Quackenbush SL, Mullins JI, Hoover EA (1996). Replication kinetics and cell tropism of an immunosuppressive feline leukaemia virus. The Journal of general virology, 77 ( Pt 7), 1411-20. (pubmed)
To elucidate in vivo cell tropism and infection kinetics of an immunodeficiency-inducing isolate of feline leukaemia virus (FeLV-FAIDS), we quantified the two major genotypes comprising FeLV-FAIDS [the replication-competent common form (clone 61E) and the replication-defective variant (clone 61C)] in lymphocyte and leukocyte populations from infected cats. Micromagnetic separation of cell subsets, virus genome-specific PCR and flow cytometry were used to demonstrate the following sequence of events in infected animals: (i) very early replication of both 61E and 61C in CD4 T cells (provirus burden 0.2 to 1 copy/cell at 2-4 weeks post-infection); (ii) lower magnitude replication of both viruses in CD8 T cells and B cells during this initial phase of infection; (iii) plateauing of CD4 cell virus burden accompanied by escalation in CD8 and B cell provirus burdens after 4 weeks; (iv) extensive infection of haemopoietic and circulating myeloid cells. FeLV-FAIDS 61E and 61C replication kinetics and lymphocyte tropisms were similar in blood and lymph nodes, where provirus burdens ranged from 0.15 to 1.0 copy/cell. Moreover, virus infection was productive; 8-48 percent of blood lymphocytes, 35-81 percent of node lymphocytes and 53-98 percent of bone marrow cells expressed FeLV capsid antigen (p27 Gag). These findings suggest that the immunosuppressive potency of FeLV-FAIDS reflects the unique cytopathicity rather than unique cytotropism of its 61C (versus 61E) component.