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Biomedical subjects

C Saxinger

Publications and source records attributed to C Saxinger.

At least 55 records · Page 3Linked to original sources
PubMed1985

Seroepidemiology of HTLV-III antibodies in a remote population of eastern Zaire.

A human retrovirus--human T cell lymphotropic virus-III (HTLV-III)--has recently emerged as the probable cause of acquired immunodeficiency syndrome (AIDS). In May 1984, 250 outpatients at a hospital in a remote area of eastern Zaire were surveyed for AIDS type illnesses and the prevalence of antibodies against HTLV-III determined by an enzyme linked immunosorbent assay using disrupted whole HTLV-III virus as the antigen. No clinical cases of AIDS were diagnosed among these patients. Overall, 31 (12.4%) had clearly positive ratios (greater than or equal to 5.0) and a further 30 (12.0%) had borderline ratios (3.0- less than 5.0). Western blots of serum samples from subjects with antibodies yielded bands consistent with HTLV-III as found in American patients with AIDS and members of groups at risk of AIDS. The prevalence of antibody was highest in childhood (p = 0.02); among adults prevalence rose slightly with age. HTLV-III antibodies were more common among the uneducated (p = 0.006), agricultural workers (p = 0.03), and rural residents (p = 0.006), but the Western blot bands were generally weak in this group. By contrast, one urban resident had strong bands. The relatively high prevalence of antibodies among the rural poor in this area of Zaire suggests that HTLV-III or a closely related, cross reactive virus may be endemic in the region. A different natural history of infection, perhaps in childhood, may also explain the findings.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Diversity of clinical spectrum of HTLV-III infection.

In a prospective follow-up volunteer study lasting 4 to 16 months, 17 of 200 homosexual men living in Finland had antibodies to human T-lymphotrophic virus type III (HTLV-III). 1 man who initially had a low titre of HTLV-III antibodies became seronegative within 6 months without any symptoms developing, and a seronegative man became seropositive. 14 men had high titres of HTLV-III antibodies when they first joined the study and during the study titres rose in all other HTLV-III-positive men except those with AIDS. Initially 9 men were symptom-free, 3 had lymphadenopathy syndrome (LAS), 3 had AIDS-related complex (ARC), and 2 had AIDS. During follow-up LAS developed in 3 symptom-free HTLV-III positive men but none of those with LAS or ARC progressed to AIDS. Most HTLV-III-positive men, including those who were otherwise symptom-free, had mucocutaneous lesions generally associated with immune deficiency. Regardless of the symptoms, those with increasing HTLV-III antibody titres showed lowered T helper/T suppressor ratios, decreased numbers of T helper cells, and/or diminished responses to tuberculin antigen (PPD). These results suggest that the clinical spectrum of HTLV-III infection ranges from transient infection through chronic provirus state, asymptomatic virus producer state, LAS or ARC, and rarely full-blown AIDS. Cofactors probably determine the final outcome of infection in the individual.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Risk of nosocomial infection with human T-cell lymphotropic virus III (HTLV-III).

Infection with human T-cell lymphotropic virus III (HTLV-III) is closely linked to the acquired immunodeficiency syndrome (AIDS). We evaluated the risk of nosocomial infection with HTLV-III by testing for antibodies to HTLV-III among hospital employees, including victims of needle-stick exposure, endoscopists, pathologists, and laboratory workers. Assays for antibody against the virus were performed by enzyme-linked immunosorbent assay and electrophoretic (Western blot) techniques. Although all 22 of our patients with AIDS and 6 of 7 with AIDS-related complex were found to have antibodies to HTLV-III when both assays were employed, none of the 85 employees with nosocomial exposure to specimens from patients with AIDS were positive for HTLV-III antibody. These studies must be regarded as preliminary, but they suggest that when current hospital isolation procedures are employed, the risk of nosocomial transmission of HTLV-III is low.

Accidents, Occupational↗
PubMed1985

Influence of the human T-lymphotropic virus/lymphadenopathy-associated virus on functions of human lymphocytes: evidence for immunosuppressive effects and polyclonal B-cell activation by banded viral preparations.

The etiologic agent for the acquired immunodeficiency syndrome (AIDS) is now firmly established as the retrovirus termed the human T-lymphotropic virus type III (HTLV-III) or the lymphadenopathy-associated virus, LAV. The disease is characterized by profound and progressive loss of immunity, but molecular evidence indicates that only a few cells in peripheral blood are being productively infected with this virus. In the present study we have investigated a disrupted HTLV-III viral preparation for biologic effects on normal lymphoid cells. Relatively dilute concentrations of this preparation were found to stimulate immunoglobulin secretion by peripheral blood lymphocytes; at the same dosages, the preparation was inhibitory for the B-cell differentiation responses that are induced with other known polyclonal B-cell activators, pokeweed mitogen, Staphylococcus aureus, and Epstein-Barr virus. This preparation was also inhibitory at high concentrations for T-lymphocyte proliferative responses to phytomitogens and antigens and resulted in a reduced expression of Tac antigen on phytohemagglutinin-activated lymphocytes. Paradoxically, incubation of lymphocytes of certain healthy donors with the HTLV-III preparation alone resulted in increased expression of Tac and Leu-12 antigens. These findings show that a disrupted preparation of HTLV-III virus can mimic many of the immunologic abnormalities present in patients with HTLV-III infection. Nonviable viral proteins may be responsible for some of the immunologic perturbations that occur in HTLV-III-infected states.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Antibodies to human T lymphotropic virus type III demonstrated by a dot immunobinding assay.

A dot immunobinding (DIB) technique was applied to the demonstration of antibodies to human T-lymphotropic virus type III (HTLV-III). By this technique IgG antibodies to HTLV-III were demonstrated in six of six Swedish patients with acquired immune deficiency syndrome and in 37 of 39 (95%) Swedish homosexual men with persistent generalized lymphadenopathy but in none of 50 Swedish healthy blood donors. Findings obtained by this method showed complete concordance with those obtained by an enzyme-linked immunosorbent assay. All sera positive by DIB were also positive by Western blotting. The DIB assay is simple and well suited for screening of sera for HTLV-III antibodies.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Immune functions in homosexual men with antibodies to HTLV-III in Finland.

The occurrence of HTLV-III antibodies in a voluntary group of 175 homosexual men in a low risk AIDS area was studied, and the findings were correlated to clinical, virological, immunological and lifestyle parameters. Fifteen of 175 men had HTLV-III antibodies; two of these had AIDS, five had LAS and two had enlarged lymph nodes. In the HTLV-III antibody negative group, no signs of AIDS or pre-AIDS were seen during a 10 month follow-up. In HTLV-III antibody positive individuals, low TH/TS ratio was mainly due to decreased number of TH cells. Most HTLV-III antibody positive cases had low responses to a specific antigen, PPD, while responses to the mitogens PHA and PWM were only slightly affected. In HTLV-III antibody negative cases, 13% had a low TH/TS ratio, mostly due to elevation of TS cells. In this group, mitogen and antigen responses were normal or only slightly affected. The results reinforce the causal relationship between HTLV-III and AIDS and suggest that the cells primarily affected by the virus infection are TH cells, responsible for antigen specific responses. Longitudinal studies are required to find out, what is the relationship of immune response to the development of clinical AIDS in HTLV-III infected individuals.

Acquired Immunodeficiency Syndrome↗
PubMed1985

HTLV-III infection in homosexuals and hemophiliacs in Sweden.

Two hundred and three homosexual (HS) men and 114 hemophiliacs in Sweden were examined for serum antibodies to human T-lymphotropic virus type III (HTLV-III) and for alterations of T-lymphocyte subsets. Sera were screened for HTLV-III antibodies by an enzyme-linked immunosorbent assay and/or a dot immunobinding assay, and positive reactions were confirmed by Western blotting. HTLV-III antibodies were demonstrated in 13 of 13 (100%) HS men with acquired immune deficiency syndrome, in 63 of 67 (94%) HS men with persistent generalized lymphadenopathy, in 17 of 45 (38%) symptomatic HS men, and in 6 of 78 (8%) asymptomatic HS men but in none of 108 male blood donors. Seropositive HS men had significantly lower T4/T8 (helper/suppressor) cell ratios and T4 cell numbers than had seronegative HS men. Seronegative HS men had decreased T-cell ratios compared to controls but not decreased T4 cell numbers. Among hemophilia A patients, HTLV III antibodies were demonstrated in 40 of 48 (83%) cases treated with American factor VIII concentrate and in 17 of 29 (59%) cases treated with both American and Swedish concentrates but in none of 13 cases treated exclusively with Swedish factor VIII. Twenty-one hemophilia B patients treated with Swedish factor IX concentrates were all seronegative, whereas one of 3 hemophilia B cases treated with imported factor IX was seropositive. T4/T8 cell ratios were significantly lower in seropositive as compared to seronegative hemophilia A patients.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Clinical and immunological findings in HTLV-III infection.

Clinical, immunological, microbiological, virological, and lifestyle parameters were followed in 200 homosexual men living in Finland. The subjects were seen at 3- to 6-month intervals starting in summer 1983. Human T-cell lymphotropic virus III (HTLV-III) antibodies detected by enzyme immunoassay and confirmed by Western blotting were seen in 18 (9%) of the cases. Initially two cases had acquired immunodeficiency syndrome, three had acquired immunodeficiency syndrome-related complex, three had lymphadenopathy syndrome, and ten were asymptomatic. During the follow-up two asymptomatic cases developed lymphadenopathy syndrome and three developed enlarged lymph nodes. Immunological studies revealed decreased T-helper cell values and/or T-helper/suppressor ratios in all clinical categories, the findings being more severe and progressive in the symptomatic cases. The finding most clearly distinguishing HTLV-III antibody positive cases from the antibody negative ones was a decreased response to a specific recall antigen, purified protein derivative of tuberculoprotein. Responses to mitogens phytohemagglutinin and pokeweed mitogen were also decreased, but to a lesser extent. The primary immunological defect associated with helper T-cell infection by HTLV-III thus seems to be loss of antigen specific immune responses. It is suggested that this is the result of previous antigenic stimulation of HTLV-III infected T-helper cells and that the cellular destruction is associated with initial mitotic activity.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Unique pattern of HTLV-III (AIDS-related) antigen recognition by sera from African children in Uganda (1972).

Of 75 sera collected in the West Nile district of Uganda over a 1-year period between 1972 and 1973, 50 (66%) had antibody reactivity to human T-cell lymphotropic virus subgroup III (HTLV-III) at low titer levels. Sera were initially screened by HTLV-III enzyme linked immunosorbent assay and sera with values less than normal mean + 2 SD were removed from testing. The remaining sera were tested for positivity by an amplified Western blotting procedure which incorporated a three-layer immunoperoxidase procedure. Immunoglobulin reactive with HTLV-III Mr 24,000, 41,000, and 76,000 proteins were present in nearly all positive sera. The antibody status of this group was unlike any normal or acquired immunodeficiency syndrome-risk group previously tested. The high prevalence and relatively low titers suggest the detection as early as 1972 of a relative or predecessor of HTLV-III or of HTLV-III itself but existing in a population acclimated to its presence. It further suggests a likely African origin of HTLV-III.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Immunosuppression in homosexual men seronegative for HTLV-III.

Clinical, microbiological, and lifestyle patterns in homosexual men showing in vitro immunological abnormalities were studied and related to the susceptibility to human T-lymphotropic virus type III (HTLV-III) infection. In a cohort of male homosexual volunteers in Finland, 90% were HTLV-III antibody negative. Ten % of the HTLV-III negative cases showed decreased T-helper/suppressor cell ratios, mostly due to elevated numbers of T-suppressor cells. In this immunosuppressed group, more signs of diarrhea, intestinal giardiasis, genital warts, and hepatitis B were observed than in the other HTLV-III antibody-negative study subjects. The type of sexual practice was not associated with the in vitro immune abnormalities. During a follow-up of up to 16 months, 4 initially HTLV-III antibody negative cases showed seroconversion. Three of these had inverted T-helper/suppressor cell ratios prior to the seroconversion. It is concluded that persons showing in vitro immunosuppression are more susceptible to HTLV-III infection when being exposed to the virus or else alteration in T-cell subsets signals a pre-antibody-positive or early phase of HTLV-III infection.

Antibodies, Viral↗
PubMed1984

Type-I HTLV antibody in urban and rural Ghana, West Africa.

The prevalence of antibodies against the newly described human T-cell lymphoma virus, type I (HTLV-I) in two communities in Ghana, West Africa, is described. There was no difference by community (urban, 3.6% and rural, 4.0%). Prevalence increased with age, being 5.9% among persons greater than 10 years old, but did not differ by sex. There was no difference when data were analysed by housing status or crowding. Non-confirmed reactions in the assay system were frequent and correlated with both prevalence and titer of antibody against malaria. Possible explanations include vector-borne transmission like that of malaria, but the relationship is more probably due to a polyclonal stimulation of B cells, enhancing the potential for detecting reactivity in the assay. Because assay systems vary and because most laboratories do not routinely use a confirmation assay, results presented by different groups must be interpreted cautiously.

Adolescent↗
PubMed1984

Functional and phenotypic comparison of human T cell leukemia/lymphoma virus positive adult T cell leukemia with human T cell leukemia/lymphoma virus negative Sézary leukemia, and their distinction using anti-Tac. Monoclonal antibody identifying the human receptor for T cell growth factor.

Adult T cell leukemia (ATL) and Sézary leukemia are malignant proliferations of T lymphocytes that share similar cell morphology and clinical features. ATL is associated with HTLV (human T cell leukemia/lymphoma virus), a unique human type C retrovirus, whereas most patients with the Sézary syndrome do not have antibodies to this virus. Leukemic cells of both groups were of the T3, T4-positive, T8-negative phenotype. Despite the similar phenotype, HTLV-negative Sézary leukemic cells frequently functioned as helper cells, whereas some HTLV-positive ATL and HTLV-positive Sézary cells appeared to function as suppressors of immunoglobulin synthesis. One can distinguish the HTLV-positive from the HTLV-negative leukemias using a monoclonal antibody (anti-Tac) that appears to identify the human receptor for T cell growth factor (TCGF). Resting normal T cells and most HTLV-negative Sézary cells were Tac-negative, whereas all ATL cell populations were Tac-positive. The observation that ATL cells manifest TCGF receptors suggests the possibility that an abnormality of the TCGF-TCGF receptor system may partially explain the uncontrolled growth of these cells.

Adult↗
PubMed1984

Adult T-cell leukemia/lymphoma in Jamaica and its relationship to human T-cell leukemia/lymphoma virus type I-associated lymphoproliferative disease.

We had shown previously that the prevalence of human T-cell leukemia/lymphoma virus type I (HTLV-I)-antibody positivity is high in Jamaican non-Hodgkin's lymphoma (NHL) patients and that virus-positive patients have the clinical features and poor prognosis of adult T-cell leukemia/lymphoma (ATL). Sixty-two % of 45 NHL patients diagnosed consecutively between 2/1/82 and 1/31/84 and studied prospectively were HTLV-I-antibody positive. Skin involvement (38%), hypercalcemia (44%), and leukemia (40%) were unusually prevalent and there was a strong association (p less than 0.05) with HTLV-I-antibody positivity. Fifty-two % of the patients had bone marrow infiltration, and 74% of these patients were HTLV-I-antibody positive (p = 0.06). Lymphadenopathy (96%), hepatomegaly (60%), and splenomegaly (25%) were detected with about the same frequency as in other series of NHL patients with advanced disease, and 61-88% of these patients were HTLV-I-antibody positive. Patients were classified into those with "typical ATL" (NHL associated with 2 of the 4 features i) hypercalcemia; ii) histologically proven skin infiltration; iii) leukemia; and iv) bone marrow infiltration, providing that the morphology of infiltrating or leukemic cells was characteristic of ATL; those "consistent with ATL" (NHL associated with 1 of these 4 features); and "non-ATL" (NHL without any of these 4 additional features). Thirty-two (71%) of the NHL patients were ATL patients, i.e., had features typical of or consistent with ATL, and 78% of these were HTLV-I-antibody positive. HTLV-I provirus was detected in tumour cells of all HTLV-I-antibody positive patients tested. Three (23%) of the non-ATL patients were HTLV-I-antibody positive. There was no correlation between histopathological features and the clinical classification or HTLV-I-antibody positivity. Median survival of ATL and non-ATL patients was 16 and 53 weeks. Although the disease was usually fulminant, 34% of the ATL patients had a subacute or chronic course. Skin involvement and leukemia were prominent in these patients. Hypercalcemia was the chief prognostic determinant. Median survival of hypercalcemic and normocalcemic ATL patients was 13 and 86 weeks (p less than 0.05). Hypercalcemia caused 10 deaths, infections 12, and death was due to tumour progression in 4 patients. Infections were usually due to pyogenic organisms and only 2 patients had systemic opportunistic infections. Six (27%) of 22 chronic lymphocytic leukemic (CLL) patients were HTLV-I-antibody positive.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1984

HTLV: epidemiology and relationship to disease.

With the discovery of the human retrovirus class, an important turning point in the understanding of the process by which cancer is caused and develops in humans has been achieved. As summarized here, clinical and epidemiologic studies have documented the close association of human T-cell leukemia virus (HTLV-I) to a particular form of T-cell malignancy, adult T-cell leukemia/lymphoma (ATL). Yet to be understood is the process involved in translating virus infection into malignant lymphoproliferation. Epidemiologic data suggest that this may involve a relatively long latent period between primary HTLV-I infection and subsequent malignancy risk. Presumably, identifiable co-factors will emerge to explain the trigger for malignant transformation. However, the restricted pattern of tumor phenotype suggest that this process is tightly linked to cells for which HTLV-I has a particularly strong infectious trophism. Interdisciplinary studies are currently under way in a number of laboratories to elucidate the molecular interactions in the HTLV-I associated malignant transformation process in order to correlate these with the epidemiologic data. Thus, lessons are likely to be learned from these molecular and epidemiologic studies which may provide new and important etiologic insights applicable to the prevention and therapy of cancer. Furthermore, with the recent discovery of HTLV-III, a cytopathic form of this class of human retrovirus, the likely cause of acquired immunodeficiency syndrome (AIDS) has been discovered. This has enormous public health implications for the detection, treatment, and prevention of this major medical epidemic. Epidemiologic studies are currently under way to identify what factors associated with virus exposure result in the full-blown AIDS syndrome. In addition, the malignancy potential of this new type of retrovirus is currently the subject of intensive investigation.

Acquired Immunodeficiency Syndrome↗