Antibody mediated complement dependent lysis of virus infected cells

Oldstone, Michael B. A.; Lampert, Peter W.

doi:10.1007/bf00198720

Cited by 27 publications

(17 citation statements)

References 39 publications

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“…Complement activation occurs in the presence of Ab, or for some viruses complement activation can be independent of Ab, leading to neutralization of cellfree virus and lysis of virus-infected cells (1,2). Complement activation by cell-free virus facilitates binding to phagocytic cells (3), whereas complement activation by infected cells promotes leukocyte attachment and cytotoxicity (4,5).…”

mentioning

confidence: 99%

Novel Mechanism of Antibody-Independent Complement Neutralization of Herpes Simplex Virus Type 1

Friedman¹,

Wang²,

Pangburn

et al. 2000

The Journal of Immunology

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The envelope surface glycoprotein C (gC) of HSV-1 interferes with the complement cascade by binding C3 and activation products C3b, iC3b, and C3c, and by blocking the interaction of C5 and properdin with C3b. Wild-type HSV-1 is resistant to Ab-independent complement neutralization; however, HSV-1 mutant virus lacking gC is highly susceptible to complement resulting in ≥100-fold reduction in virus titer. We evaluated the mechanisms by which complement inhibits HSV-1 gC null virus to better understand how gC protects against complement-mediated neutralization. C8-depleted serum prepared from an HSV-1 and -2 Ab-negative donor neutralized gC null virus comparable to complement-intact serum, indicating that C8 and terminal lytic activity are not required. In contrast, C5-depleted serum from the same donor failed to neutralize gC null virus, supporting a requirement for C5. EDTA-treated serum did not neutralize gC null virus, indicating that complement activation is required. Factor D-depleted and C6-depleted sera neutralized virus, suggesting that the alternative complement pathway and complement components beyond C5 are not required. Complement did not aggregate virus or block attachment to cells. However, complement inhibited infection before early viral gene expression, indicating that complement affects one or more of the following steps in virus replication: virus entry, uncoating, DNA transport to the nucleus, or immediate early gene expression. Therefore, in the absence of gC, HSV-1 is readily inhibited by complement by a C5-dependent mechanism that does not require viral lysis, aggregation, or blocking virus attachment.

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mentioning

confidence: 99%

Novel Mechanism of Antibody-Independent Complement Neutralization of Herpes Simplex Virus Type 1

Friedman¹,

Wang²,

Pangburn

et al. 2000

The Journal of Immunology

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“…A chapter on the immunosurveillance of virus infected cells is i~resented elsewhere in this volume [42].…”

Section: Ill Structural Features Of Virusesmentioning

confidence: 99%

Antibody and complement-dependent viral neutralization

Cooper

Welsh

1979

Springer Semin Immunopathol

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“…Antiviral antibody-mediated complement-dependent lysis (ACDL) of virusinfected cells has been described for RNA animal viruses such as arenaviruses, coronaviruses, enteroviruses, orthomyxoviruses, paramyxoviruses, retroviruses, rhabdoviruses, rhinoviruses, togaviruses, and DNA animal viruses such as HSV, papovaviruses, and poxviruses (reviewed by Oldstone and Lampert, 1979;. Many of these studies employed virusinfected cells, antiviral antibody, and complement, each of which was obtained from different animal sources.…”

Section: Antiviral Antibody-mediated Complement-dependent Lysismentioning

confidence: 99%

Immunopathology

1983

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Antibody mediated complement dependent lysis of virus infected cells

Cited by 27 publications

References 39 publications

Novel Mechanism of Antibody-Independent Complement Neutralization of Herpes Simplex Virus Type 1

Novel Mechanism of Antibody-Independent Complement Neutralization of Herpes Simplex Virus Type 1

Antibody and complement-dependent viral neutralization

Immunopathology

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