title: Phenotype of intramyocardial leukocytic infiltrates in acquired immunodeficiency syndrome (AIDS): a postmortem immunohistochemical study in 34 consecutive cases.
abstract: In 34 hearts, obtained at autopsy in consecutive AIDS cases, leukocytic phenotype and presence of viral antigens were investigated in paraffin-embedded (34 cases) and frozen myocardial sections (10 cases) by different monoclonal antibodies. The total frequency of focal lymphocytic infiltrates with and without myocell necrosis was 26.4 and 32.3%, respectively. In six control cases (HIV-negative i.v. drug abusers dying from acute fulminating hepatitis), these infiltrates were absent. In AIDS patients, the number of infiltrative foci per section, their wall distribution (subendocardial, middle layer, subepicardial), number of leukocytes per focus, and cell phenotype (prevalence of CD8+ suppressor/cytotoxic T-lymphocytes with CD4/CD8 ratio of 0.6 +/- 0.09 SE, absence of B-cells and granulocytes) were similar in cases with and without myocell necrosis. Significant differences were not observed between homosexual and i.v. drug abuser patients. In inflammatory foci associated with myocell necrosis CD45+/CD68+ monocytes prevailed, as a possible manifestation of nonspecific reparative process. In addition, in both AIDS patients and HIV-negative drug abusers, a population of CD68+ dendritic monocytes (histiocytes) characterized by a restricted CD45 expression (PanLeu-/9.4+) was found dispersed in the interstitium, with a significant higher frequency in the subendocardial layer. Histologic evidences of myocardial virus infections were not observed. Cytomegalovirus (CMV) antigens, however, were found in frozen sections of five of the six cases with lymphocytic infiltrates, supporting the view that this virus can be one of the possible causes of myocarditis in AIDS. Moreover, in two of these CMV-positive cases, a concomitant expression of HIV1 antigens in isolated intramyocardial leukocytes was also observed.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Institute of Biomedical Science, Medical School, University of Milan, Italy.
authors.forename: C
authors.initials: C
authors.lastname: Parravicini
authors.forename: G
authors.initials: G
authors.lastname: Baroldi
authors.forename: G
authors.initials: G
authors.lastname: Gaiera
authors.forename: A
authors.initials: A
authors.lastname: Lazzarin
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000150:complications / Q000276:immunology / Q000473:pathology*; D000328:Adult; D000911:Antibodies, Monoclonal; D015703:Antigens, CD / Q000032:analysis; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D000956:Antigens, Viral / Q000032:analysis; D001344:Autopsy; D015704:CD4 Antigens / Q000032:analysis; D016827:CD8 Antigens / Q000032:analysis; D002452:Cell Count; D002465:Cell Movement; D016616:Cryoultramicrotomy; D003587:Cytomegalovirus / Q000276:immunology; D005260:Female; D006678:HIV / Q000276:immunology; D006649:Histocompatibility Antigens / Q000032:analysis; D006801:Humans; D007150:Immunohistochemistry; D017493:Leukocyte Common Antigens; D007962:Leukocytes / Q000737:chemistry / Q000276:immunology / Q000473:pathology*; D008297:Male; D009205:Myocarditis / Q000209:etiology / Q000276:immunology / Q000473:pathology; D009206:Myocardium / Q000737:chemistry / Q000473:pathology*; D010232:Paraffin; D010641:Phenotype; D000097382:CD68 Molecule
chemical_list: D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D000956:Antigens, Viral; D015704:CD4 Antigens; D016827:CD8 Antigens; D006649:Histocompatibility Antigens; D017493:Leukocyte Common Antigens; D010232:Paraffin; C067980:CD68 antigen, human; D000097382:CD68 Molecule