Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Early events of HIV infection of the CNS are not yet clear. HIV infection in most recent cases, generally shows a prolonged interval between diagnosis and death. HIV infection, months to years before the patient's death, may or may not result in early neurologic symptoms. AIDS patients with spinal cord symptoms often show a sudden onset of long tract signs and a temporally related altered mental status indicating the appearance of both myelitis and encephalitis. Immunohistochemical localization of the HIV cell-surface receptor protein, CD4, and of HIV antigens in cerebral and lymph node venular endothelial cells suggests that a natural occurrence or induction of CD4 protein in some endothelial cells allows transmission of HIV from circulating infected white blood cells preferentially to certain tissues through endothelial cell infection. HIV immunolocalization is present in perivascular astrocytes, particularly in long white matter tracts, and on the surface of oligodendrocytes. HIV immunoreactivity is mostly in macrophages and multinucleated cells in a typical autopsy case, but this may be due to the clearing of HIV antigen from early sites of infection by the hematogenous cells. Not all immunoreactivity for HIV antigens is necessarily due to HIV gene products. Cross reacting epitopes, such as that of HIV envelope glycoprotein gp120 and neuroleukin, may be "seen" not only by antibodies on tissue sections, but by an AIDS patient's immune system, thus targeting a CNS antigen for immune-complex formation. Evidence for hypersensitivity disease in the CNS in AIDS includes the frequent findings of demyelination, perivenous chronic inflammation, chronic vasculitis, and perivenous hemorrhages. The white matter demyelination so frequently reported in all areas of the CNS in AIDS could be the result of a combination of factors that include direct HIV vasculitis, opportunistic infections, and hypersensitivity responses. The blood-brain barrier is breached when immune-related antigens interact on CNS vascular endothelial cells. Perhaps the CD4 antigen, which responds to interaction with antigen-presenting cells and enhances cellular immune activity, is induced or increased in the CNS in association with immune activity and in the presence of a leaky blood-brain barrier. Therefore, with or without HIV in the CNS, hypersensitivity disease, including demyelination, may be the result of long-standing activity of the immune system in AIDS patients.
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PMID:Immunohistochemistry of human immunodeficiency virus in the central nervous system and an hypothesis concerning the pathogenesis of AIDS meningoencephalomyelitis. 249 Dec 41

The use of monospecific antisera for the analysis by radioimmunoassay and immunofluorescence study of two major viral proteins, gp69/71 and p30 of murine leukemia virus, that could be of significance in the pathogenesis of immune complex glomerulonephritis of mice, particularly NZB and B/WF(1) hybrid mice, yielded the following conclusions. A remarkably high concentration of viral envelope glycoprotein, gp69/71, was detected in the spleen and serum of New Zealand mice (NZB, NZW, B/WF(1), and W/BF(1)); the concentration in the spleen was 10-fold greater than that found in AKR mice and 30-fold greater than that present in C57BL/6 mice. The gp69/71 was deposited along with bound immunoglobulins, apparently as an immune complex, in the diseased kidneys of mice, and the glomerular site and extent of deposition of gp69/71 was related to the severity of the glomerulonephritis. This study suggests that the pathogenesis of immune complex glomerulonephritis (and vasculitis) in mice is related to the expression of this specific viral envelope glycoprotein and to the host immune response to this protein.
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PMID:The viral envelope glycoprotein of murine leukemia virus and the pathogenesis of immune complex glomerulonephritis of New Zealand mice. 427 68

Herpes simplex (HSV) and varicella-zoster (VZV) skin infections share so many histological similarities that distinguishing between them may prove to be impossible. We developed and characterized a new monoclonal antibody, VL8, IgG kappa isotype, directed to the VZV envelope glycoprotein gpI. Immunohistochemistry with VL8 appeared highly sensitive and specific on formalin-fixed paraffin-embedded biopsies and a clear-cut distinction between HSV and VZV infections was possible. The pattern of VL8 immunolabelling in VZV infections was strikingly different from that found in HSV infections studied with polyclonal antibodies to HSV I and II. Double immunolabelling revealed the VL8 positivity of sebaceous cells, endothelial cells, Mac 387- and CD68-positive monocyte-macrophages, and factor XIIIa-positive perivascular, perineural and interstitial dendrocytes. Intracytoplasmic VL8 labelling of endothelial cells and perivascular dendrocytes was found at the site of leukocytoclastic vasculitis.
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PMID:Comparative immunohistochemical study of herpes simplex and varicella-zoster infections. 838 79