Summary auto-generated
This study investigated how CD9, a cell surface molecule, contributes to feline immunodeficiency virus (FIV) infection. Researchers found that anti-CD9 monoclonal antibody (vpg15) blocks FIV infection, but not by preventing virus entry. Using PCR analysis, they demonstrated that viral reverse transcripts appeared in cells treated with anti-CD9 antibody within 3 hours of infection, confirming that virus entry and early replication events occurred normally. However, productive virus production was blocked, as shown by absent p24 capsid protein and viral proteins in Western blots. The inhibitory effect was independent of virus subtype, passage history, or cell tropism—anti-CD9 antibody equally blocked both primary and laboratory-adapted FIV strains. Notably, CD9-negative 3201 cells remained susceptible to infection, indicating CD9 is not absolutely required. However, artificially expressing CD9 on 3201 cells enhanced infection approximately 4-fold, suggesting CD9 acts as a facilitator of viral replication. The researchers propose that CD9 may function as a molecular chaperone assisting virus transport or assembly, representing a novel post-entry control point in lentivirus replication that could be targeted therapeutically.
Key findings
- Anti-CD9 antibody inhibits FIV infection at a post-entry stage, after virus entry and reverse transcription have occurred, not at initial virus binding or fusion
- The inhibitory effect of anti-CD9 antibody is independent of virus subtype, strain, passage history, and cell tropism, affecting both primary and laboratory-adapted isolates equally
- CD9 is not obligatory for FIV infection since CD9-negative 3201 cells remain susceptible, but ectopic CD9 expression enhances infection by at least 4-fold
- CD9 likely functions as a facilitator of viral replication, possibly as a molecular chaperone assisting in virus transport or assembly during the replication cycle
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Abstract
A monoclonal antibody which blocks infection with feline immunodeficiency virus (FIV) was found previously to react with the cell surface molecule CD9, implicating CD9 in the process of virus entry. We report here that inhibition by anti-CD9 antibody does not operate at the level of virus entry but at a subsequent stage in the virus life-cycle. Moreover, inhibition of infection is independent of the passage history of the virus or the virus subtype. Inhibition of FIV infection by anti-CD9 antibody does not operate in 3201 cells, which do not express this surface antigen. However, ectopic expression of CD9 on 3201 cells enhances infection with FIV, suggesting that the role of CD9 may be direct rather than via cellular signalling pathways. These results suggest a novel control point in the lentivirus life- cycle which might be susceptible to modulation by natural antagonists.