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Biomedical subjects

J Goudsmit

Publications and source records attributed to J Goudsmit.

At least 325 records · Page 18Linked to original sources
PubMed1988

HIV-antibody seroconversions in Dutch haemophiliacs using heat-treated and non heat-treated coagulation factor concentrates.

A national multicentre study was performed to investigate the effects of donorselection and the use of heat-treated plasma products on seroconversion to HIV in 157 Dutch haemophiliacs. All patients included in the study were seronegative for HIV antibodies in 1983. Thirteen percent (20/157) seroconverted between 1983 and 1986. Nineteen of 20 seroconversions could be related to the use of non heat-treated products in the year preceding HIV antibody seroconversion. One seroconversion occurred in a person using heat-treated non donor screened product. Seroconversion rate decreased as a result of the policy to discourage high risk blood donors and no seroconversions were observed following the introduction of donor screening in 1985.

Blood Coagulation Factors↗
PubMed1988

Effect of zidovudine on serum human immunodeficiency virus antigen levels in symptom-free subjects.

18 men with longstanding human immunodeficiency virus (HIV) antigenaemia but no symptoms received zidovudine in low-dose regimens (250 mg 6-hourly, 500 mg 6-hourly, or 500 mg 12-hourly) with or without acyclovir. Serum HIV antigen rose in only 1 patient and declined significantly in 13 (to below cut-off values in 9). In the 1 subject from whom HIV antigen positive cerebrospinal fluid was obtained, the fluid was antigen negative after 12 weeks of treatment. Acyclovir treatment alone or in addition did not seem to influence serum antigen levels. In 7 untreated men serum antigen levels rose or remained stable during follow-up. CD4+ cell counts increased in 14/18 treated subjects and 1/7 untreated subjects. No disease progression was observed in either group. Regression of enlarged lymph nodes was seen in the zidovudine-treated subjects. Adverse reactions to the study drugs were infrequent and mild. Anaemia caused symptoms in 2, but serious leucopenia or neutropenia was not observed.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Neurological and neuropathological features of human immunodeficiency virus infection in children.

A progressive encephalopathy occurs in 30 to 50% of infants and children infected with the human immunodeficiency virus (HIV). The expression of HIV antigen in the cerebrospinal fluid appears to correlate with the clinical occurrence of progressive encephalopathy. The signs of progressive encephalopathy in children with HIV infection, including loss of developmental milestones, impaired brain growth, and progressive motor dysfunction, indicate a poor prognosis and almost invariably a fatal outcome. Neuropathological findings in these children, including virus-laden macrophages and multinucleated giant cells are unique to this condition. Opportunistic or reactivated latent infections and neoplasms of brain occur in children with HIV infection but are uncommon. These findings support the hypothesis that the progressive encephalopathy observed in HIV-infected children is caused by primary infection of the brain with this virus. Epidemiological data predict increasing numbers of HIV-infected women and children. Research aimed at an understanding of the mechanism(s) of mother-to-infant transmission of HIV infection is urgently needed so that strategies for the prevention and treatment of such infection in children may be planned.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Natural antibodies to HIV-tat epitopes and expression of HIV-1 genes in vivo.

The tat regulatory protein of HIV-1 was expressed as a fusion protein in E. coli and used as antigen to detect antibodies against HIV-tat (anti-tat) in the serum of HIV-1 infected children and adults. HIV-1-infected children showed a higher frequency (55%) of anti-tat than HIV-1-infected adults (36%). Anti-tat were present in only 15% (3/20) of acutely infected individuals. Forty percent (10/25) of individuals with prolonged HIV-1 infection but without antigen were anti-tat positive. Only 13% (3/23) of HIV-1-antibody-positive individuals with prolonged HIV-1 antigenemia were anti-tat positive and titers of anti-tat antibodies declined with time. Pepscan analysis identified the amino terminus of HIV-tat as the major antibody-binding site. Antibodies to HIV-tat occurred as a harbinger of HIV-1 antigen expression and disappeared thereafter, possibly reflecting the transience of HIV-tat expression. Because of the low antigenicity of HIV-tat, antibodies to this regulatory protein are not a reliable marker for either early HIV-1 infection or subsequent disease progression.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Antibodies to HTLV-I in populations of the southwestern Pacific.

Sera collected from 1,102 individuals in 14 populations of the southwestern Pacific between 1956 and 1979 were tested by ELISA for antibodies to human T-cell leukemia virus type I (HTLV-I). Selected sera were also tested by particle agglutination and immunoblotting. Six of the populations had prevalences of antibodies greater than 4%, two populations had prevalences greater than 15%. Six populations had antibody prevalences of 2% or less. Three populations from the coast and northern islands of New Guinea had high prevalences of antibodies, while three New Guinea highland groups had virtually none. One population from the Solomon Islands had a high prevalence, while two others had very low prevalences. Two populations from small remote islands in Vanuatu both had high prevalences. Pacific sera did not neutralize a standard strain of virus readily neutralized by Japanese, European, and American sera. We conclude that infections with HTLV-I, some acquired more than 20 years ago, are widespread throughout the southwestern Pacific, even in several very isolated populations, although others have been spared. Some strains of HTLV-I in populations of the Pacific may have substantially different envelope proteins from prototype strains of America, Europe, and Japan.

Adolescent↗
PubMed1988

No predictive value of GC phenotypes for HIV infection and progression to AIDS.

The genetic polymorphism of group-specific component (GC) was investigated with isoelectric focusing in 351 homosexual men at risk for HIV infection, 96 male patients with AIDS, and 86 heterosexual controls. No significant differences in GC phenotype distribution were seen between controls and any of the at risk groups or patients, neither between HIV-Ab-positive/Ag-negative and HIV-Ab-positive/Ag-positive homosexual men nor between HIV-Ab-positive/Ag-positive homosexual men and AIDS patients, suggesting that the GC system is not involved in the infective susceptibility or progression of HIV infection to AIDS-related complex and AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Biological significance of the antibody response to HIV antigens expressed on the cell surface.

Human antibodies to HIV antigens expressed on the surface of infected cells may inhibit cell fusion with uninfected CD 4-positive cells and mediate killing of the infected cells by effector cells bearing the Fc receptor. Sequential sera from ten HIV-antibody seroconverted men, of which five progressed to ARC or AIDS (CDC stage IV) during the follow-up period of two years, were tested for the ability to inhibit CD 4-dependent cell fusion, (CFI) and to mediate antibody-dependent cellular cytotoxicity (ADCC). Nine patients developed HIV-specific ADCC and seven CFI-antibodies using the HIV strain HTLV-IIIB as target antigen. These antibodies appeared approximately at the same time 2-12 months after primary infection, defined as antibody seroconversion or antigenaemia. ADCC antibodies were detectable at higher titers as compared to CFI-antibodies. All sera of asymptomatic individuals (CDC stage II and III) were CFI antibody positive and had a higher mean ADCC titer as compared to sera from patients progressing to AIDS or ARC. ADCC and CFI antibodies coincided in some cases in the complete absence of core antibodies. Because the relationship between ADCC and CFI was not exclusive it is concluded that distinct domains of the HIV envelope induce natural antibodies mediating ADCC and CFI.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Temporal development of cross-neutralization between HTLV-III B and HTLV-III RF in experimentally infected chimpanzees.

Sera from chimpanzees inoculated respectively with HTLV-III B, LAV, HTLV-III RF and brain tissue from an AIDS patient were analysed for neutralizing activity by two methods: a cell fusion inhibition test (CFI) using HTLV-III B infected cells as inoculum and CD4+ cells as target and a replication inhibition test (RIT) using cell-free HTLV-III B as well as HTLV-III RF as inoculum and also CD4+ cells as target. All chimpanzees seroconverted for HTLV-III B antibodies within 2 months after inoculation and the ten sera included in the study recognized the HTLV-III B core proteins p17 and p24 and the transmembrane protein gp41 by immunoblotting. The HTLV-III B external envelope gp120 was recognized by eight sera with antibodies active in the CFI (CFI-Ab) or in the RIT (VN-Ab) using HTLV-III B as inoculum, while neither of two sera without such reactivity did. HTLV-III B CFI-Ab and HTLV-III B VN-Ab concurred in nine of ten serum samples. LAV and HTLV-III B infection induced HTLV-III B CFI-Ab and HTLV-III B VN-Ab within 9 months after inoculation in all four chimpanzees tested. However, only the serum of one of the four animals also neutralized HTLV-III RF. HTLV-III RF inoculation evoked only HTLV-III RF VN-Ab within nine months. Between 11 and 18 months neutralizing activity to both HTLV-III B and HTLV-III RF was found in all four sera of chimpanzees inoculated with HTLV-III B, LAV or HTLV-III RF.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Transmission of HIV and AIDS by plasmapheresis for Guillain-Barré syndrome.

A 58-year-old patient suffering from Guillain-Barré syndrome was successfully treated with plasma exchange therapy. Two- and half year later she developed AIDS. The only risk factor of this patient was plasmapheresis and it appeared, retrospectively, that one of the plasma donor samples contained antibodies to HIV. Knowing the exact moment of infection of our patient we documented the transfer of HIV antibodies from donor to patient, a HIV antigen peak two weeks after transmission (reflecting the initial virus replication in the patient) and subsequently the occurrence of patients' HIV antibodies and the reoccurrence of HIV antigen at the moment AIDS was diagnosed.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Human immunodeficiency virus type 1 neutralization epitope with conserved architecture elicits early type-specific antibodies in experimentally infected chimpanzees.

Chimpanzees are susceptible to infection by divergent strains of human immunodeficiency virus type 1 (HIV-1), none of which cause clinical or immunological abnormalities. Chimpanzees were inoculated with one of four strains of HIV-1: human T-lymphotropic virus (HTLV) type IIIB, lymphadenopathy virus (LAV) type 1, HTLV type IIIRF, or an isolate from the brain of a patient with acquired immunodeficiency syndrome. Within 6 months after inoculation with the closely related strains HTLV-IIIB or LAV-1, six chimpanzees developed serum antibodies to the C-terminal half (amino acids 288-467) of the HTLV-IIIB external envelope glycoprotein gp120. Sera from five of those chimpanzees had HTLV-IIIB cell-fusion-inhibiting antibody titers greater than or equal to 20 at that time, indicating that they neutralized the infecting strain of HIV-1 in vitro. No antibodies to the carboxyl terminus of HTLV-IIIB gp120 were observed in sera of chimpanzees inoculated with HTLV-IIIRF or with the brain-tissue strain, and those sera did not neutralize HTLV-IIIB. A rabbit immunized with the C-terminal portion of gp120 acquired neutralizing antibodies that bound to four domains of the HTLV-IIIB external envelope as analyzed by reactivity to 536 overlapping nonapeptides of gp120. One of these domains in the variable region V3, with the amino acid sequence IRIQRGPGRAFVTIG (amino acids 307-321), bound to all chimpanzee sera that neutralized HTLV-IIIB but not to the serum of the HTLV-IIIRF-inoculated chimpanzee that did not neutralize HTLV-IIIB. The HTLV-IIIRF sequence at the same location, ITKGPGRVIYA, was recognized by the serum of the HTLV-IIIRF-inoculated chimpanzee but not by any sera of the HTLV-IIIB-inoculated or LAV-1-inoculated chimpanzees. The HTLV-IIIB residues RIQR and AFV and the HTLV-IIIRF residues lysine and VIYA, flanking a highly conserved beta-turn (GPGR), appear to be critical for antibody binding and subsequent type-specific virus neutralization. This neutralization epitope, putatively consisting of a loop between two cysteine residues (amino acids 296 and 331) connected by a disulfide bond, is immunodominant in HIV-1-infected chimpanzees and induces antibodies restricted to the homologous viral strain.

Amino Acid Sequence↗
PubMed1988

Decline in CD4+ cell numbers reflects increase in HIV-1 replication.

Changes in CD4+ cell numbers were studied in relation to the presence of HIV-1 antigen (HIV-1-Ag) in serum from homosexual men followed prospectively. During 30 months of follow-up the mean CD4+ cell number (x 10(9) per liter) was stable in 134 at entry HIV-1 antibody (HIV-1-Ab) seropositives, who remained HIV-1-Ag negative (from 0.59 to 0.62) and declined in 38 at entry HIV-1-Ab seropositives who were persistently HIV-1-Ag positive (from 0.43 to 0.34). In sera of 9 of 65 HIV-1-Ab seroconverters HIV-1-Ag was detected only once, 3 months before or concomitantly with antibody seroconversion. Another 11 men became persistently HIV-1-Ag positive with antibody seroconversion or 2-6 weeks thereafter. A decline in CD4+ cell numbers was seen between 6 months before and the moment of HIV-1-Ab seroconversion, independently of duration and level of antigen expression. This indicates initial HIV-1 replication in both HIV-1-Ag negatives and positives. Following antibody seroconversion, HIV-1-Ag negatives had higher CD4+ cell numbers than HIV-1-Ag positives. Similarly to those who were HIV antigenemic from entry of the study, the HIV-1-Ab seroconverters who concomitantly with seroconversion or shortly thereafter became HIV-1 antigenemic showed a steady and significant (p = 0.01) decline in CD4+ cell numbers. In those who remained HIV-1-Ag negative after antibody seroconversion, CD4+ cell numbers were stable during follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Numbers of CD4+ cells and the levels of core antigens of and antibodies to the human immunodeficiency virus as predictors of AIDS among seropositive homosexual men.

The relation between serological and immunologic profiles and the risk of developing AIDS was assessed in 306 initially asymptomatic, human immunodeficiency virus-infected homosexual men studied for 30 mo. Twenty-nine men developed AIDS (attack rate, 16.8%). The attack rate in core antibody-negative men was 35.7%; this rate was 43.9% in antigen-positive men, 51.9% in men with low (less than 0.5 x 10(9)/L) CD4+ cell counts, 6.8% in core antibody-positive men, 6.9% in antigen-negative men, and 6.1% in men with normal CD4+ cell counts. The disappearance of core antibody, the expression of antigen, and the occurrence of low CD4+ cell counts preceded AIDS by a median of 624, 544, and 466 d, respectively. Seronegativity for core antibody preceded AIDS in 21 of 26 patients, 20 of whom were also antigen positive. Four more cases of AIDS developed among the antigen-negative, core antibody-positive men with low CD4+ cell counts. Only one patient with AIDS escaped detection by using these three markers.

AIDS-Related Complex↗
PubMed1988

Diagnostic value of specific IgM antibodies in primary HIV infection.

Sequential serum samples from 55 homosexual men with primary HIV infection were tested for IgM anti-HIV. An early IgM response was found in 27 out of 55 (49%). In five cases IgM anti-HIV was detected 1-3 1/4 months prior to IgG anti-HIV seroconversion, as detected by a commercially available ELISA, but in no case was IgM detected prior to IgG anti-HIV seroconversion, as detected by the more sensitive GACRIA (IgG antibody captive radio-immunoassay, see Subjects and methods) and immunoblot assays. In 22 out of 23 men (96%) the primary IgM response did not persist beyond 3 months. HIV antigenaemia was found before HIV antibody seroconversion in 6 out of 55 (11%) and concomitant with HIV antibody seroconversion in 8 out of 55 (15%) subjects. A 'flu-like' illness that might be ascribed to primary HIV infection was found in 37 out of 50 men (74%). A blood sample was taken from 11 men during or within 2 weeks of the illness: no serological markers of HIV infection were detected in four subjects, HIV antigen, IgM and IgG anti-HIV were detected in another four, HIV antigen was the only marker of HIV infection in two subjects, and in one subject, IgM and IgG anti-HIV were detected but not HIV antigen. These results indicate that no conclusive value can be attached to a negative IgM test in suspected primary HIV infection, and that any role for IgM anti-HIV testing in blood donor screening is highly questionable.

Acquired Immunodeficiency Syndrome↗