Viral mimicry of the complement system

Bernet, John; Mullick, Jayati; Singh, Akhilesh K.; Sahu, Arvind

doi:10.1007/bf02970145

Cited by 80 publications

(67 citation statements)

References 135 publications

(83 reference statements)

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“…We refer to this phenomenon as interface mimicry. Mimicry of host components is a general strategy employed by pathogens in their efforts to evade immune system detection and hijack host cellular machinery for their own purposes (21)(22)(23)(24)(25). Given that PPIs are responsible for mediating many cellular events, and given that these interactions depend on specific physical interfaces between proteins, interface mimicry is expected to be a common mechanism by which viruses modulate the biology of their hosts.…”

Section: Resultsmentioning

confidence: 99%

Structural principles within the human-virus protein-protein interaction network

Franzosa

Xia

2011

Proc. Natl. Acad. Sci. U.S.A.

119

144

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General properties of the antagonistic biomolecular interactions between viruses and their hosts (exogenous interactions) remain poorly understood, and may differ significantly from known principles governing the cooperative interactions within the host (endogenous interactions). Systems biology approaches have been applied to study the combined interaction networks of virus and human proteins, but such efforts have so far revealed only low-resolution patterns of host-virus interaction. Here, we layer curated and predicted 3D structural models of human-virus and human-human protein complexes on top of traditional interaction networks to reconstruct the human-virus structural interaction network. This approach reveals atomic resolution, mechanistic patterns of hostvirus interaction, and facilitates systematic comparison with the host's endogenous interactions. We find that exogenous interfaces tend to overlap with and mimic endogenous interfaces, thereby competing with endogenous binding partners. The endogenous interfaces mimicked by viral proteins tend to participate in multiple endogenous interactions which are transient and regulatory in nature. While interface overlap in the endogenous network results largely from gene duplication followed by divergent evolution, viral proteins frequently achieve interface mimicry without any sequence or structural similarity to an endogenous binding partner. Finally, while endogenous interfaces tend to evolve more slowly than the rest of the protein surface, exogenous interfaces-including many sites of endogenous-exogenous overlap-tend to evolve faster, consistent with an evolutionary "arms race" between host and pathogen. These significant biophysical, functional, and evolutionary differences between host-pathogen and within-host protein-protein interactions highlight the distinct consequences of antagonism versus cooperation in biological networks. structural bioinformatics | structural systems biology | virus-host interaction I n host-virus protein-protein interactions (PPIs), components from the viral system invade and modulate the biological networks of the host in a highly antagonistic manner. As a result of this competitive relationship, the organizational, functional, and evolutionary principles of the host-virus PPI network are expected to differ from the better-understood principles governing the cooperative PPI network naturally occurring within the host. However, the evolved strategies by which viral pathogens evade the surveillance of the host immune system and hijack host cellular machinery for their own replication are not completely understood.Traditional pathogen research studies host-virus PPIs in a oneat-a-time fashion. Recently, systems biology approaches have been applied to immunology (1) and pathogen research (2). Significant progress has been made in genome-wide mapping of host-pathogen PPIs for selected pathogens (3-8). This work has been successful in revealing systematic trends in host-pathogen interaction networks, e.g., that viruses tend to targ...

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Section: Resultsmentioning

confidence: 99%

Structural principles within the human-virus protein-protein interaction network

Franzosa

Xia

2011

Proc. Natl. Acad. Sci. U.S.A.

119

144

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“…The high vaccination doses had no visible adverse effects on health status of either both breeds. During the first week post vaccination, viral antigens may have stimulated haemolytic complement activity as a result of the CPW in virus neutralization by proposed mechanisms earlier, such as (1) deposition of complement proteins to the virus, blocking virus attachment and entry; (2) aggregation of virion-lectin complexes, causing increased phagocytosis of C3b-coated viral particles and destruction by macrophages; (3) activation of the entire complement pathway, resulting in lysis of the virus; or (4) generation of inflammatory and specific immune responses (Cooper and Nemerow, 1984;Friedman et al, 2000;Bernet et al, 2003). Complement and antibodies are important mechanisms in combating viral infections, but whether they operate alone or in concerted action depends on the type of virus (Friedman et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Reciprocal Antibody and Complement Responses of Two Chicken Breeds to Vaccine Strains of Newcastle Disease Virus, Infectious Bursal Disease Virus and Infectious Bronchitis Virus

et al. 2006

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“…However, to regulate host immune responses and succeed as pathogens, viruses have developed mechanisms to limit complement function(s) towards immune evasion strategies. Important examples of viruses which regulate host complement system are poxviruses, herpes viruses, retroviruses, paramyxoviruses and picornaviruses [13]. It has been reported that expression of C-reactive protein (CRP), which is known to be required for complement activation, found to be increased during HIV-1 disease progression [112].…”

Section: Complement Proteins During Viral Infectionmentioning

confidence: 99%

Immune Regulation and Evasion of Mammalian Host Cell Immunity During Viral Infection

et al. 2013

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The mammalian host immune system has wide array of defence mechanisms against viral infections. Depending on host immunity and the extent of viral persistence, either the host immune cells might clear/restrict the viral load and disease progression or the virus might evade host immunity by down regulating host immune effector response(s). Viral antigen processing and presentation in the host cells through major histocompatibility complex (MHC) elicit subsequent anti-viral effector T cell response(s). However, modulation of such response(s) might generate one of the important viral immune evasion strategies. Viral peptides are mostly generated by proteolytic cleavage in the cytosol of the infected host cells. CD8 ? T lymphocytes play critical role in the detection of viral infection by recognizing these peptides displayed at the plasma membrane by MHC-I molecules. The present review summarises the current knowledge on the regulation of mammalian host innate and adaptive immune components, which are operative in defence mechanisms against viral infections and the variety of strategies that viruses have evolved to escape host cell immunity. The understanding of viral immune evasion strategies is important for designing anti-viral immunotherapies.

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Viral mimicry of the complement system

Cited by 80 publications

References 135 publications

Structural principles within the human-virus protein-protein interaction network

Structural principles within the human-virus protein-protein interaction network

Reciprocal Antibody and Complement Responses of Two Chicken Breeds to Vaccine Strains of Newcastle Disease Virus, Infectious Bursal Disease Virus and Infectious Bronchitis Virus

Immune Regulation and Evasion of Mammalian Host Cell Immunity During Viral Infection

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