2002/08/01 by Rachael C. Rigden, Carlos P. Carrasco, Artur Summerfield +2
Agricultural and Biological Sciences · Biochemistry, Genetics and Molecular Biology · Medicine · #Animal Disease Management and Epidemiology #Viral Infections and Immunology Research #Virus-based gene therapy research
paper · doi:10.1046/j.1365-2567.2002.01460.x
crossref issued 2002/08/01 · crossref published 2002/08/01 · crossref published-online 2002/08/01 · crossref published-print 2002/08/01 · openalex publication_date 2002/08/01 · crossref created 2003/03/12 · crossref deposited 2023/10/16 · openalex created_date 2025/10/10 · crossref indexed 2026/07/31 · openalex updated_date 2026/08/01
Macrophages play critical roles in innate defences against virus infections, particularly pertinent to the rapid immune response required following emergency vaccination against foot-and-mouth disease virus (FMDV). Consequently, macrophage-FMDV interaction was studied in vitro, in the absence of specific antibodies, to mimic the animal early postvaccination. A gradual loss of infectivity and viral antigen was observed over 48 hr, and no evidence of productive virus replication was found. From the pathological viewpoint, an important observation was that the majority of macrophages carried infectious virus for at least 10 hr. Pronase and mild acid treatments showed the virus to be primarily on the cell surface during the first 4 hr. Thereafter, it became internalized (pronase- and pH resistant), but remained infectious for 10-24 hr. The internalization process was dependent on microfilament activity, while the survival of infectious virus related to live virus-dependent inhibition of macrophage protein synthesis. Infectious centre assays demonstrated that this infectious virus - whether on the cell surface or internalized - was actually being released from the cells. This is interesting considering that FMDV is highly pH labile. Together, these characteristics suggest that the virus had been internalized by a process such as macropinocytosis, and fusion with endosomes was delayed or impaired. This mechanism whereby the virus could 'piggyback' on or in the macrophage, becoming internalized but not degraded for at least 10 hr, are important considerations in FMD pathogenesis. Such 'virus-transporting' macrophages would be in a position to carry infectious FMDV to different sites in the body, where it could be released to infect other cells for replication.