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Biomedical subjects

M Torten

Publications and source records attributed to M Torten.

At least 19 recordsLinked to original sources
PubMed2001

The number and distribution of immune cells in the cervicovaginal mucosa remain constant throughout the menstrual cycle of rhesus macaques.

A number of studies have shown that the ovarian hormone cycle affects genital tract immunoglobulin (Ig) levels and T cell function in both humans and rhesus monkeys. We hypothesized that shifts in immune cell populations occurring in response to hormone cycles are involved in the observed changes in genital tract immunity. To test this hypothesis, we characterized the type, number, and distribution of immune cells in the cervicovaginal mucosa at different stages of the menstrual cycle. Tissues from 18 normal female rhesus macaques were studied by immunohistochemistry and computerized morphometric analysis. The number and distribution of CD1a+ Langerhans' cells, CD2+, CD3+, CD4+, and CD8+ T cells, CD20+ B cells, and surface Ig+ plasma cells did not change in samples collected at the different stages of the cycle. However, in no relation to the stage of the menstrual cycle, the number of Langerhans' cells and other immune cell types was different in the various regions of the cervicovaginal mucosa examined. In addition, variation in thickness of the ectocervical and vaginal epithelium during a normal menstrual cycle of rhesus macaques is not accompanied by changes in intraepithelial immune cell populations. We conclude that steroid hormones do not influence genital mucosal immunity by changing the number or distribution of immune cells in the lower reproductive tract.

Animals↗
PubMed1994

Infection of cats with molecularly cloned and biological isolates of the feline immunodeficiency virus.

Molecularly cloned viruses are considered essential reagents for characterizing viral domains responsible for infectivity and disease pathogenesis in the host. The infectivity and hematological alterations associated with two molecularly cloned isolates of feline immunodeficiency virus (FIV-pPPR and FIV-pF34) and an uncloned isolate (FIV-PPR) were assessed by inoculation of cats. Inoculated cats were tested for viral antibody, viremia, and clinical pathological disease. Peripheral blood mononuclear cells isolated from inoculated cats were assayed for virus infection by virus isolation, amplification of proviral DNA (by polymerase chain reaction), and in situ hybridization for viral RNA. Over 50% of the cats inoculated with cloned virus FIV-pF34 failed to seroconvert even when coinfected with feline leukemia virus; these cats were consistently virus positive only by amplification of proviral DNA. All cats inoculated with cloned virus FIV-pPPR seroconverted and were found virus positive by at least two of three virus detection assays. Both cloned viruses were less capable of suppressing CD4:CD8 ratios when compared to the biological isolates from which they were cloned. Isolates which replicate efficiently in feline peripheral blood mononuclear cells (PBMC), i.e., FIV-pPPR or biological FIV-PPR, caused greater virus load and lower CD4:CD8 ratios when compared to cloned FIV-pF34, which replicates efficiently in feline adherent cell lines and macrophages but poorly in primary feline PBMC. Molecular clones FIV-pF34 and FIV-pPPR will be useful reagents for characterization of viral determinants of virus load and possibly, cell tropism in vivo.

Animals↗
PubMed1994

Evaluation of in vivo and in vitro interactions of feline immunodeficiency virus and feline leukemia virus.

OBJECTIVE: To determine the potential mechanisms for disease potentiation where feline immunodeficiency virus (FIV) infection of persistently feline leukemia virus (FeLV)-infected cats results in more severe FIV disease and increased mortality than FIV infection of specific pathogen-free cats. DESIGN AND METHODS: To determine whether pseudotype formation resulting in expanded cell tropism may be an important mechanism, cellular targets and tissue distribution of FIV and FeLV were determined by in situ hybridization and/or immunohistochemistry. To determine whether FeLV can transactivate the FIV long terminal repeat (LTR) resulting in increased FIV expression, in vitro transient expression assays were performed. To examine whether persistent FeLV infection can cause the deletion of a suppressive T-lymphocyte population, peripheral blood mononuclear cell (PBMC) cultures from persistently FeLV-infected cats were infected with FIV and monitored for FIV antigen levels. RESULTS: Macrophages were the predominant target of FIV infection and were disseminated in a similar pattern in lymphoid and nonlymphoid tissues of both FIV-infected and FeLV/FIV-coinfected cats. FeLV-infected cells expressing FIV RNA were not present. Significant transactivation of the FIV LTR in FeLV-infected cells was not demonstrated. FIV antigen production was similar upon in vitro infection of PBMC from FeLV-infected and uninfected cats. CONCLUSIONS: Neither direct virus/virus interactions, such as FeLV/FIV pseudotype formation or transactivation of the FIV LTR in FeLV-infected cells, nor deletion of a regulatory cell subset from the blood of FeLV-infected cats, was found to be the mechanism of disease potentiation.

Animals↗
PubMed1993

Delayed seroconversion following naturally acquired caprine arthritis-encephalitis virus infection in goats.

One hundred eight milking goats from a dairy that had been using a modified caprine arthritis-encephalitis virus (CAEV) eradication program were tested for CAEV antibodies by serologic methods and for proviral CAEV DNA by use of polymerase chain reaction (PCR) technology. All goats were free of clinical symptoms of CAEV infection. Twenty-seven of the 108 goats were considered seropositive, on the basis of ELISA results. Proviral CAEV DNA was detected, using PCR techniques, in mononuclear leukocytes in blood samples obtained from 25 of the these 27 seropositive goats. Twenty of the 81 seronegative goats also had positive PCR test results. Ten of these goats seroconverted by 8 months later, and virus was readily isolated from mononuclear leukocytes in venous blood samples after the goats had seroconverted. Virus was also isolated from mononuclear leukocytes in blood samples collected from 4 of 11 goats that were seronegative, but had positive PCR test results. These results indicated that seroconversion can be delayed for many months following natural infection with CAEV. Delayed seroconversion appears to be a feature of CAEV infection, which may have direct implications for CAEV eradication programs and epidemiologic studies that rely on serologic methods to detect infected goats.

Animals↗
PubMed1992

Detection of feline immunodeficiency virus (FIV) nucleic acids in FIV-seronegative cats.

A study was undertaken to determine the rate of viral transmission among naive specific-pathogen-free (SPF) cats living in close contact with feline immunodeficiency virus (FIV)-infected cats. Twenty SPF cats were housed in the same rooms with experimentally FIV-infected seropositive and virus culture-positive cats for 2 to 4 years and were monitored for the presence of FIV nucleic acids and antibodies. Only 1 of the 20 cats became seropositive and virus culture positive and developed signs of disease. Genomic DNA from bone marrow and peripheral blood mononuclear cells (PBMC) of 10 of 19 healthy-appearing seronegative cats became positive for FIV DNA by the polymerase chain reaction. Twenty-eight SPF cats housed as groups in separate quarters and never exposed to FIV-infected cats were uniformly negative for FIV DNA. FIV RNA transcripts were detected in concanavalin A-stimulated PBMC cultures from 4 of 10 FIV DNA-positive, seronegative cats by in situ hybridization. PBMC from three of four naive SPF cats acquired FIV nucleic acids after the cats were transfused with blood and bone marrow from FIV genome-positive, seronegative donors. Three of five FIV-seronegative cats housed for years with naturally FIV-infected cats in a private household were also found to harbor FIV DNA, indicating that the same phenomenon occurred in the field. These findings demonstrate that cats living in close contact with FIV-infected seropositive cats can acquire FIV nucleic acids without developing detectable levels of serum antibodies or disease.

Animals↗
PubMed1991

Progressive immune dysfunction in cats experimentally infected with feline immunodeficiency virus.

Within 6 months of infection with the Petaluma isolate of feline immunodeficiency virus, specific-pathogen-free domestic cats exhibited a decrease in the percentage and number of circulating CD4+ lymphocytes and in the CD4+/CD8+ T-cell ratio, along with a marginally significant depression of pokeweed mitogen-induced lymphocyte proliferation in vitro. There was no loss of responsiveness to concanavalin A during this stage, and the cats were capable of mounting a satisfactory antibody response to a T-dependent, synthetic polypeptide immunogen. The pokeweed mitogen response deficit became clearly demonstrable by 11 to 12 months postinfection. A decline in the lymphocyte proliferative response to concanavalin A and a diminished ability to mount an in vivo antibody response to the T-dependent immunogen evolved by 25 to 44 months postinfection. Virus infection did not affect the ability of cats to mount an antibody response to a T-independent synthetic polypeptide immunogen. These data indicate that feline immunodeficiency virus produces a slowly progressive deterioration of T-cell function but does not affect the ability of B cells to recognize and respond to a T-independent antigenic stimulus.

Amino Acid Sequence↗
PubMed1991

Development of IL-2-independent feline lymphoid cell lines chronically infected with feline immunodeficiency virus: importance for diagnostic reagents and vaccines.

Two interleukin 2 (IL-2)-independent feline immunodeficiency virus (FIV) producer cell lines (FL-4 and FL-6) were produced by selecting cells from an IL-2-dependent culture of mixed peripheral blood lymphocytes infected with FIV. The new cell lines have been stable for over 1 year and spontaneously produce FIV with an average reverse transcriptase titer of 300,000 cpm/ml and an average sucrose gradient purified viral protein concentration of 1 mg/l. FIV produced from these cultures is highly infectious in vitro and in vivo. The FL-6 cell line was phenotyped as expressing the feline CD8 and Pan-T antigens, while the FL-4 cell line expressed the CD4, CD8, and Pan-T antigens. Both cell lines, however, express high levels of viral core and envelope proteins. Paraformaldehyde-inactivated whole virus and similarly inactivated whole-cell virus preparations induced a strong antibody response to core and envelope antigens in immunized cats. The establishment of FIV-producing feline IL-2-independent peripheral blood lymphocyte lines should be valuable for the development of FIV-diagnostic reagents and vaccines and also as a model for human acquired immunodeficiency syndrome vaccine development.

Animals↗
PubMed1990

Type C retroviral expression in spontaneous feline olfactory neuroblastomas.

Three cases of spontaneous olfactory neuroblastoma (ONB) in domestic cats were morphologically and immunocytochemically characterized. Diagnostic light microscopic features included Flexner and Homer-Wright rosettes, while ultrastructurally the cells had neuritic processes, intracellular intermediate filaments, and intercellular junctions. Immunocytochemically, the tumors stained positively for neuron-specific enolase, cytokeratins, and S-100 protein antigens. In each case, a key finding was the identification of numerous mature type C retroviral particles within the tumors. In one case, budding of viral particles from the plasmalemma of tumor cells suggested the source of mature particles. This cat and one other were tested, and both were serologically positive for feline leukemia virus (FeLV). The virus in the tumors was identified as FeLV by polymerase chain reaction and immunocytochemistry. No other neoplasms were found in any of the cats, nor was there similar evidence of active viral infection in other non-tumor tissues, including the brain. Although the relationship between FeLV infection and ONB is uncertain, our findings indicate that FeLV should be investigated as an etiologic agent of ONB.

Animals↗
PubMed1990

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

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 infedted 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.

Animals↗
PubMed1985

A novel immunoassay with direct relevance to protection against organophosphate poisoning.

Antiparaoxon immune sera were employed in a new immunoassay based on competition between acetylcholinesterase and antibodies for the binding of paraoxon. Unlike radioimmunoassay, the new assay described herein can be extended to predict the feasibility of antibodies to confer in vivo protection of acetylcholinesterase against organophosphate poisoning. The toxicity of paraoxon was reduced in mice which were preinjected with the immune sera.

Acetylcholinesterase↗
PubMed1982

Interleukin 2 and stimulator lymphoblastoid cells will induce human thymocytes to bind and kill K562 targets.

Human thymocytes cultured in the presence of IL-2 and an irradiated B cell line became cytotoxic to K562 target cells. Thymocytes cultured alone or with only IL-2 exhibited almost no killing, but thymocytes cultured in the presence of stimulator cells alone exhibited low levels of cytotoxic activity. Removal of Fc gamma receptor-bearing cells from the activated thymocyte population almost completely abolished the binding and lytic activity. Separation of thymocytes into Fc microns+ and Fc microns-cells before culturing with IL-2 and stimulator cells revealed that only the Fc microns+ subpopulation developed into K562 killer cells. These findings indicate that modulation of Fc microns to Fc gamma receptors on the thymocyte cell surface is part of the maturation process of this particular subset of cytotoxic cells. Morphologically, most of the activated Fc gamma+ K562-binding cells were large, granulated lymphocytes. Only very few of the round, nongranulated small thymocytes were bound to K562 target cells.

Cell Differentiation↗
PubMed1977

Chemoimmunotherapy for canine lymphosarcoma.

Thirty-two dogs with naturally occurring multicentric lymphosarcoma were randomly assigned to one of two treatment groups. One half of the animals received combination chemotherapy plus vitamin injections (controls) while the other half received indentical chemotherapy plus injections of chemically-modified tumor cell extract in Freund's complete adjuvant (vaccinates). Clinical staging revealed no bias between groups but showed that prognosis could be closely correlated with the severity of disease at initial presentation. Twenty dogs (62%), including 11 vaccinates and 9 controls, responded favorably to chemotherapy and were evaluated for length of first remission and total survival time. Both parameters were significantly longer in vaccinated dogs than in controls. These data suggest that immunological stimulation may be a helpful adjunct to conventional therapy in selected types of cancer when immunological principles are observed.

Animals↗
PubMed1977

Dynamic changes in the epidemiology of canicola fever in Israel. Natural adaptation of an established serotype to a new reservoir host.

Investigation of human leptospirosis caused by the serotype canicola revealed a significant shift in the chain of infection of this disease. The adaptation of an old and well-established serotype to a new and abundant host, the Norway rat, provides a new means for spreading and transferring canicola fever to man and farm animals. The changes in the epidemiology of leptospirosis described should serve as a warning to epidemiologists responsible for suggesting proper prophylactic measures.

Adult↗