatitis A virus

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Cited by 24 publications
(18 citation statements)
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“…The lack of any comparable precipitation of virus mixed with FCS or fraction 1 could be due to either antigenic differences between the human and bovine geM molecules, or the antigenic masking of ~x2i with other proteins present in FCS. The latter explanation is plausible because Seelig et al (1984) have demonstrated that fibronectin inhibits the detection of HAV by solidphase RIA and that HAV may complex with a number of serum components to give immune complexes in vivo (Margolis et al, t988;Margolis & Nainan, 1990).…”
Section: Discussionmentioning
confidence: 99%
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“…The lack of any comparable precipitation of virus mixed with FCS or fraction 1 could be due to either antigenic differences between the human and bovine geM molecules, or the antigenic masking of ~x2i with other proteins present in FCS. The latter explanation is plausible because Seelig et al (1984) have demonstrated that fibronectin inhibits the detection of HAV by solidphase RIA and that HAV may complex with a number of serum components to give immune complexes in vivo (Margolis et al, t988;Margolis & Nainan, 1990).…”
Section: Discussionmentioning
confidence: 99%
“…It is known that during viraemia, virus can be isolated from serum in association with immune complexes (Margolis et al, 1988;Margolis & Nainan, 1990). Virus grown in vitro is associated with host cell-derived material (Lemon & Binn, 1985) and has been shown to interact with the serum protein fibronectin (Seelig et al, 1984). It is possible that virion-bound host components play a role in virus attachment and dissemination.…”
Section: Introductionmentioning
confidence: 99%
“…Fibronectin is able to bind to several viruses (1,4,5,(40)(41)(42), and a recent study has shown that a virus-binding domain is located in the type III 1 repeat (42). A peptide containing the III 1 region efficiently bound to HIV in vitro, and when the virus was incubated with the III 1 fragment before being added to lymphocytes, HIV attachment and internalization were enhanced (42).…”
Section: Discussionmentioning
confidence: 99%
“…Although cell lines originating from tissues other than liver, such as fibroblasts and kidney cells, are also susceptible to HAV infection (9, 11) and although HAV antigen and the putative receptor for HAV could be detected in different organs, such as kidney, spleen, and gastrointestinal tract (2, 6, 10, 18), no extrahepatic sites of HAV replication have been clearly identified. The data on the ubiquitous expression of a receptor for HAV and the ability of HAV to replicate in a number of nonliver cells in cell cultures, but obviously not in the organism, suggest that HAV may be targeted to the liver by a particular mechanism.Data from several laboratories showed that HAV virions are partially associated with immunoglobulin A (IgA) molecules (19,22) and other host organism-derived materials, such as fibronectin or ␣ 2 -macroglobulin (21,23,24,35,43). As viruses may find entry into host cells via receptors specific for molecules of the host organism ligated to the virion (13,16,20,26) and as the liver plays a central role in IgA metabolism by eliminating IgA as well as antigen-IgA complexes (4), we wondered if HAV-specific IgA ligated to HAV supports the targeting of HAV to the liver and is able to mediate the entry of HAV into hepatocytes via receptors specific for the IgA molecule and if such a carrier-mediated mechanism may result in viral infection.…”
mentioning
confidence: 99%
“…Data from several laboratories showed that HAV virions are partially associated with immunoglobulin A (IgA) molecules (19,22) and other host organism-derived materials, such as fibronectin or ␣ 2 -macroglobulin (21,23,24,35,43). As viruses may find entry into host cells via receptors specific for molecules of the host organism ligated to the virion (13,16,20,26) and as the liver plays a central role in IgA metabolism by eliminating IgA as well as antigen-IgA complexes (4), we wondered if HAV-specific IgA ligated to HAV supports the targeting of HAV to the liver and is able to mediate the entry of HAV into hepatocytes via receptors specific for the IgA molecule and if such a carrier-mediated mechanism may result in viral infection.…”
mentioning
confidence: 99%