Human Immunodeficiency Virus Infection of the CNS: Characterization of 'Neurotropic' Strains

Neurologic abnormalities have been reported in over 50% of patients with the acquired immune deficiency syndrome (AIDS), and in some cases can be the only clinical manifestation of infection with the human immunodeficiency virus (HIV) (Snider et al. 1983; Nielson et al. 1984; Petito et al. 1985; Levy et al. 1985; Navia et al. 1986a, b; de la Monte et al. 1987, Gabuzda and Hirsch 1987; Navia and Price 1987; Elder and Sever 1988; Price et al. 1988; Rosenblum et al. 1988). Substantial evidence suggests that many of the neurologic symptoms, particularly vacuolar myelopathy and progressive dementia, are the direct consequence of HIV infection of the CNS (Epstein et al. 1984–85; Ho et al. 1985a; Lipkin et al. 1985; Anders et al. 1986; Sharer et al. 1986; Cornblath et al. 1987). This apparent capacity of HIV to induce neuropathology is not surprising, since other members of the lentivirus family (for example, visna and caprine arthritis encephalitis virus) are also “neurotropic”. In the case of visna, the virus has been shown to infect cells of the choroid plexus, alveolar macrophages/monocytes, astrocytes, and oligodendrocytes, both in infected animals and in tissue culture (Brahic et al. 1984; Narayan et al. 1985; Gendelman et al. 1986; Hasse 1986). However, the neurotropism of HIV raises important questions as to (a) whether specific “neurotropic” strains of HIV exist, (b) what cells in the brain are infected, and (c) what genetic factors of “neurotropic” HIV impart the ability to infect cells of the CNS.