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Abstract
BackgroundOver the last several decades it has been noted, using a variety of different methods, that cells infected by a specific gammaretrovirus are resistant to infection by other retroviruses that employ the same receptor; a phenomenon termed receptor interference. Receptor masking is thought to provide an earlier means of blocking superinfection, whereas receptor down regulation is generally considered to occur in chronically infected cells.ResultsWe used replication-competent GFP-expressing viruses containing either an amphotropic murine leukemia virus (A-MLV) or the gibbon ape leukemia virus (GALV) envelope. We also constructed similar viruses containing fluorescence-labeled Gag proteins for the detection of viral particles. Using this repertoire of reagents together with a wide range of antibodies, we were able to determine the presence and availability of viral receptors, and detect viral envelope proteins and particles presence on the cell surface of chronically infected cells.ConclusionsA-MLV or GALV receptors remain on the surface of chronically infected cells and are detectable by respective antibodies, indicating that these receptors are not downregulated in these infected cells as previously proposed. We were also able to detect viral envelope proteins on the infected cell surface and infected cells are unable to bind soluble A-MLV or GALV envelopes indicating that receptor binding sites are masked by endogenously expressed A-MLV or GALV viral envelope. However, receptor masking does not completely prevent A-MLV or GALV superinfection.
Highlights
Over the last several decades it has been noted, using a variety of different methods, that cells infected by a specific gammaretrovirus are resistant to infection by other retroviruses that employ the same receptor; a phenomenon termed receptor interference
It was later shown that chicken embryos productively infected by Rous Sarcoma Virus (RSV) were resistant to avian leukosis virus [2]
Cells productively infected with gammaretroviruses are resistant to challenge infection
Summary
Over the last several decades it has been noted, using a variety of different methods, that cells infected by a specific gammaretrovirus are resistant to infection by other retroviruses that employ the same receptor; a phenomenon termed receptor interference. Rubin and co-workers discovered, many years ago, that chicken embryos productively infected with Rous Sarcoma Virus (RSV) were resistant to subsequent RSV challenge [1] This phenomenon was designated as viral superinfection interference. Cells productively infected with gammaretroviruses are resistant to challenge infection This is thought to occur because primary viral envelope expression prevents superinfection by interfering with the binding of viruses that recognize the same receptor. It remains unclear how access of most gammaretroviruses to their receptors are blocked; in superinfection it is unclear whether the envelope protein interacts with the receptor and down modulates its expression on the cell surface or whether the receptor is masked at the cell surface by viral envelope proteins. Evidence exists for both mechanisms [4,5,6,7]
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