Document 0065
 DOCN  M9650065
 TI    Human immunodeficiency virus type 1 infection alters chemokine beta
       peptide expression in human monocytes: implications for recruitment of
       leukocytes into brain and lymph nodes.
 DT    9605
 AU    Schmidtmayerova H; Nottet HS; Nuovo G; Raabe T; Flanagan CR; Dubrovsky
       L; Gendelman HE; Cerami A; Bukrinsky M; Sherry B; Picower Institute for
       Medical Research, Manhasset, NY 11030, USA.
 SO    Proc Natl Acad Sci U S A. 1996 Jan 23;93(2):700-4. Unique Identifier :
       AIDSLINE MED/96149367
 AB    Two chemokine (chemoattractant cytokines) beta peptides, macrophage
       inflammatory proteins 1 alpha and 1 beta (MIP-1 alpha and MIP-1 beta),
       were induced in human monocyte cultures following infection with the
       human immunodeficiency virus type 1 (HIV-1). Induction depended on
       productive viral infection: not only did the kinetics of MIP-1 peptide
       induction closely follow those of viral replication, but monocyte
       cultures inoculated with heat-inactivated virus or infected in the
       presence of AZT failed to produce these chemokine beta peptides. In
       addition, HIV infection markedly altered the pattern of beta chemokine
       expression elicited by tumor necrosis factor (TNF), itself a potent
       proinflammatory cytokine upregulated during the development of AIDS.
       Reverse transcription (RT)-PCR and RT-in situ PCR studies on brain
       tissue from patients with AIDS dementia demonstrated elevated MIP-1
       alpha and MIP-1 beta mRNA expression relative to comparable samples from
       HIV-1-infected patients without dementia. Cells expressing chemokines in
       HIV-1-infected brains were identified morphologically as microglia and
       astrocytes. As MIP-1 alpha and MIP-1 beta are potent chemoattractants
       for both monocytes and specific subpopulations of lymphocytes, this
       dysregulation of beta chemokine expression may influence the trafficking
       of leukocytes during HIV infection. These data, taken together, suggest
       a mechanism by which HIV-1-infected monocytes might recruit uninfected T
       cells and monocytes to sites of active viral replication or
       inflammation, notably the brain and lymph nodes.
 DE    AIDS Dementia Complex/METABOLISM  Base Sequence
       Brain/CYTOLOGY/METABOLISM  Chemotaxis, Leukocyte  Comparative Study
       Human  HIV Infections/*METABOLISM  HIV-1/*GROWTH & DEVELOPMENT  Lymph
       Nodes/CYTOLOGY/METABOLISM  Molecular Sequence Data  Monocytes/DRUG
       EFFECTS/*METABOLISM/VIROLOGY  Monokines/*BIOSYNTHESIS/GENETICS  RNA,
       Messenger/ANALYSIS  Support, Non-U.S. Gov't  Support, U.S. Gov't, P.H.S.
       Tumor Necrosis Factor/PHARMACOLOGY  *Up-Regulation (Physiology)  JOURNAL
       ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).