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Biomedical subjects

W D Hardy

Publications and source records attributed to W D Hardy.

At least 73 records · Page 4Linked to original sources
PubMed1983

The Parodi-Irgens feline sarcoma virus and simian sarcoma virus have homologous oncogenes, but in different contexts of the viral genomes.

We have identified the oncogene and the putative transforming protein of the Parodi-Irgens feline sarcoma virus (PI-FeSV). The PI-FeSV is defective and needs a helper virus for its replication. The v-onc sequences in the PI-FeSV were found to be related to the v-sis sequences of the simian sarcoma virus (SSV). PI-FeSV nonproducer cells express two viral RNAs, a 6.8-and a 3.3-kilobase RNA. The 6.8-kilobase RNA contains gag, sis, and env sequences but lacks the pol gene. The 3.3-kilobase RNA, on the other hand, contains only env sequences. We have detected one feline leukemia virus-related protein product in these cells, namely, a 76-kilodalton protein which contains determinants of the feline leukemia virus gag proteins p15 and p30. The v-sis sequences in the PI-FeSV have been located near the 5' end of the viral genome. Taken together, these results imply that the p76 protein contains both feline leukemia virus gag and sis sequences and probably is the transforming protein of this virus. In contrast, in SSV the sis sequences are located towards the 3' end of the viral genome, and the sis protein is thought to be expressed via a subgenomic RNA. PI-FeSV and SSV therefore use different schemes to express their onc-related sequences. The v-sis sequences in the PI-FeSV contain restriction sites which reflect the different origin of the v-sis sequences in the PI-FeSV and SSV. The homologous oncogenes of the PI-FeSV and SSV thus were transduced by two different retroviruses, feline leukemia virus and the simian sarcoma-associated virus, apparently from the genomes of different species.

Base Sequence↗
PubMed1983

Naturally occurring retroviruses (RNA tumor viruses). I.

This is the first of two papers describing the naturally occurring retroviruses (RNA tumor viruses). Here, the general properties of these viruses and the biology of the fish, reptilian, chicken, and mouse retroviruses are described. In the next issue of Cancer Investigation the biologic properties of the cat, cattle, primate, and newly discovered human retroviruses will be discussed.

Animals↗
PubMed1983

Naturally occurring retroviruses (RNA tumor viruses). II.

This is the second of two papers describing the biology of the naturally occurring RNA tumor viruses (oncoviruses). It will appear in two parts. In the first paper [Cancer Investigation 1(1):67-83 (1983)] the general properties of this class of viruses and the biology of the retroviruses of the "lower" vertebrates was discussed. In this paper the oncoviruses of the "higher" animals are described. Part one deals with cat retroviruses.

Animals↗
PubMed1982

Isolation and characterization of circulating feline leukemia virus-immune complexes from plasma of persistently infected pet cats removed by ex vivo immunosorption.

IgG and circulating IgG immune complexes (CIC) were purified from plasma of three pet cats persistently infected with feline leukemia virus (FeLV) by adsorption to, and elution from, Staphylococcus aureus Cowan I. CIC were then separated from free IgG by sucrose gradient ultracentrifugation and were analyzed for the presence of FeLV structural proteins and corresponding specific antibodies. Radioimmunoprecipitation analysis indicated that FeLV envelope (gp70) and major core (p30) proteins, along with cat IgG heavy and light chains, were present in the CIC from all three cats. Further analysis of the CIC from one of the cats also revealed the presence of FeLV core proteins p15 and p12. IgG purified from isolated CIC was also shown to bind specifically to purified FeLV gp70, p30, and p15. These data provide direct evidence for FeLV-specific CIC in the plasma of persistently viremic pet cats, and suggest these animals are immunologically response to the virus even though free antibodies against the major structural proteins cannot be demonstrated in standard assays.

Animals↗
PubMed1982

Search for evidence of feline leukemia virus infection in humans with leukemias, lymphomas, or soft tissue sarcomas.

Two-hundred and thirty-nine patients, including 66 with soft tissue sarcomas and 173 with hematologic cancers, were investigated for evidence of infection with feline leukemia virus (FeLV). Included in this group were 2 patients with acute lymphocytic leukemia who had lived in the same household with leukemic cats. None of the patients demonstrated measurable levels of neutralizing antibody to FeLV or had detectable FeLV antigens in peripheral blood normal leukocytes or leukemic cells. In a smaller number of patients, there was no evidence of antibody to FOCMA or of FOCMA on tumor cells in the bone marrow.

Adult↗
PubMed1981

Prevalence and sequelae of feline leukemia virus infection in laboratory cats.

Over a 4-year period, 1,683 pound-source cats received at a research institution were screened for feline leukemia virus (FeLV) infection, using an indirect fluorescent antibody test. Viremia was detected in 83 of the cats, for a prevalence of 4.9%. During this period, FeLV infection was detected in 5 kittens on a research project; lymphoma or anemia developed 6 to 17 months after the infections were detected. It was concluded that apparently healthy cats infected with FeLV may not be appropriate for some biomedical research projects.

Animals↗
PubMed1981

Epidemiologic association between virus-negative feline leukemia and the horizontally transmitted feline leukemia virus.

About two-thirds of the natural cases of feline leukemia-lymphoma are assumed to be caused by the feline leukemia virus (FeLV) because they occur in cats, which harbor this agent, and FeLV will induce the disease under laboratory conditions. Epidemiological evidence is presented which associates cases of naturally occurring 'virus negative' feline leukemia with exposure to FeLV.

Animals↗
PubMed1981

Shared interspecies antigenic reactivities among hamster and feline oncoviruses.

Group-reactive antisera against the major internal protein p30 of the hamster sarcoma virus (HaSV) showed interspecies reactivity in immunodiffusion even with sera of low titer against HaSV. Antisera were prepared by sc injection of virus into male New Zealand White rabbits. The cross-reactivity between interspecies antigens of feline and hamster RNA tumor viruses was stronger than between either virus with murine leukemia virus. Molecular hybridization data, obtained from nucleic acid hybridization between the viral RNA's and complementary DNA's of murine and feline oncovirus origin, were consistent with the immunologic results. THe implications of these observations were discussed.

Animals↗
PubMed1980

Development of virus non-producer lymphosarcomas in pet cats exposed to FeLv.

Naturally occurring oncoviruses of several species are transmitted contagiously and cause lymphosarcoma (LSA) or leukaemia in their hosts. All naturally occurring oncoviruses replicate in vivo in the tumours they induce or, as with bovine leukaemia virus, can be isolated from tumour cells grown in short-term cell culture. However, we have shown that feline leukemia virus (FeLV) is not present in a significant minority of pet cats that develop LSA. Unlike experimentally induced virus-negative leukaemias and sarcomas of other species, LSA cells from FeLV-negative LSA cats lack any FeLV proteins, including p15 or p12, and complete functional copies of FeLV provirus and thus do not produce FeLV when grown in cell culture. Thus, except for FeLV, the naturally occurring animal leukaemogenic oncoviruses seem to induce only virus-producing lymphoid tumours. Our earlier findings prompted a study to determine the frequency of occurrence of FeLV non-producer (NP) LSA in pet cats and whether NP LSAs develop in cats exposed to FeLV. We report here epidemiological data which indicate that development of NP LSAs in pet cats is associated with exposure to FeLV and suggest that FeLV may be the aetiological agent for FeLV NP feline LSAs. Thus, feline NP LSAs may be suitable for studying the potential viral aetiology and mechanism of leukaemogenesis of human lymphoid tumours in which no oncoviruses have, as yet, been proved to cause the disease.

Animals↗
PubMed1980

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.

Animals↗