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H Alter

Publications and source records attributed to H Alter.

18 recordsLinked to original sources

Sera from HTLV-III/LAV antibody-positive individuals mediate antibody-dependent cellular cytotoxicity against HTLV-III/LAV-infected T cells.

The causative agent of the acquired immunodeficiency syndrome (AIDS) has been shown to be a human retrovirus called human T lymphotropic virus (HTLV)-III or lymphadenopathy-associated virus (LAV). The nature of the protective immune response against this virus is currently unknown. We report here results using an antibody-dependent cellular cytotoxicity (ADCC) assay which has been developed for measuring a specific immune response against HTLV-III/LAV. Forty-four sera were examined for their ability to mediate ADCC against HTLV-III/LAV-infected T cells. Sera from healthy HTLV-III/LAV seropositive individuals in the presence of mononuclear cells from healthy HTLV-III/LAV seronegative donors exhibited significantly higher levels of ADCC activity compared to sera from patients with AIDS. Western blot analysis of serum samples indicated that antibody reactivity with the p24 protein of HTLV-III/LAV correlated with higher levels of ADCC activity than did reactivity with Gp120/160. The observation that sera from healthy HTLV-III/LAV seropositive individuals mediated higher levels of ADCC activity than did sera obtained from subjects with AIDS suggests that ADCC may represent a protective immune response to infection with HTLV-III/LAV.

Acquired Immunodeficiency Syndrome

Increased detection of hepatitis C virus (HCV)-infected blood donors by a multiple-antigen HCV enzyme immunoassay.

A new, multiple-antigen enzyme immunoassay (EIA-2) for hepatitis C virus (HCV) antibodies was evaluated in parallel with the previously available c100-3 HCV EIA (EIA-1) in 14,068 volunteer blood donors as well as in 25 cases of transfusion-associated hepatitis C for which recipient and donor samples were available. When compared to EIA-1, the EIA-2 was more sensitive in detecting HCV-infected blood donors. The EIA-2 detected an additional 1 in 1000 EIA-1-negative, surrogate marker-negative donors who were infected with HCV as demonstrated by polymerase chain reaction (PCR). The specificity of the EIA-2 was comparable to that of the EIA-1, but the two tests appear to detect different populations of false-positive donors. Recombinant immunoblot assay-indeterminate donors were detected five times more frequently by the EIA-2; PCR demonstrated that 21 percent of these donors were infected with HCV. The greater sensitivity of EIA-2 was also found in 25 transfusion recipients with non-A, non-B hepatitis; however, in 16 percent of these cases of posttransfusion HCV infection, the EIA-2 failed to detect an HCV-seropositive donor. These data indicate that EIA-2 testing will significantly reduce, but probably not eliminate, the risk of transfusion-associated HCV infection; we estimate this residual per-unit risk to be 1 in 2000 to 1 in 6000 units transfused. On a national level, it is projected that the replacement of the anti-HCV EIA-1 with the EIA-2 will initially prevent up to 40 additional cases of transfusion-associated hepatitis C per day.

Blood Donors