Jörg W. Eichberg

Two of three chimpanzees given plasma from patients with acquired immune deficiency syndrome (AIDS) or pre-AIDS showed serum antibodies to type III human T-cell leukemia virus (HTLV-III) 10 to 12 weeks after transfusion. One animal also developed lymphadenopathy, transient depression of the ratio of T4 to T8 lymphocytes, and impaired blastogenic responses. No opportunistic infections occurred. Adenopathy persisted for 32 weeks, and antibody to HTLV-III persisted for at least 48 weeks. This transmission of HTLV-III by lymphocyte-poor plasma confirms the potential risk of such plasma or plasma derivatives to recipients. The susceptibility of the chimpanzee to HTLV-III infection and the ability to simulate the human lymphadenopathy syndrome in this animal makes it a valuable model for further study of AIDS.

The use of a human immunodeficiency virus (HIV) immune globulin (HIVIG) in prevention of HIV infection in chimpanzees was investigated in the hope of ultimate application to interruption of vertical transmission. In previous experiments, no protection was observed when relatively high challenge doses were used. This study shows that HIVIG protected against a challenge dose (10 CID50) tenfold lower than that used previously. The protected animal remained free of HIV infection as determined by cocultivation and by polymerase chain reaction (PCR), and did not mount a primary immune response detectable by enzyme-linked immunosorbant assay (ELISA) and neutralization assays. These results imply that HIV vaccines should induce neutralizing antibody and may not need to induce cell-mediated immunity in order to be protective against exposure to HIV. They also provide an experimental basis for the conduct of clinical trials to evaluate prevention of maternal-infant transmission by HIVIG.

Anti-idiotypic antibodies (anti-Id) that contain an internal image component that mimics the surface antigen of hepatitis B virus (HBsAg) were used to immunize chimpanzees. Four injections of the rabbit anti-Id preparation elicited an antibody response to HBsAg (anti-HBs). The antibody specificity appeared to be against the anti-Id, since the anti-Id immunogen was shown to bind the chimpanzee anti-HBs. Two chimpanzees immunized with the anti-Id, along with two control animals that were either untreated or received a nonimmune rabbit immunoglobulin G preparation, were challenged with infectious hepatitis B virus. Both control chimpanzees developed clinical and serological characteristics consistent with an active hepatitis B virus infection, whereas the two anti-Id treated chimpanzees were protected from infection. Since chimpanzees provide a relevant model of a human response to hepatitis B virus immunization and infection, these results indicate that anti-Id preparations such as that described here might be candidates for vaccines against human diseases.