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Biomedical subjects

W D Hardy

Publications and source records attributed to W D Hardy.

At least 109 records · Page 6Linked to original sources
PubMed1977

Horizontal transmission of feline leukemia virus under natural conditions in a feline leukemia cluster household.

Ten post-weanling 4-month-old cats, designated "tracers", were placed in a feline leukemia cluster household to determine the efficiency of horizontal transmission of feline leukemia virus (FeLV). The tracer cats were confirmed as negative for prior exposure to FeLV. Following the placement in the leukemia cluster environment, the tracer cats were serologically monitored at intervals of 3-6 weeks for a total period of 1 year. The tests employed included the detection of FeLV using fixed-cell immunofluorescence and the detection and titration of antibody to : (1) the feline oncornavirus-associated cell membrane antigen (FOCMA), as detected by membrane immunofluorescence; (2) viable FeLV, using serum neutralization; (3) virion core protein p30, using radioimmunoprecipitation; and (4) virion glycoprotein gp70, using radioimmunoprecipitation. All of the tracers had evidence of horizontal infection by FeLV, by several criteria. Seven of the 10 had virus that could be isolated from plasma. All of these 7 developed a terminal illness within 18 months; 3 developed aplastic anemia, 3 infectious peritonitis, and 1 lymphoma. The remaining 3 were negative for FeLV by both virus isolation and fixed-cell immunofluorescence. These 3 did, however, develop high antibody titers by all four criteria and they remained healthy throughout the examination period. These results clearly indicate that unprotected pros-weanling cats brought into a leukemia exposure household environment have a high risk of becoming infected with FeLV. Furthermore, a large proportion of the cats are at risk for development of persistent viremia and FeLV-related diseases.

Anemia, Aplastic↗
PubMed1977

Feline oncornavirus-associated cell-membrane antigen (FOCMA): distinction between FOCMA and the major virion glycoprotein.

The humoral antibody response of feline leukemia virus (FeLV)-exposed cats to the feline oncornavirus-associated tumor cell-membrane antigen (FOCMA) is directly correlated with immunosurveillance against tumor development under natural conditions. By means of membrane immunofluorescence and radioimmunoprecipitation, the antibody response to FOCMA was found to be independent of the antibody response to the major envelope and core proteins of FeLV, gp70 and p30. This was especially true for healthy viremic cats, where antigenemia with circulating FeLV gp70 and p30 apparently binds any free antibody to these proteins, but high levels of FOCMA antibody are often concurrently present. Exhaustive in vitro absorption of highly immune nonviremic serum with gp70 and p30 also failed to remove FOCMA antibody activity. These results indicate that FOCMA is not one of these major FeLV structural proteins.

Animals↗
PubMed1977

Horizontal transmission of feline leukemia virus under experimental conditions.

Thirty-seven specific-pathogen-free (SPF) cats ranging from newborn to 1 year were inoculated with the Rickard strain of feline leukemia virus (FeLV). Each inoculated cat shared a cage with a control SPF cat for 40 weeks post inoculation. After 4-5 weeks, 20 of the inoculated cats became group-specific antigen (gsa)-positive; the other 17 remained gsa-negative but developed virus neutralizing and feline oncornavirus cell membrane-associated antigen antibody titers. Seventeen of the control cats in contact with the gsa-positive cats developed evidence of FeLV infection 4-18 weeks after virema was detected in their inoculated cage mates. Of the control cats in contact with inoculated cats that remained gsa-negative, none developed evidence of FeLV infection. Data indicated that the gsa-positive state in cats inoculated with FeLV correlated with the capacity for horizontal transmission of the virus.

Animals↗
PubMed1976

Humoral immune responses of cats to feline leukemia virus: comparison of responses to the major structural protein p30 and to a virus-specific cell membrane antigen (FOCMA).

Radioimmunoprecipitation was used to test cat sera for ability to bind to the purified major internal protein p30 of feline leukemia viurs (FeLV), to the endogenous cat virus (RD-114), and to murine leukemia virus (MuLV). The data were compared with results of tests for antibody to the feline oncornavirus-associated cell membrane antigen FOCMA and for the presence of viremia. In contrast to the general lack of free antibody to FeLV p30 in a random sample of healthy cats, high levels of antibody to FeLV p30 and FOCMA were found in normal animals from high-leukemia-cluster households. Titers of greater than or equal to 200 for p30 and greater than or equal to 32 for FOCMA were found in nonviremic animals; a percentage of animals with high FOCMA titers and lower or no p30 binding activity were viremic. Animals with neoplasms were low or negative for FOCMA antibody and did not have high titers of free p30 antibody. The p30 binding activity could be divided into three main categories: high binding with FeLV p30 and much lower activity with RD-114 and MuLV p30's, as seen with hyperimmune sera; high binding with FeLV and RD-114 p30's and low activity with MuLV p30, possibly indicative of specific antibody to both of the aforementioned proteins; and low level binding to all three p30's.

Animals↗
PubMed1976

Feline leukemia virus infection: age-related variation in response of cats to experimental infection.

Sixty-seven specific-pathogen-free cats of various ages (newborn, 2 wk, 1 mo, 2 mo, 4 mo, and 1 yr) were inoculated ip with either the Rickard (R) or the Kawakami-Theilen (KT) strain of feline leukemia virus (FeLV). Susceptibility to FeLV was judged by induction of a) FeLV group-specific antigens (gsa) in leukocytes, b) FeLV-related disease, c) antibody to feline oncornavirus-associated cell membrane antigen (FOCMA), and d) virus-neutralizing (VN) antibody. Susceptibility to FeLV-decreased with age. Persistent viremia and FeLV-related disease developed in 100% of cats inoculated as newborns, in 85% of cats inoculated at 2 weeks to 2 months of age, and in 15% of cats inoculated at 4 months or 1 year of age. Cats susceptible to FeLV leukemogenesis became persistently FeLV gsa-positive (viremic) at 4 weeks post inoculation and thereafter and produced little or no FOCMA or VN antibody. Cats that resisted leukemogenesis by FeLV all developed persistent FOCMA and VN titers and never became FeLV gsa-positive. The disease in inoculated cats was influenced by virus strain; FeLV-R induced predominantly thymic lymphosarcoma, whereas FeLV-KT caused fatal nonregenerative anemia without concurrent neoplasia.

Age Factors↗
PubMed1976

Biology of feline leukemia virus in the natural environment.

The feline leukemia virus (FeLV) was discovered in 1964 in a cluster of cats with lymphosarcoma. The observed clustering of cases of feline lymphosarcoma suggested that FeLV was an infectious agent for cats. The development of a simple immunofluorescent test for FeLV permitted a seroepidemiological study to be undertaken on the distribution of the virus in cats living in their natural environment. Over 2000 cats were tested, and the results showed conclusively that FeLV is an infectious agent for cats. This finding has now been independently confirmed using three different test procedures. After the infectious nature of FeLV was discovered, a simple FeLV test and removal program was devised to control the spread of the virus in the natural environment. The spread of FeLV was controlled in 45 households by removing the FeLV-infected cats, while in 25 households, where the infected cats were left in contact with the uninfected cats, 12% of the uninfected cats became infected. The ultimate control of FeLV awaits the development of an effective FeLV vaccine, which now seems feasible since we have already experimentally immunized some cats with attenuated FeLV. Although FeLV is infectious for cats there is no evidence that FeLV can infect humans.

Animals↗
PubMed1976

Immune response to leukemia virus and tumor-associated antigens in cats.

Cats represent an unusually valuable model for studying the role of the immune response to leukemia, lymphoma, and other mesodermal neoplasms. The agents that cause spontaneous feline leukemias, lymphomas, and fibrosarcomas, the feline leukemia and sarcoma viruses, are well characterized. A specific tumor cell membrane antigen, designated the feline oncornavirus-associated cell membrane antigen (FOCMA) has also been described. Feline leukemia and feline sarcoma viruses are antigenically indistinguishable, and FOCMA is common for both. Both laboratory-induced and spontaneous feline leukemias, lymphomas, and fibrosarcomas are available for study. A clear correlation has been shown between the resistance of cats to development of lethal tumors following inoculation of feline sarcoma virus and the presence of high humoral antibody titers to FOCMA. The geometric mean antibody titer to FOCMA for cats that resisted growth of fibrosarcomas was more than 20-fold higher than the mean for cats that succumbed to lethally progressing tumors. Cats with induced or spontaneous leukemia or lymphoma also have either no detectable FOCMA antibody or very low levels. Conversely, some cats resist development of leukemia or lymphoma following natural exposure to feline leukemia virus in leukemia cluster households, and these cats have high FOCMA antibody titers. These results support the concept of a natural immunosurveillance mechanism against leukemia or lymphoma development in an outbred mammalian species.

Animals↗
PubMed1975

Immunosurveillance of naturally occurring feline leukemia.

When compared to their housemates that subsequently developed leukemia, cats that remained healthy had five-to tenfold higher (geometric mean) humoral antibody titers to the feline oncornavirus-associated cell membrane antigen. This is compatible with the application of the immunosurveillance hypothesis to the natural development of leukemia in an outbred mammalian species.

Animals↗
PubMed1975

Association of feline leukemia virus with lymphosarcoma and other disorders in the cat.

Two hundred fifty Boston cats with disorders such as lymphosarcoma, myeloproliferative disease, anemia, glomerulonephritis, pregnancy abnormalities, feline infectious peritonitis, toxoplasmosis, and various bacterial infections were examined for feline leukemia virus (FeLV) by immunofluorescence. Antibody titers against feline oncornavirus-associated cell membrane antigen (FOCMA) were tested in 133 of these cats. The tests for FeLV and FOCMA antibody were also conducted among healthy cats not known to have been exposed to FeLV, as well as among healthy cats from households where FeLV was known to be present. Most of the cats with lymphosarcoma and the other aforementioned disorders were infected with FeLV and low FOCMA antibody titers. Healthy cats known to have been exposed to FeLV were often viremic, but those that remained healthy were able to develop high FOCMA antibody titers. Healthy cats without known prior exposure to FeLV were unlikely to be viremic but often had detectable FOCMA antibody titers, indicating that some exposure occurs under natural conditions in the Boston area. The association of FeLV with infections other than lymphosarcoma was assumed to be caused by the immunosuppresive effect of FeLV, thus allowing development of disease.

Abortion, Veterinary↗
PubMed1975

Expression of virus-associated antigens and immune cell functions during spontaneous regression of the Friend viral murine leukemia.

Spontaneous regression and/or remission of Friend virus (FV)-induced splenic erythroblastic leukemia was observed in CD-1 mice infected with several isolates of FV. Regression of splenic tumor was accompanied by the loss of both specific FV-induced cell membrane antigen (FVMA) and virus group-specific antigens (gsa) from the spleen cells. The frequency (percentage) of immunoglobulin-positive cells (B) and thetapositive cells (T) in the spleen was markedly decreased during leukemia progression, but there was a subsequent increase during regression. The appearance of gsa-positive (gsa+) cells in peripheral blood correlated well with the early progressive and regressive phase of leukemia (up to 7 weeks after infection). Later, the presence of these cells became unpredictable in regard to status of disease. Gsa+ blood cells reappeared in most mice with regressed splenic tumors, suggesting persistence of the virus complex in the animals. Antibody responsiveness as determined by the numbers of hemolytic plaque-forming cells, PFC, after a single immunization with sheep red blood cells (SRBC), was suppressed in leukemia progression and recovered, spontaneously, during regression of leukemia. However, hemolytic PFC elicited by antigen in both progressors and regressors expressed the specific virus-induced membrane antigen, FVMA, detectable by the PFC-inhibition test with specific antiserum and complement. Recovery of immunological responsiveness also included the spontaneous appearance of virus-neutralizing antibody to FV. However, this was not paralleled by the appearance of antibody to FVMA. Traces of anti-FVMA antibody activity were occasionally detectable in serum of both progressors and regressors and did not correlate with virus neutralization, in individual mice; This may explain the susceptibility of regressors to secondary relapse and to reinfection.

Animals↗
PubMed1975

Stimulation of erythropoietic differentiation in BALB/c mice infected with Rauscher leukemia virus.

The function of phenylhydrazine (PHZ) hemolysis in ameliorating the anemia induced in mice by a slow-acting strain of Rauscher leukemia virus (RLV-A) was described. After cessation of treatment with PHZ, mid-stage RLV-A-infected, anemic mice responded with massive reticulocytoses and a rebound in hematocrit above control levels. RLV-infected mice, subjected to PHZ-induced hemolysis or phlebotomy, produced high levels of plasma erythropoietin (Ep); this suggested that Ep mediated the PHZ-induced differentiation. In addition, administration of exogenous Ep induced a wave of erythroid maturation in RLV-infected anemic mice, which indicated that virus-infected erythroid precursors could still respond to the hormone governing normal differentiation.

Anemia↗
PubMed1975

Naturally occurring persistent feline oncornavirus infections in the absence of disease.

Healthy feline leukemia virus (FeLV)-infected cats from leukemia cluster environments were followed for up to 23 months for development of disease and evidence of alteration in the hemogram. The incidence of disease development in FeLV-postive cats was more than fivefold higher than the incidence for FeLV-negative cats. Ten cases of leukemia developed in 69 infected cats, whereas one case of leukemia occurred in 59 uninfected cats. The incidence for development of diseases other than leukemia was 30.4 percent for FeLV-infected cats as opposed to 6.8 per cent for uninfected cats. This could be a result of the immunosuppressive effects of FeLV. Felv-infected cats had no evidence of subclinical anemia. Mean packed cell volumes and total leukocyte counts were about the same for infected and uninfected animals. The only variation seen in healthy FeLV-infected cats was a decreased mean lymphocyte count. The difference between mean lymphocyte count for FeLV-infected and uninfected animals was significant at the 0.999 level. These findings suggest that the incubation period for feline leukemia may be very prolonged under natural conditions and that an increased susceptibility to unrelated infectious diseases exists during this period. This increased susceptibility was apparently not associated with anemia or depressed total leukocyte counts.

Animals↗
PubMed1975

Horizontal transmission of feline leukemia virus in cats.

Traditionally, cancer has not been considered an infectious disease although some multiple cases of leukemia in man and cattle have been reported. The discovery that feline lymphosarcoma was associated with an RNA virus (feline leukemia virus(FeLV)) meant that infectious transmission of the disease was a possibility. The critical question was whether the predominant method of transmission from one animal to another was 'vertical' (via the gametes) or 'horizontal' (via contagion or infection). A number of epidemiological studies have shown that the chances of healthy cats contracting lymphosarcoma are greatly increased when a cat with the disease lives in close proximity. It does not matter whether the healthy cats are related to the sick animal or not. It has also been established that viremic normal cats have an approximately 900 times greater chance of developing leukemia than cats whose FeLV status is unknown. Infectious FeLV is present in the excretions and blood of viremic animals. In the natural environment, feline lymphosarcoma occurs in clusters. The results in pet cats have been supported by experiments with cat colonies under controlled conditions and prove that horizontal transmission of FeLV occurs. This does not mean that epigenetic (infection in utero or via the milk) or vertical transmission cannot also occur. It should be possible to break the cycle of horizontal transmission of the virus by vaccination and thus control FeLV-related diseases.

Animals↗
PubMed1975

Immune response of healthy and leukemic cats to the feline oncornavirus-associated cell membrane antigen.

Feline leukemia is an infectious disease caused by a horizontally transmitted virus. Infection of animals or cultured cells with feline oncornaviruses results in the expression of a specific cell membrane antigen, feline oncornavirus-associated cell membrane antigen (FOCMA). The humoral antibody response to FOCMA is directly correlated with tumor progression. The measurement of this antibody is a useful tool for determining virus exposure. Using this procedure it was determined that cats living in leukemia "cluster" households as well as cats used as contact controls in virus injection experiments have a risk of infection of 90% or higher.

Animals↗