Scanning and transmission electron microscopic studies of complement-mediated lysis and antibody-dependent cell-mediated cytolysis of herpes simplex virus-infected human fibroblasts.
The morphologic aspects of complement-mediated and antibody-dependent cell-mediated cytolysis (ADCC) of human fibroblasts (HuFs) infected by herpes simplex virus (HSV) is described. Human antiviral antibody (antiHSV) was shown by transmission and scanning electron microscopy ( TEM and SEM) to cause the deposition of an amorphous material over the surface of infected cells and virus particles. Associated with antiHSV treatment, the HuFs underwent endocytosis, with the appearance of pinocytotic vesicles immediately beneath the plasma membrane. The addition of complement resulted in lysis of the infected HuFs and massive dilatation of the perinuclear cisternae, but the virus particles associated with the cell surface did not appear lysed. Instead, an additional deposit was noted on the enveloped particles after the addition of complement (C). Human peripheral blood mononuclear leukocytes (MNLs) also lysed the antibody-coated, infected HuFs. Lymphocytes formed broad-based areas of attachment to the antiHSV-treated cells. Beneath these areas of contact occurred focal cytoplasmic changes that preceded cell lysis. Monocytes showed multiple points of binding and sent cytoplasmic projections over the surface of the infected HuFs. Virus particles and segments of target cell cytoplasm were gathered into vacuoles of the monocyte. In accord with the above morphologic findings, the relative roles that antibody, C, and leukocytes may play in human viral diseases is discussed.[1]References
- Scanning and transmission electron microscopic studies of complement-mediated lysis and antibody-dependent cell-mediated cytolysis of herpes simplex virus-infected human fibroblasts. Daniels, C.A., Bodner, S., Trofatter, K.F. Am. J. Pathol. (1980) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
