IMMUNOLOGY OF HIV INFECTION IN THE FETUS AND NEWBORN

Abstract

In a recently published edition of Immunology of HIV Infection,47 focused primarily on adults, the view was expressed that “HIV should serve as an immunologic Rosetta stone.”95 For those of us interested in the ontogeny of immunity and how infectious agents may affect the developing immune systems, the three languages of our immunologic Rosetta stones* actually began to be deciphered around the time that HIV-1 was acquired by humans in the early 1950s.94, 139 Thus, immunological competence of the fetus and newborn was first unraveled when it was pointed out that newborns are not “immunologically null” because plasma cells, the producers of antibodies, could be found in stillbirths with congenital syphilis. The discovery of the X-linked agammaglobulinemia opened the door to the study of other genetic immunodeficiencies,112 which led to the differentiation of the humoral and cellular immune systems and furthered our knowledge of the ontogeny and phylogeny of immunity. Some of these primary immunodeficiencies have provided models for several of the immune disturbances induced by HIV. A third Rosetta stone was decoded by studies of in utero and intrapartum infections, such as by toxoplasma and rubella, cytomegalo- and herpes simplex viruses, and their impact on the developing immune systems of the fetus and newborn, serving also as models for HIV.89 In this article, we discuss information obtained from these different immunologic fields as they relate to HIV infection in the fetus and newborn. Focus is placed on newer understanding of thymic–viral interactions and related aspects.