title: Human immunodeficiency virus type 1 infection alters enzymatic and ultrastructural features of peripheral blood monocytes.
abstract: BACKGROUND
  Human immunodeficiency virus-1 (HIV-1) infected monocytes are now believed to serve as a reservoir for HIV-1 infection, and to play a role in viral rebound phenomena in certain groups of patients who failed or stopped highly active antiretroviral therapy (HAART). Data characterizing the morphological changes of peripheral blood monocytes in HIV-1-infected individuals are limited.
  
  
  METHODS
  In this study, we collected monocytes from 21 asymptomatic HIV-1-infected individuals with CD4 count more than 500 cells/mm(3) and healthy individuals. The monocytes ultrastructural morphologic changes and α-naphthyl butyrate esterase (ANBE) activity were compared between the two groups.
  
  
  RESULTS
  In monocytes from patients infected with HIV-1, activity of α-naphthyl butyrate esterase (ANBE) was markedly increased compared with normal monocytes. In both light microscopic and ultrastructural studies, the cytoplasm of monocytes from HIV-1-infected patients contained a haphazard appearing network of thin fibrils. Cell surface expression of the activation marker HLA-DR molecule was upregulated. There were no discernible differences between the cell surface expression of CD4, CD14, and CD16 molecules comparing normal monocytes to those from HIV-1-infected patients. α-naphthyl butyrate esterase (ANBE) was markedly increased compared with normal monocytes. In both light microscopic and ultrastructural studies, the cytoplasm of monocytes from HIV-1-infected patients contained a haphazard appearing network of thin fibrils. Cell surface expression of the activation marker HLA-DR molecule was upregulated. There were no discernible differences between the cell surface expression of CD4, CD14, and CD16 molecules comparing normal monocytes to those from HIV-1-infected patients.
  
  
  CONCLUSIONS
  Possibly, changes in the activity of ANBE along with a disrupted appearing cytoplasmic fibril network contribute to monocyte dysfunction in HIV-1-infected patients.
authors.affiliation: Department of Pathology, Detroit Medical Center, Wayne State University, 3990 John R, Detroit, MI, 48201, USA.
authors.forename: Ali M
authors.initials: AM
authors.lastname: Gabali
authors.forename: Tarek
authors.initials: T
authors.lastname: Jazaerly
authors.forename: Ronald
authors.initials: R
authors.lastname: Cleveland
authors.forename: Lawrence
authors.initials: L
authors.lastname: Kass
keywords: CD14; CD16; CD4; human immunodeficiency virus-1; monocyte; α-naphthyl butyrate esterase