Feline leukaemia provirus load during the course of experimental infectionand in naturally infected cats

Citation
R. Hofmann-lehmann et al., Feline leukaemia provirus load during the course of experimental infectionand in naturally infected cats, J GEN VIROL, 82, 2001, pp. 1589-1596
Citations number
38
Categorie Soggetti
Microbiology
Journal title
JOURNAL OF GENERAL VIROLOGY
ISSN journal
00221317 → ACNP
Volume
82
Year of publication
2001
Part
7
Pages
1589 - 1596
Database
ISI
SICI code
0022-1317(200107)82:<1589:FLPLDT>2.0.ZU;2-D
Abstract
Feline leukaemia virus (FeLV) infection in domestic cats can vary in its ou tcome (persistent, transient, no infection) for reasons that are not entire ly known. It was hypothesized that the initial virus and provirus load coul d significantly influence the course of retrovirus infection. To determine the role of provirus loads, two methods of PCR, a nested PCR and a fluoroge nic probe-based (TaqMan) real-time quantitative PCR, which were specific to the U3 region of FeLV-A were established. FeLV provirus in naturally and e xperimentally infected cats was then measured. Only 3 weeks after experimen tal FeLV-A infection, persistently infected cats demonstrated higher provir us loads and lower humoral immune responses than cats that had overcome ant igenaemia. Lower initial provirus loads were associated with successful hum oral immune responses. Unexpectedly, provirus in the buffy-coat cells of tw o cats that tested negative for the p27 antigen (a marker for viraemia) was also detected. In 597 Swiss cats, comparison of p27 antigen levels with PC R results revealed broad agreement. However, similar to the experimental si tuation, a significant number of animals (10%) was negative for the p27 ant igen and FeLV-positive by PCR. These cats had a mean provirus load 300-fold lower than that of animals testing positive for the p27 antigen. In conclu sion, an association between the provirus load and the outcome of FeLV infe ction was found. Detection of provirus carriers should contribute to furthe r the control of FeLV. In addition, quantification of provirus loads will l ead to a better understanding of FeLV pathogenesis and antiretrovirus prote ctive mechanisms.