An in vitro focus-induction assay for xenotropic murine leukemia virus, feline leukemia virus C, and the feline--primate viruses RD-114/CCC/M-7.
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Aberrant viruses in cells infected with murine sarcoma virus-feline leukemia virus.
This study describes an unusual type of virus seen when a feline leukemia virus (FeLV) pseudotype of murine sarcoma virus (MuSV) obtained by cocentrifugation procedures infected feline embryo cells (FEF) and two Crandell cat cell lines (CrFK1, CrFK2). When all three cell cultures were infected with MuSV-FeLV, only FEF and CrFK2 were transformed and only these showed normal and aberrant virus. The CrFK1 infected with MuSV-FeLV did not transform but did replicate normal type-C virus with a 50-A intermediate coat. The virus replicated in the two transformed lines showed three particles; a normal particle with a 50-A intermediate coat, a normal particle with a 100-A intermediate coat, and an aberrant particle with a 100-A intermediate coat.
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Zidovudine toxicity to cats infected with feline leukemia virus.
Feline leukemia virus (FeLV) infection of cats is a model for the acquired immunodeficiency syndrome in humans. The toxicity of zidovudine was evaluated in SPF cats experimentally infected with FeLV. At initiation of the zidovudine study, all cats were antibody positive for FeLV antigens but clinically asymptomatic. Four cats were also viremic. Thirteen, 6- to 10-month-old cats were divided into five dosage groups and given zidovudine po at 0, 7.5, 15, 30, or 60 mg/kg daily in three equally divided doses for 32 to 34 days. Titers of circulating virus antigen remained constant; however, three of six cats receiving the higher doses of zidovudine (greater than or equal to 30 mg/kg) showed an increase in antibody titers to FeLV. Administration of zidovudine resulted in a progressive anemia, dependent upon dose and time. Macrocytes were observed prior to the development of anemia and were also found in several nonanemic cats. Repeated measures regression analyses indicated that an increased dose of zidovudine was associated with decreased packed cell volume, red blood cell count, and hemoglobin. As determined from the packed cell volume, the analyses indicate that anemia is induced only by the two highest doses of zidovudine. The regression model indicates that daily doses of 60 and 30 mg/kg are expected to induce anemia by Day 4 and Day 13, respectively. Progressive absolute neutropenia was observed in the greater than or equal to 30 mg/kg groups. Histopathologic lesions consisted of marked bone marrow hypercellularity in cats given greater than or equal to 30 mg/kg zidovudine and splenic extramedullary hematopoiesis in cats given greater than or equal to 15 mg/kg. Thus, oral toxicity of zidovudine in the cat is manifested by a dose-related anemia and neutropenia as observed in humans.
Anemia↗
Hematopoietic target cells of anemogenic subgroup C versus nonanemogenic subgroup A feline leukemia virus.
Feline leukemia viruses (FeLVs) belonging to interference subgroup C induce fatal anemia resembling human pure red cell aplasia (PRCA). Subgroup A FeLVs, although closely related genetically to FeLVs of subgroup C, do not induce PRCA. The determinants for PRCA induction by a molecularly cloned prototype subgroup C virus (FeLV-Sarma-C [FSC]) have been localized to the N-terminal 241 amino acids of the surface glycoprotein (SU) gp70. To investigate whether the anemogenic activity of FSC reflects a unique capacity to infect erythroid progenitor cells, we used correlative immunogold, immunofluorescence, and cytological staining to study prospectively the hemopoietic cell populations infected by either FSC or FeLV-FAIDS-61E-A (F6A), a prototype of subgroup A virus. The results demonstrated that although only FSC-infected animals developed erythrocyte aplasia, the env SU and the major core protein (p27) were expressed in a surprisingly large fraction of the lymphoid, erythroid, and myeloid lineage marrow cells in both FSC- and F6A-infected cats. Between days 8 and 17 postinoculation, gp70 and p27 were detected in 43 to 73% of erythroid, 25 to 75% of lymphoid, and 35 to 50% of myeloid lineage cells, regardless of whether the cats were infected with FSC or F6A. Thus, anemogenic subgroup C and nonanemogenic subgroup A FeLVs have similar hemopoietic cell tropism and infection kinetics, despite their divergent effects on erythroid progenitor cell function. Acute anemia induction by subgroup C FeLV, therefore, does not reflect a unique tropism for marrow erythroid cells but rather indicates a unique cytopathic effect of the SU on erythroid progenitor cells.
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Increased risk for lymphoma and glomerulonephritis in a closed population of cats exposed to feline leukemia virus.
Feline leukemia virus (FeLV)-associated diseases were observed in a household in eastern Connecticut having 134 cats over a period of five and a half years. FeLV-positive cats had a much higher mortality rate (34.6 deaths per 1000 cat-months of follow-up) than did FeLV-negative cats (8.9 deaths per 1000 cat-months of follow-up). The leading cause of death was glomerulonephritis followed by lymphoma. The relative risk for virus-positive cats as compared to virus-negative cats for the two diseases was 9.9 and 9.6, respectively. The major risk factors for the development of lymphoma were virus positivity and low antibody titer to the feline oncornavirus-associated cell membrane antigen (FOCMA). No significant differences in cancer incidence were seen between the two major breeds (Abyssinian and Burmese) in the household. An older age at arrival in the house decreased death rates for all causes in the household, but it did not significantly affect death rates from lymphoma, although there was a positive trend.
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Feline oncornavirus-associated cell membrane antigen. VI. Cytotoxic antibody in cats exposed to feline leukemia virus.
Feline leukemia virus (FeLV)-infected specific pathogen-free (SPF) cats, normal uninfected SPF cats, and healthy cats from leukemic households were tested for antibody reactive to the feline oncornavirus-associated cell membrane antigen (FOCMA)-containing target cell line FL-74 by microcytotoxicity and indirect membrane immunofluorescence. Of the infected SPF animals, 81% showed concordant reactivity for the two tests. In contrast, only 55% of the healthy cats known to be naturally exposed to FeLV for long periods showed such concordance. FOCMA antibody could not be detected in normal SPF cats by either indirect membrane immunofluorescence or microcytotoxicity. Most cats in the FeLV-infected SPF group developed antibody detectable by both procedures by the fifth week post inoculation. Antibody detectable by membrane immunofluorescence persisted in a high percentage (75-90%) of the animals throughout the observation period of 19 weeks; after 9 weeks, fewer cats had antibody that was also detectable by microcytotoxicity.
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Endogenous env elements: partners in generation of pathogenic feline leukemia viruses.
Feline leukemia viruses (FeLVs), which are replication-competent oncoretroviruses of the domestic cat species, are contagiously transmitted in natural environments. They are capable of inducing either acute antiproliferative disease or, after prolonged latency, lymphoid malignancies in this animal population. Current knowledge of the recombinational events between infectious FeLV and noninfectious endogenously inherited FeLV-like elements is reviewed, and the potential role of the derived recombinant viruses in pathogenesis is discussed. Major observations made are as follows: (1) Up to three fourths of the exogenous FeLV envelope glycoprotein (SU), beginning from the N-terminal end, can be replaced by sequences from an endogenous FeLV to produce biologically active chimeric FeLVs. The in vitro replication efficiency or cell tropism of the recombinants appears to be influenced by the amount of SU sequences replaced by the endogenous partner, as well as by the locus of origin of the endogenous sequences. (2) Generation of FeLV recombinants in tissue culture cells corresponds closely to the findings from natural tumors. There is direct evidence, based on molecular genetic analysis, for the prevalence of recombinant proviruses in naturally arising FeLV-induced lymphomas. (3) Certain recombinants harboring an altered primary neutralizing epitope in the middle of SU corresponding to the endogenous FeLV sequence can evade immunity developed against common FeLV infection. In several other recombinants, the epitope sequence is found to be frequently mutated during the process of recombination. (4) FeLV variants with altered epitope, although they may not be efficient in replication in vivo, apparently are capable of causing focal infection in target organs. Evidence is also presented that when coinfected with an exogenous FeLV, the epitope sequence in the variants is reverted to the exogenous type, providing an explanation why this sequence is found to be conserved in all natural isolates of FeLV. (5) A prototype chimeric polyprotein containing most of the SU from the endogenous source is abnormally processed and becomes trapped in the endoplasmic reticulum. A functional consequence of such trapping is interference with specific FeLV infection. (6) Some recombinants, while only poorly replicating in the host, may have the ability to infect target erythroid progenitor cells for the induction of strong cytopathic effect. (7) Some other recombinants appear to potentiate lymphomagenesis by exogenous FeLV and others to acquire properties to infect CNS endothelial cells, an event that could potentially be related to FeLV-induced neuropathogenicity. (8) Of multiple recombinant viruses, a specific recombinant species was found to occur in each of the three cats examined in which lymphoma was experimentally induced, and it was exclusively seen in one of these cats. This recombinant FeLV may potentially be a candidate for strong leukemogenic function. In addition to commonly encountered virus envelope changes, another prominent viral factor involved in tumorigenesis is mutated FeLV transcription regulatory sequences, most frequently with enhancer duplication or triplication. Although only a limited amount of information is available in the area of insertional mutagenesis in FeLV neoplastic disease, activation of certain key nuclear transcription factor genes has been documented.
Amino Acid Sequence↗
Retinal neoplasia and dysplasia. I. Induction by feline leukemia virus.
Feline leukemia virus, a naturally occurring C-type virus (oncorna virus), was injected systemically and intraocularly into fetal and newborn kittens. A light microscopy study of the resultant ocular tumor changes was carried out. One animal developed an intraocular tumor of apparent retinal origin. Eight animals showed intraocular neoplastic cell infiltration. The most common ocular change observed was retinal dysplasia. Sequential histologic examination of enucleated eyes showed diffuse intraocular inflammation after viral inoculation. In the developing retinas progressive disorganization and necrosis were documented, with subsequent reorganization into cell clumps and dysplastic rosette structures. The retinal pigment epithelium showed proliferation and intraretinal migration. The mature retina exhibited full-thickness folds and tubes associated with infoldings of the retinal pigment epithelium.
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Cooperating events in lymphomagenesis mediated by feline leukemia virus.
Feline leukemia virus (FeLV)-mediated lymphomagenesis in the domestic cat has been examined as a model of lymphoid malignancy in a naturally outbreeding population. The pathogenesis of two distinct, naturally occurring types of FeLV-induced tumors has been investigated: (1) a thymic lymphoma of T-cell origin, typical of FeLV-induced lymphoma, and (2) an extrathymic, extranodal lymphoma of non-B non-T-cell origin. The genetic features of these tumors are clearly distinguishable, and include determinants encoded both by the virus and the host. Virally encoded determinants of pathogenesis include the long terminal repeat (LTR) and the envelope SU protein. Cellular determinants include the involvement of a set of proto-oncogenes, and other factors characteristic of the specific cell type of origin of the tumor. Functional studies are aimed at evaluating the action and interaction of these genetic determinants in the pathogenesis of lymphoma in an animal model system.
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Selective host range restriction of goat cells for recombinant murine leukemia virus and feline leukemia virus type A.
We isolated a strain of normal goat fibroblasts which was uniquely selective in that it allowed the replication of xenotropic murine leukemia virus but not polytropic recombinant murine leukemia virus. In addition, feline leukemia virus type A replication was severely diminished in these goat cells, whereas feline leukemia virus type B and feline endogenous RD114-CCC viruses replicated efficiently. No other known cells exhibit this pattern of virus growth restriction. These goat cells allow the study of xenotropic murine leukemia virus in mixtures which also contain recombinant murine leukemia virus and may be helpful in eliminating feline leukemia virus type which often coexists in feline sarcoma or leukemia virus mixtures with other feline leukemia virus types.
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Prevalence of disease in nonviremic cats previously exposed to feline leukemia virus.
Feline leukemia virus status and antibody titer to feline oncornavirus-associated cell membrane antigen (FOCMA) were determined on plasma from 183 outpatient cats and 61 cats from 2 closed, FeLV-positive, multiple-cat households. Cats with FOCMA antibody titer had a significantly (P less than 0.02) higher prevalence of history of disease than did cats without FOCMA antibody. Diseases included upper respiratory tract infections, abscesses, ear infections, lower urinary tract infections, gastrointestinal disease, pneumonia, uterine infection, lymphadenopathy, fever of unknown origin, and bacterial infections. The FOCMA antibody titer was determined by use of an indirect fluorescent antibody test; titer greater than or equal to 1:16 was considered to be positive results. Lower mean FOCMA antibody titer was observed in young cats with history of disease (P less than 0.05) than in young cats without history of disease or in older cats with or without history of disease. Prevalence of FOCMA antibody titer was identical (38%) in young and adult cats, indicating cats likely were exposed to FeLV as kittens because a higher prevalence of FOCMA antibody titer in older cats would otherwise be expected.
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A common proviral integration region, fit-1, in T-cell tumors induced by myc-containing feline leukemia viruses.
Feline leukemia viruses carrying transduced v-myc genes (myc-FeLV) induce tumors of clonal origin, suggesting that activated myc alone is not sufficient for tumorigenesis. To investigate the hypothesis that insertional mutagenesis plays a role by activating genes which collaborate with v-myc, we looked for evidence of common proviral integration sites in these tumors. By inverse polymerase chain reaction we identified a 6-kb domain, designated fit-1, in which FeLV proviruses were inserted in four of nine (44%) T-cell tumors induced by myc-FeLV. The fit-1 locus was mapped to feline chromosome B2 and appears to be distinct from known oncogenes located on this chromosome. Fit-1 represents a novel common proviral integration region which may harbor a cellular gene which acts in concert with the myc gene in T-cell tumorigenesis.
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Infection of feline embryo adherent cells with feline leukemia virus: feline oncornavirus-associated cell membrane antigen expression and morphologic transformation.
Feline embryo adherent cells were infected with the Richard or Kawakami-Theilen strains of feline leukemia virus (FeLV) and examined for feline oncornavirus-associated cell membrane antigen (FOCMA), viral group-specific antigen (gsa) production, and in vitro evidence of transformation. As early as 10 days after infection, when more than half of the infected cells were gsa positive, FOCMA was detected on 5-10 percent of the cells. Transitory morphologic alterations (epithelioid appearance and rounding) were first noted in most cultures around 20-30 days post infection. At this time, approximately 50% of the cells in infected cultures expressed FOCMA. Morphologic characteristics of transformed fibroblastic cells (rounded shape, disordered alignment, and low adhesion to substratum), as well as enhanced agglutinability by plant lectins and ability to grow in agar, were demonstrated in one of four FeLV-infected, FOCMA-positive cultures. Findings showed that FOCMA may be expressed in FeLV-infected monolayer cells independent of transformation as assessed by in vitro criteria.
Agglutination Tests↗
Tumorigenic potential of a recombinant retrovirus containing sequences from Moloney murine leukemia virus and feline leukemia virus.
A recombinant retrovirus, termed MoFe2-MuLV, was constructed in which the U3 region of T-lymphomagenic Moloney murine leukemia virus (Mo-MuLV) was replaced by that of FeLV-945, a provirus of unique long terminal repeat (LTR) structure identified only in non-T-cell, non-B-cell lymphomas of the domestic cat. The LTR of FeLV-945 is unusual in that it contains only a single copy of the transcriptional enhancer followed 25 bp downstream by a 21-bp sequence in triplicate in tandem. Infectivity of MoFe2-MuLV was demonstrated in vitro in SC-1 cells and in vivo in neonatal NIH-Swiss mice. Tumors occurred in MoFe2-MuLV-infected animals following a latency period of 4 to 10 months (average, 6 months). The results of Southern blot analysis of the T-cell receptor beta locus demonstrated that all tumors were lymphomas of T-cell origin. MoFe2-MuLV LTRs were amplified by PCR from tumor DNA and were characterized by nucleotide sequence analysis. LTRs from the tumors that occurred with relatively shorter latency predominantly retained the original MoFe2-MuLV sequence intact and unaltered. Tumors that occurred with relatively longer latency contained LTRs that also retained the 21-bp sequence triplication characteristic of the original virus but had acquired various duplications of enhancer sequences. The repeated identification of enhancer duplications in late-appearing tumors suggests that the duplication affords a selective advantage, although apparently not in the efficient induction of T-cell lymphoma. Proto-oncogenes known to be targets of insertional mutagenesis in the majority of Mo-MuLV-induced tumors or in feline non-T-cell, non-B-cell lymphomas were shown not to be rearranged in any tumor examined. Mink cell focus-inducing (MCF) proviral DNA was readily detectable in some, but not all, tumors. The presence or absence of MCF did not correlate with the kinetics of tumor induction. These studies indicate that the single-enhancer, triplication-containing FeLV LTR, typical of non-T-cell, non-B-cell lymphomas in cats, is competent in the induction of T-cell lymphoma in mice. The findings suggest that the mechanism of MoFe2-MuLV-mediated lymphomagenesis may differ from that of Mo-MuLV-mediated disease, considering the possible involvement of novel oncogenes and the variable presence of MCF recombinants.
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Neutralization of feline leukemia virus with feline antisera to leukocyte alloantigens.
The possibility that normal cellular antigens might serve as targets for antibody neutralization of the feline leukemia virus was investigated. Xenospecific antiserum directed to normal feline cells was shown to inactivate feline leukemia virus grown in fibroblasts. Cat antisera to normal feline leukocyte alloantigens were then prepared, after which persistent viremia was induced in the donor cats. Such alloantisera neutralized virus taken from plasma of the appropriate cat but did not neutralize virus from a different cat. The virus neutralization was dependent on the presence of complement. These results indicate that alloantigens are present at the virus surface and raise the possibility that such antigens may play a role in the natural immune response directed to retrovirus infections.
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Diagnosis of feline leukemia virus and feline immunodeficiency virus infections.
Feline leukemia virus is an oncogenic retrovirus that can result in a wide variety of neoplastic and non-neoplastic diseases, including immunosuppression. Diagnosis of FeLV infection can be achieved by several methods, including virus isolation; IFA assay of a peripheral blood smear; and detection of a viral protein (called p27) by ELISA testing of whole blood, plasma, serum, saliva, or tears. Commercially available ELISA kits have revolutionized FeLV testing and have become very popular as "in-house" procedures. This article discusses the interpretation of ELISA results and compares them with IFA assay findings. Feline immunodeficiency virus is a lentivirus that causes immunosuppression, but not neoplasia, in cats. It originally was called feline T-lymphotropic lentivirus. Differentiating FIV infection from the immunosuppressive type of FeLV infection requires virus isolation or serology. The most rapid method for diagnosis of FIV infection is ELISA testing for antiviral antibody.
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Feline leukemia virus and feline immunodeficiency virus.
Ophthalmic manifestations of FeLV or FIV infection can occur in all ocular tissues and may be manifestations of direct viral effects or secondary to viral-related malignant transformation. Additionally, the manifestations of common feline ophthalmic pathogens may be more severe and poorly responsive to therapy because of the immunosuppressive effects of FeLV or FIV infection. Prompt diagnosis of underlying viral infection in cats with ophthalmic disease is paramount for accurate diagnosis and prognosis and is required for appropriate therapeutic decision making.
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Prevalence of canine distemper virus, feline immunodeficiency virus and feline leukemia virus in captive African lions (Panthera leo) in Japan.
Sero-prevalences of canine distemper virus (CDV), feline immunodeficiency virus (FIV) and feline leukemia virus (FeLV) were evaluated in 20 captive lions in two Japanese zoos. Anti-CDV antibody was detected in 13 of 20 lions. We could pursue antibody responses against CDV in three lions back to 1996. Sera collected in 1996 were negative for anti-CDV antibody, therefore, all of them showed sero-conversion in 2000. This result suggested that the epidemic of CDV infection in this zoo might have happened between 1996 and 2000. The lions were also examined for FIV and FeLV infections. We had no evidence for FeLV infection but eight lions were sero-positive for anti-FIV antibody.
Animals↗