Human respiratory syncytial virus (RSV) is the leading cause of severe bronchiolitis and pneumonia in infants. RSV vaccine development has been stifled for the past 23 years because infants vaccinated with formalin-inactivated (FI) RSV have experienced exacerbated disease upon RSV infection. This exacerbated disease phenomenon is poorly understood, in part because of the lack of a primate model that exhibits a similar exacerbated disease state. Vaccination of African green monkeys with either FI RSV or a genetically engineered subunit vaccine termed FG glycoprotein reduced replication of challenge virus. However, only vaccination with FI RSV induced an enhanced pulmonary pathologic response to RSV infection. Pulmonary inflammatory scores in the FG glycoprotein-vaccinated monkeys were no greater than in monkeys vaccinated with adjuvant alone. This is the first demonstration of RSV vaccine-induced enhanced pathology in a primate and illustrates that a subunit vaccine has the potential of circumventing this exacerbated disease phenomenon.

Mibolerone, an androgen analog (17 beta-hydroxy-7-alpha, 17-dimethylestr-4-en-3-one), induces a slow but progressive involution of the bursa of Fabricius when fed to chickens at microng levels during the first 7 weeks of life. Chickens receiving mibolerone remained immunologically competent, evidenced by: 1) their antibody response to nonreplicating antigens and infectious antigens; 2) the number of antibody-producing cells in their spleens; 3) the stimulation of their peripheral leukocytes with the plant mitogen phytohemagglutinin; and 4) their capacity to resist challenge with Marek's disease virus and Newcastle disease virus after vaccinations with turkey herpes-virus and the B-1 LaSota strain. This, coupled with the fact that it prevents experimental lymphoid leukosis, makes mibolerone a potential agent to be used under field conditions for the control of lymphoid leukosis.