Complement Control Proteins, CD46, CD55, and CD59, as Common Surface Constituents of Human and Simian Immunodeficiency Viruses and Possible Targets for Vaccine Protection

Montefiori, David C.; Cornell, Robert J.; Zhou, Ji; Zhou, Jian‐Liang; Hirsch, Vanessa M.; Johnson, Philip R.

doi:10.1006/viro.1994.1622

Cited by 127 publications

(85 citation statements)

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“…Other studies, however, show that intact HIV activates complement only in the presence of antiviral Abs (25,26). Sensitivity to complement-mediated lysis is influenced by the actual composition of the viral membrane, as in vitro studies demonstrated that some primary isolates of HIV are highly resistant to complement-mediated lysis due to the incorporation of host cell-derived complement control proteins, including CD46, CD55, and CD59 (27,28).…”

Section: Discussionmentioning

confidence: 99%

Cutting Edge: Productive HIV-1 Infection of Dendritic Cells via Complement Receptor Type 3 (CR3, CD11b/CD18)

Bajtay

Speth

Erdei

et al. 2004

The Journal of Immunology

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In the present study, we demonstrate that macrophage-tropic HIV-1 opsonized by complement and limited amounts of anti-HIV-IgG causes up to 10-fold higher productive infection of human monocyte-derived dendritic cells than HIV treated with medium or HIV opsonized by Ab only. Enhanced infection is completely abolished by a mAb specific for the ligand-binding site of CD11b (i.e., α-chain of complement receptor 3, receptor for iC3b), proving the importance of complement receptor 3 in this process. Inhibition of complement activation by EDTA also prevents enhanced infection, further demonstrating the role of complement in virus uptake and productive infection. Since HIV is, even in the absence of Abs, regularly opsonized by complement, most probably the above-described mechanism plays a role during in vivo primary infection.

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Section: Discussionmentioning

confidence: 99%

Cutting Edge: Productive HIV-1 Infection of Dendritic Cells via Complement Receptor Type 3 (CR3, CD11b/CD18)

Bajtay

Speth

Erdei

et al. 2004

The Journal of Immunology

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“…In the rabbit this presents an advantage over a free-virus inoculum since it has been shown that HIV is very susceptible to neutralization by normal rabbit serum (Spear et al, 1991). This may be an anomaly due to the inability of human complement control proteins carried on particles from human cells (Montefiori et al, 1994) to prevent activation of rabbit complement around virions. If virus budding from rabbit cells carries the equivalent rabbit complement control proteins, then free virus particles are likely to be resistant to this form of neutralization.…”

Section: Discussionmentioning

confidence: 99%

Human immunodeficiency virus type 1 infection of human CD4-transgenic rabbits

Dunn

Mehtali

Houdebine³

et al. 1995

Journal of General Virology

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“…This finding is not surprising because it has been reported that HIV particles contain native DAF/CD55, MCP/CD46 and CD59 proteins. [30][31][32][33] The ability to incorporate these proteins in the native conformation represents a critical advance for viral vector technology, since previous use of CRPs to protect MLV and baculovirus vectors required the generation of chimeric molecules with heterologous transmembrane domains for efficient incorporation. 16,28 The formation of the chimeric CRPs was problematic because a number of chimeric forms of the molecules were not incorporated into the viral particles or caused reduced infectivity.…”

Section: Complement-resistant Lentiviral Vectorsmentioning

confidence: 99%

Complement regulatory proteins are incorporated into lentiviral vectors and protect particles against complement inactivation

et al. 2004

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Lentiviral vectors pseudotyped with G glycoprotein from vesicular stomatitis virus (VSV-G) and baculovirus gp64 are inactivated by human complement. The extent of vector inactivation in serum from individual donors was examined and results showed wide donor-dependent variation in complement sensitivity for VSV-G-pseudotyped lentivectors. Amphotropic envelope (Ampho)-pseudotyped vectors were generally resistant to serum from all donors, while gp64-pseudotyped vectors were inactivated but showed less donor-to-donor variation than VSV-G. In animal sera, the vectors were mostly resistant to inactivation by rodent complement, whereas canine complement caused a moderate reduction in titer. In a novel advance for the lentiviral vector system, human complement-resistant-pseudotyped lentivector particles were produced through incorporation of complement regulatory proteins (CRPs). Decay accelerating factor (DAF)/CD55 provided the most effective protection using this method, while membrane cofactor protein (MCP)/ CD46 showed donor-dependent protection and CD59 provided little or no protection against complement inactivation. Unlike previous approaches using CRPs to produce complement-resistant viral vectors, CRP-containing lentivectors particles were generated for this study without engineering the CRP molecules. Thus, through overexpression of native DAF/CD55 in the viral producer cell, an easy method was developed for generation of lentiviral vectors that are almost completely resistant to inactivation by human complement. Production of complement-resistant lentiviral particles is a critical step toward use of these vectors for in vivo gene therapy applications. Gene Therapy (2005) 12, 238-245.

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Complement Control Proteins, CD46, CD55, and CD59, as Common Surface Constituents of Human and Simian Immunodeficiency Viruses and Possible Targets for Vaccine Protection

Cited by 127 publications

References 0 publications

Cutting Edge: Productive HIV-1 Infection of Dendritic Cells via Complement Receptor Type 3 (CR3, CD11b/CD18)

Cutting Edge: Productive HIV-1 Infection of Dendritic Cells via Complement Receptor Type 3 (CR3, CD11b/CD18)

Human immunodeficiency virus type 1 infection of human CD4-transgenic rabbits

Complement regulatory proteins are incorporated into lentiviral vectors and protect particles against complement inactivation

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