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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0009498,
umls-concept:C0020094,
umls-concept:C0023493,
umls-concept:C0024299,
umls-concept:C0033684,
umls-concept:C0042760,
umls-concept:C0042776,
umls-concept:C0054966,
umls-concept:C0108793,
umls-concept:C0205725,
umls-concept:C0332307,
umls-concept:C0445356,
umls-concept:C1167395,
umls-concept:C2587213
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pubmed:issue |
9
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pubmed:dateCreated |
1995-12-14
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pubmed:abstractText |
The current study was undertaken to determine whether the human T cell leukemia/lymphoma oncovirus type I (HTLV-I) and the herpesvirus human cytomegalovirus (HCM) incorporate host cell-derived C regulatory proteins. Our experiments showed that both CD59 and CD55 were associated with the external membrane of HTLV-I derived from MT2 cells, since virus could be captured by mAbs to these proteins, and antisera to CD55 and CD59 induced C-mediated lysis of HTLV-I virions. Additionally, both CD55 and CD59 were detected by immunoblot analysis of purified HTLV-I. Purified HCMV produced in human foreskin fibroblasts (HFF) also contained both CD55 and CD59, as detected by immunoblot analysis. However, treatment with anti-CD55, but not anti-CD59, reduced the HCMV infectious titer in the presence of C. Additional studies determined whether HTLV-I-associated CD55 and CD59 participated in the resistance of the virus to C-mediated lysis. Treatment of virus with phosphatidylinositol-specific phospholipase C (PI-PLC), which removes glycosylphosphatidylinositol-anchored CD55 and CD59, increased the sensitivity of HTLV-I to C-mediated destruction in the presence of anti-HTLV-I Abs. Reconstitution of PI-PLC-treated virus with purified CD55 and CD59 restored resistance to C. These experiments show that HTLV-I and HCMV acquire C control proteins from host cells. Together with our previous experiments showing that both CD55 and CD59 are present on HIV-1, these studies demonstrate a mechanism by which a variety of enveloped viruses may acquire resistance to C-mediated destruction.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
155
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4376-81
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:7594597-Antigens, CD55,
pubmed-meshheading:7594597-Antigens, CD59,
pubmed-meshheading:7594597-Cell Line,
pubmed-meshheading:7594597-Complement Inactivator Proteins,
pubmed-meshheading:7594597-Cytomegalovirus,
pubmed-meshheading:7594597-Human T-lymphotropic virus 1,
pubmed-meshheading:7594597-Humans,
pubmed-meshheading:7594597-Viral Envelope Proteins,
pubmed-meshheading:7594597-Virion
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pubmed:year |
1995
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pubmed:articleTitle |
Host cell-derived complement control proteins CD55 and CD59 are incorporated into the virions of two unrelated enveloped viruses. Human T cell leukemia/lymphoma virus type I (HTLV-I) and human cytomegalovirus (HCMV).
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pubmed:affiliation |
Department of Immunology/Microbiology, Rush Presbyterian-St. Luke's Medical Center, Chicago, IL 60612, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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