Summary auto-generated
This study examined how fusion regulatory protein-1 (FRP-1), identical to the 4F2/CD98 heavy chain, affects cell fusion induced by paramyxoviruses. Researchers tested seven anti-FRP-1 monoclonal antibodies (MAbs) on human parainflenza virus type 2 (HPIV-2) and Newcastle disease virus (NDV)-infected HeLa cells. While most anti-FRP-1 MAbs enhanced cell fusion in NDV-infected cells, the MAb HBJ127 unexpectedly suppressed HPIV-2-induced cell fusion, delaying multinucleated giant cell formation. This suppression was not due to reduced virus replication, decreased viral protein expression, or altered surface expression of the viral HN and F glycoproteins required for fusion. The inhibitory effect was confirmed in cells transiently expressing only the HPIV-2 HN and F proteins, though the effect was weaker than in virus-infected cells. These findings demonstrate that FRP-1 has multifunctional roles in virus-mediated cell fusion, capable of both enhancing and suppressing fusion depending on the specific virus-cell system, despite both viruses belonging to the same Rubulavirus genus.
Key findings
- The anti-FRP-1 MAb HBJ127 suppressed cell fusion in HPIV-2-infected cells while enhancing fusion in NDV-infected cells, despite both viruses belonging to the same genus Rubulavirus
- Suppression of HPIV-2-induced cell fusion by HBJ127 was not due to reduced virus replication or altered expression of viral glycoproteins HN and F
- FRP-1 molecules demonstrate multifunctional regulatory capacity, capable of transducing both cell fusion-enhancing and fusion-suppressing signals depending on the virus-cell system
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Abstract
Fusion regulatory protein-1 (FRP-1) regulates virus-mediated cell fusion and induces poly-karyocyte formation of monocytes without any fusogen. We have recently reported that FRP-1 and the 4F2/CD98 heavy chain are identical molecules. Cell fusion in Newcastle disease virus (NDV)-infected HeLa cells was enhanced when cells were incubated with anti-FRP-1 MAb. Anti-FRP-1 MAbs also induced human immunodeficiency virus gp160-mediated cell fusion. However, HBJ127, an anti-FRP- 1/4F2/CD98 MAb that enhanced cell fusion in NDV-infected cells, delayed human parainfluenza virus type 2 (HPIV-2)-induced cell fusion in HeLa cells, although these viruses belong to the same genus Rubulavirus. No anti-FRP-1 MAbs enhanced cell fusion in HPIV-2-infected HeLa cells. Anti-FRP-1 MAbs including HBJ127 showed no effect on virus growth and expression levels of virus-specific poly-peptides in HPIV-2-infected HeLa cells, indicating that the delay in cell fusion by an anti-FRP-1 MAb is not due to suppression of virus replication. When HeLa cells were transfected with an expression vector harbouring HPIV-2 HN and F genes, cell fusion was also suppressed by HBJI27, but the effect was weak in comparison with virus-infected cells. These data indicate anti- FRP-1 antibodies not only induce/enhance, but also inhibit/delay virus- induced cell fusion and therefore FRP-1 molecules are multifunctional.