Feline leukemia virus infection as a potentiating cofactor for the primary and secondary stages of experimentally induced feline immunodeficiency virus infection

Abstract

Preexistent feline leukemia virus (FeLV) infection greatly potentiated the severity of the transient primary and chronic secondary stages of feline immunodeficiency virus (FIV) infection. Of 10 FeLV-FIV carrier cats, 5 died of experimentally induced FIV infection, compared with 2 deaths in 10 cats infected only with FeLV and 1 death in 7 cats infected only with FIV. FIV-infected cats with preexistent FeLV infections developed severe depression, anorexia, fever, diarrhea, dehydration, weight loss, and leukopenia 4 to 6 weeks after infection and were moribund within 2 weeks of the onset of signs, whereas cats infected only with FIV developed much milder self-limiting gross and hematologic abnormalities. Pathologic findings in dually infected cats that died were similar to those observed previously in cats dying from uncomplicated primary FIV infection but were much more widespread and severe. Coinfection of asymptomatic FeLV carrier cats with FIV did not increase the levels of FeLV p27 antigen present in their blood over that seen in cats infected with FeLV alone. The amount of proviral FIV DNA was much higher, however, in dually infected cats than in cats infected only with FIV; there was a greater expression of FIV DNA in lymphoid tissues, where the genome was normally detected, and in nonlymphoid tissues, where FIV DNA was not usually found. Dually infected cats that recovered from the primary stage of FIV infection remained more leukopenic than cats infected with FIV or FeLV alone, and their CD4+/CD8+ T-lymphocyte ratios were inverted. One of these cats developed what was considered to be an opportunistic infection. It was concluded, therefore, that a preexistent FeLV infection in some way enhanced the expression and spread of FIV in the body and increased the severity of both the resulting transient primary and chronic secondary stages of FIV infection. This study also demonstrated the usefulness of the FIV model in studying the role of incidental infectious diseases as cofactors for immunodeficiency-causing lentiviruses.

4 Haematological disorders associated with feline retrovirus infections

“…Neutropenia is severe (i.e. < 500 cells/~l) in FIV-inoculated neonatal kittens (George et al, 1993) and in cats with pre-existing asymptomatic FeLV infection (Pedersen et al, 1990). Dually infected cats have more severe clinical signs of primary FIV infection and a higher rate of fatal infections and/or gastrointestinal complications.…”

“…Histological marrow evaluations during the neutropenic phase of experimental acute FIV infection occasionally reveal myeloid hyperplasia with a shift to immature precursors, lymphoid follicles, and/or marrow lymphocytosis (Pedersen et al, 1990;Beebe et al, 1992;Callanan et al, 1992b, Mandell et al, 1992. However, serial marrow aspirates on a cohort of inoculated cats failed to detect significantly increased frequencies of marrow lymphocytes, plasma cells, or eosinophils when compared to uninfected control cats (Mandell et al, 1992).…”

Detection of feline immunodeficiency proviral DNA in peripheral blood lymphocytes by the polymerase chain reaction

“…There are some reports of detection of provirus DNA by the PCR method in HIV infection, and its usefulness (Ou et al, 1988;Albert and Feny6, 1990). Pedersen et al (1990) reported cases in which PCR was used for FIV infection. They used two primer pairs in the gag region of FIV.…”

“…If the single PCR products from the cats in which proviral DNA was not detected are subjected to detection of DNA by Southern blot or dot-blot hybridization using radioisotopes, DNA detection will be more sensitive. Pedersen et al (1990) also detected the PCR products by Southern blot hybridization using radiolabeled probes. However, these procedures are troublesome for routine PCR procedures.…”

Feline immunodeficiency virus: A brief review

“…Virus can be isolated from blood, lymphoid organs, saliva (particularly from clinically ill cats) and cerebrospinal fluid (Pedersen et al, 1987 ;Yamamoto et aL, 1988Yamamoto et aL, , 1989, and grown in vitro in lymphocytes, both T4 and T8 (Pedersen et al, 1987Brown et al, 1991b), macrophages (Brunner & Pedersen, 1989 ;Dow et al, 1990) and astrocytes (Dow et al, 1990 ;Koolen & Egberink, 1990) . Replication occurs best in lymphocytes and macrophages which have been activated or are themselves replicating (Brunner & Pedersen, 1989 ;Pedersen et al, 1990) . In addition, some strains of FIV can also grow in other cell types, for example the feline fibroblast cell line Crfk (Pedersen et al, 1987) .…”