By H. Friedman
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It is possible that the critical step in HIV-1 neuroinvasion is the presence of HIV-1 receptors on brain endothelia. The role of host factors is also critical in the invasion of the meninges by pathogenic bacteria, such as E. coli. coli invasion into the CNS may occur via ligand-receptor interactions (1, 2). HIV-1 is circulating in the blood as cell-free and cell-associated virus. Since HIV-1 penetrates into the cerebrospinal fluid early after the primary infection during the asymptomatic phase, when the plasma contains a high concentration of cell-free virus, the cell-free virus may be an important source of the CNS infection.
Third, the induction of chemokines and pro-inflammatory cytokines could facilitate mononuclear cell transmigration into the CNS. Fourth, the damage to the barrier function would allow direct entry of the virus into the brain. CONCLUSIONS HIV-1 binding to receptors on brain endothelia, possibly CCR3 and CXCR4, may initiate a cascade of effects that culminate in increased transcellular penetration of the BBB by the virus and invasion of the CNS. Cocaine may open the paracellular route across the BBB and modulate the immune system to increase HIV-1 neuroinvasion.
1993. Influence of social isolation, gender, strain, and prior novelty on plus-maze behaviour in mice. Physiol and Behav. 54(4):729-36 22 Barondes SH, Cohen HD. 1968. Delayed and sustained effect of acetoxycycloheximide in mice. Proc Nat Acad Sci USA. 58:157-164 23 Barondes SH, Cohen HD. 1968. Memory impairment after subcutaneous injection of acetoxycycloheximide. Science. 160:556-7 24 Cohen HD, Barondes. 1968. Effect of acetoxycycloheximide on learning and memory of a light-dark discrimination.
Neuroimmune Circuits, Drugs of Abuse and Infectious Diseases by H. Friedman