Summary auto-generated
This study investigated chronic K virus infection in nude mice, which lack T cell-mediated immunity but retain B cell function. Nude mice were inoculated intracranially with K virus and monitored for 28 weeks using serological methods, virus assays, and immunohistological staining. Although infection was clinically asymptomatic, it progressed slowly with highest virus titers in spleens, kidneys, and intestines. Mice mounted prompt IgM and IgG antibody responses, yet virus persisted and spread locally. Vascular endothelial cells remained the primary replication site, but unlike normal mice, nude mice developed multifocal infection of renal tubular epithelial cells, indicating altered viral tropism during chronic infection. Infected cells appeared in scattered clusters suggesting cell-to-cell spread. The central nervous system showed no histologically detectable K virus involvement, and no tumors developed. These findings demonstrate that B cell-mediated immunity alone is insufficient to clear K virus infection or prevent local progression, although it prevents systemic dissemination and fatal disease. The results suggest T cell-mediated immunity is essential for complete viral eradication and latency establishment.
Key findings
- Nude mice developed slowly progressive K virus infection despite prompt antibody responses, contrasting with transient infection in immunologically normal mice
- Highest virus titers occurred in intestines, kidneys, and spleens, with infected cells clustering in patterns suggesting local cell-to-cell spread
- K virus altered its cellular tropism during chronic infection, extensively infecting renal tubular epithelial cells in nude mice, unlike the endothelial-only involvement in normal mice
- B cell-mediated humoral immunity alone limited systemic dissemination but failed to prevent local viral progression or achieve clearance
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Abstract
Nude (nu/nu) mice were inoculated intracranially with 106.5 newborn mouse 50% lethal doses of K virus and were studied over a period of 28 weeks using serological methods, virus assay and immunohistological staining for viral antigens. K virus infection of nude mice, although clinically asymptomatic, was slowly progressive despite prompt IgM and IgG antibody response. The highest titres of K virus infectivity were reached in spleens, kidneys and intestines. Vascular endothelial cells represented the major site of viral replication, as has been shown to be the case in immunologically normal mice, with extensive involvement of intestinal capillaries. In addition, however, unlike immunologically normal mice, nude mice inoculated with K virus developed multifocal infection of renal tubular epithelial cells. Nude mice did not develop histologically detectable evidence of central nervous system involvement by K virus, and K virus infection did not result in neoplasia. Infected vascular endothelial cells and renal tubular epithelial cells in animals studied at 16 and 27 weeks after inoculation were grouped in scattered clusters, suggesting local spread of infection. The present study indicates that nude mice with preserved B cell function but impaired T cell-mediated immunity are able to limit systemic dissemination of K virus but are unable to prevent local progression of infection by cell-to-cell spread. K virus is capable of altering its cellular tropism during chronic infection.