Author's Response

Brain Pathology, an interesting and well done study on HIV-1 encephalitis was published (Cosenza MA, Zhao M-L, Si Q, Lee SC [2002] Human brain parenchymal microglia express CD14 and CD45 and are productively infected by HIV1 in HIV-1 encephalitis. Brain Pathol 12:442-455). The authors reported activated microglia to be the major target of HIV-1 infection. Microglial cells are considered bone marrowderived cells that populate the CNS parenchyma early in embryonic development. In contrast to perivascular microglia that are constantly replaced by blood-derived monocytes, under adult physiologic conditions, there is little or no repopulation of parenchymal microglia. Activation of microglial cells is considered to be a hallmark of various pathological conditions of the CNS, including infection and inflammation, neurodegenerative disorders, ischemia and trauma. Cosenza and co-workers analyzed differences in microglial subpopulations due to their localization (parenchymal versus perivascular) and mentioned, that no marker would exist to distinguish microglia from monocytes. In fact this is only true for the distinction of activated parenchymal microglia and blood-derived monocytes/macrophages. As described by the authors, microglial CD14 expression in normal human CNS differs depending on localization (resting parenchymal microglia CD14-, perivascular microglia/macrophages CDl4+) and in diseased CNS on the state of activation (resting parenchymal microglia CD14-, activated parenchymal microglia CD14+, perivascular microglia CD14+). The authors claimed that in their study “unlike previous reports” they “report for the first time the expression of CD14 in activated parenchymal microglia.” However, the CD14 expression pattern in normal and in diseased human brain was previously described. Several studies have reported: i) resting parenchymal microglia to lack CD14 in vivo (6, 7) and ii) activated microglia/ macrophages to express CD14 in multiple sclerosis lesions (4, 8), in acute bacterial or viral CNS infections (3, 5) and in HIV-1 encephalitis (6). Cellular sources and time kinetics of CD14 expression was also recently reported by our group following stroke (1), and traumatic brain injury (2).