ArticleJournal of virology2008
Identification of hot spots in the variola virus complement inhibitor (SPICE) for human complement regulation.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 40 citations in OpenAlex.
- Monkeypox virus clade IIb isolate exhibits reduced virulence relative to clade IIa isolates in multiple murine models.Journal of virology · 2026Article
- The grand escape - how pathogens outsmart the human complement system.Immunobiology · 2025Review
- Teaching a new mouse old tricks: Humanized mice as an infection model for Variola virus.PLoS pathogens · 2021Article
- Virus-Encoded Complement Regulators: Current Status.Viruses · 2021Review
- Role of Electrostatic Hotspots in the Selectivity of Complement Control Proteins Toward Human and Bovine Complement Inhibition.Frontiers in molecular biosciences · 2021Article
- Orthopoxvirus K3 orthologs show virus- and host-specific inhibition of the antiviral protein kinase PKR.PLoS pathogens · 2021Article
- Interactions of viruses and the humoral innate immune response.Clinical immunology (Orlando, Fla.) · 2020Review
- T Lymphocytes as Measurable Targets of Protection and Vaccination Against Viral Disorders.International review of cell and molecular biology · 2019Review
- Spatially conserved motifs in complement control protein domains determine functionality in regulators of complement activation-family proteins.Communications biology · 2019Article
- Characterization of genetic predisposition and autoantibody profile in atypical haemolytic-uraemic syndrome.Immunology · 2018Article
- Species Specificity of Vaccinia Virus Complement Control Protein for the Bovine Classical Pathway Is Governed Primarily by Direct Interaction of Its Acidic Residues with Factor I.Journal of virology · 2017Article
- Regulator-dependent mechanisms of C3b processing by factor I allow differentiation of immune responses.Nature structural & molecular biology · 2017Article
- Viral-derived complement inhibitors: current status and potential role in immunomodulation.Experimental biology and medicine (Maywood, N.J.) · 2017Review
- Complement Evasion Strategies of Viruses: An Overview.Frontiers in microbiology · 2017Review
- Regulators of complement activity mediate inhibitory mechanisms through a common C3b-binding mode.The EMBO journal · 2016Article
- Mutational analysis of Kaposica reveals that bridging of MG2 and CUB domains of target protein is crucial for the cofactor activity of RCA proteins.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Complement regulator CD46: genetic variants and disease associations.Human genomics · 2015Review
- The origin of the variola virus.Viruses · 2015Review
- Dissection of functional sites in herpesvirus saimiri complement control protein homolog.Journal of virology · 2013Article
- Disabling complement regulatory activities of vaccinia virus complement control protein reduces vaccinia virus pathogenicity.Vaccine · 2011Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Variola virus, the causative agent of smallpox, encodes a soluble complement regulator named SPICE. Previously, SPICE has been shown to be much more potent in inactivating human complement than the vaccinia virus complement control protein (VCP), although they differ only in 11 amino acid residues. In the present study, we have expressed SPICE, VCP, and mutants of VCP by substituting each or more of the 11 non-variant VCP residues with the corresponding residue of SPICE to identify hot spots that impart functional advantage to SPICE over VCP. Our data indicate that (i) SPICE is approximately 90-fold more potent than VCP in inactivating human C3b, and the residues Y98, Y103, K108 and K120 are predominantly responsible for its enhanced activity; (ii) SPICE is 5.4-fold more potent in inactivating human C4b, and residues Y98, Y103, K108, K120 and L193 mainly dictate this increase; (iii) the classical pathway decay-accelerating activity of activity is only twofold higher than that of VCP, and the 11 mutations in SPICE do not significantly affect this activity; (iv) SPICE possesses significantly greater binding ability to human C3b compared to VCP, although its binding to human C4b is lower than that of VCP; (v) residue N144 is largely responsible for the increased binding of SPICE to human C3b; and (vi) the human specificity of SPICE is dictated primarily by residues Y98, Y103, K108, and K120 since these are enough to formulate VCP as potent as SPICE. Together, these results suggest that principally 4 of the 11 residues that differ between SPICE and VCP partake in its enhanced function against human complement.
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