Chronic HIV-infection in CNS--neurological manifestations.
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Biomedical subjects
Publications and source records attributed to A Sönnerborg.
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The mean plasma content of malondialdehyde (MDA) in 30 patients in different stages of HIV infection was found to be about 30% higher than that in controls. The phenomenon was not correlated to the degree of immunodeficiency and was noted early in the course of the disease. This indicates a higher degree of basal lipid peroxidation, which might contribute to the tissue damage seen in these patients. A new reverse phase liquid chromatography method was used for quantitative measurements of MDA in plasma after reaction of this compound with thiobarbituric acid.
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The antibody response in 20 homosexual men with symptomatic primary HIV infection was studied with ten different antibody assays (enzyme-linked immunosorbent assays, indirect immunofluorescence assays, radioimmunoprecipitation [RIPA], and western blot). HIV antibodies were detectable by all the assays within 2 months after onset of illness. RIPA and western blot were more sensitive than the other assays--all serum samples obtained at 2 weeks and after were reactive. In all cases, the first serum sample reactive by RIPA precipitated gp160 whereas, by western blot, antibodies to p24 were first recognised. This study shows the necessity of including gp160 and p24 in any assay to detect early antibody response in primary HIV infection. 5 patients were studied by virus isolation. During the 2 first weeks after onset of symptoms, HIV was demonstrated in cell-free plasma in all cases and, in 4 cases, also in peripheral blood mononuclear cells. Samples obtained later contained demonstrable infectious virus in only 1 of 4 cases. Thus a phase of viraemia precedes the antibody response in symptomatic primary HIV infection.
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Human immunodeficiency virus (HIV) has been isolated from plasma in 6 of 7 patients showing clinical symptoms of a primary HIV infection. Parallel cultures from peripheral blood mononuclear cells (PBMC) yielded virus in 5 patients. In one case, virus could only be isolated from the cerebrospinal fluid but not from peripheral blood. Detectable viremia was transient and preceded the appearance of HIV specific antibodies. After cessation of acute symptoms, the frequency of HIV isolations was similar to that of asymptomatic carriers (23 and 26%, respectively). The role of the immune response in terminating detectable viremia remains to be established.
The human immunodeficiency virus (HIV)-specific lymphocyte proliferation response was determined for 40 persons at different stages of HIV infection. The specific response to purified HIV virion antigens from strain HTLV-IIIB was poor, occurred in only 9 of the 40 subjects, was not improved with the addition of interleukin-2, and was more frequent in symptom-free individuals (46%) than in patients with lymphadenopathy syndrome (10%). Reactivity to subcomponent p24 was better than that to whole HIV; reactivity was present in five of six infected persons and increased with the addition of exogenous interleukin-2. Reactivities to subcomponents (g)p41 and gp120 were also measured. This is the first evidence of a specific cell-mediated immune response to HIV antigen in HIV-infected persons. Monkeys immunized with purified HIV or with purified p24 displayed cellular immunoreactivity both to whole HIV and to subcomponents. In contrast to the poor reactivity to HIV antigen, the lymphocytes of the patients had good specific cell proliferation responses to cytomegalovirus and herpes simplex virus challenge and a normal response to the addition of phytohemagglutinin. The results suggest a functional defect in peripheral lymphocytes of some HIV-infected individuals on the basis of their response to whole HIV antigen and a better response to gag protein.
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The NBT reduction of granulocytes was determined in 11 patients with HTLV-III infection. The reaction was measured in granulocytes both in resting state and after stimulation with Escherichia coli, as well as with and without addition of plasma. In 5 patients with AIDS, the NBT reduction was significantly decreased in all these types of experiments, when compared with 12 healthy controls. In 6 patients with the lymphadenopathy syndrome (LAS), the NBT reduction of resting granulocytes was significantly higher than that of the controls. The findings could in general not be explained by superinfections. The elevated NBT test during the long term LAS stage reflects a release of free oxygen radicals, against which treatment might be directed.
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Serum specimens from 111 human immunodeficiency virus type 1 (HIV-1) infected and 183 HIV-1 seronegative patients were analysed for antibodies to hepatitis C virus (HCV), hepatitis B virus (HBV) and hepatitis A virus (HAV) by enzyme linked immunoassay (ELISA) and radioimmunoassay. Anti-HCV and anti-HBV antibodies were found in the vast majority (89 and 83%, respectively) of intravenous drug addicts (IVDA), independent of the type of drug abuse or whether the patients were HIV-1 infected or not. Anti-HAV antibodies were found in 60% of the IVDA. Anti-HCV antibodies were found in anti-HIV-1 positive homosexual men (14%) and anti-HIV-1 negative heterosexual persons (8%), but not in HIV-1 seronegative homosexual men. Also anti-HAV antibodies were found to a small extent in these groups. In contrast, anti-HBV antibodies were common in the homosexual men. The absorbance values of the positive reactions in the anti-HCV ELISA were lower for HIV-1 seropositive patients than those for HIV-1 seronegative subjects, particularly in the late stages of HIV-1 infection. These data suggest that HCV infection is transmitted as readily as HBV infection by intravenous drug abuse and that all three types of hepatitis virus infection are common in IVDA. Although transmission of HCV is primarily mediated by blood, sexual transmission may also occur. HIV-1 infection seems to be associated with unusually low levels of anti-HCV antibodies, especially in the late stages of HIV-1 infection.
Serum samples were analysed for IgM and IgG antibodies to parvovirus by ELISA and for parvovirus B19 DNA by polymerase chain reaction (PCR) in 69 HIV-1 infected Swedish patients with anemia and in 37 HIV-1 infected subjects without anemia. In 5/69 anemic patients, parvovirus B19 DNA was detected despite the lack of IgM antibody activity to the virus. The detection of parvovirus B19 DNA was significantly correlated to the degree of anemia in the anemic patients. In two patients who had a chronic anemia, a persistent parvovirus infection was detected by PCR, but not by serology, for 1 and 1.5 years, respectively. The results suggest that persistent parvovirus infection is a rare cause of anemia, but important to identify, since the infection is potentially treatable with intravenous immunoglobulin.
The nosocomial transmission of hepatitis C involving three subjects participating in a research project in a Swedish hospital is described. One person contracted acute hepatitis C and another participant had an asymptomatic seroconversion. A temporal relationship between participation in the experiments and seroconversion for hepatitis C, and virology with phylogenetic analyses, suggest that they most probably contracted hepatitis C from a third subject who unknowingly had chronic hepatitis C. Faulty nursing and procedural routines were identified as the probable cause of the transmission. Our findings reinforce the need for medical personnel to strictly adhere to universal precautions worked out to prevent the transmission of blood-borne viruses and underline the importance of a continuous supervision of nursing and procedural routines, even in hospitals with well-educated staff and presumably high standards.
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