Virus complement evasion strategies

Favoreel, Herman; Walle, Gerlinde R. Van de; Nauwynck, Hans; Pensaert, Maurice

doi:10.1099/vir.0.18709-0

Cited by 99 publications

(68 citation statements)

References 109 publications

(67 reference statements)

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“…Alphaherpesviruses, like other herpesviruses, are able to interfere with the host's innate and adaptative immune responses. A growing list of immune evasion mechanisms is described [139], such as, for example, inhibition of TAP proteins [66] or Fc receptor activity of viral glycoproteins [43].…”

Section: Pathogenesis and Clinical Signsmentioning

confidence: 99%

Ruminant alphaherpesviruses related to bovine herpesvirus 1

et al. 2006

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-Herpesviruses have mainly co-evolved with their hosts for millions of years. Consequently, different related host species may have been infected by various genetically related herpesviruses. Illustrating this concept, several ruminant alphaherpesviruses have been shown to form a cluster of viruses closely related to bovine herpesvirus 1 (BoHV-1): namely bovine herpesvirus 5, bubaline herpesvirus 1, caprine herpesvirus 1, cervid herpesviruses 1 and 2 and elk herpesvirus 1. These viruses share common antigenic properties and the serological relationships between them can be considered as a threat to BoHV-1 eradication programmes. BoHV-1 is a herpesvirus responsible for infectious bovine rhinotracheitis, which is a disease of major economic concern. In this article, the genetic properties of these ruminant alphaherpesviruses are reviewed on a comparative basis and the issue of interspecific recombination is assessed. The pathogenesis of these infections is described with emphasis on the host range and crossing of the host species barrier. Indeed, the non bovine ruminant species susceptible to these ruminant alphaherpesviruses may be potential BoHV-1 reservoirs. The differential diagnosis of these related infections is also discussed. In addition, available epidemiological data are used to assess the potential of cross-infection in ruminant populations. A better knowledge of these ruminant alphaherpesvirus infections is essential to successfully control infectious bovine rhinotracheitis.

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Section: Pathogenesis and Clinical Signsmentioning

confidence: 99%

Ruminant alphaherpesviruses related to bovine herpesvirus 1

et al. 2006

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“…Although gC2 has a tenfold stronger affinity for C3b 44 , only gC1 can also inhibit the interaction of C3b with C5 and properdin 45 . Other glycoproteins of the herpes virus family have Fc-receptor properties and can deplete antibody recognition and the activation of the classical pathway 43,46 . Iginactivating proteins have also been identified in bacteria, such as S. aureus and group G streptococci 35 .…”

Section: Direct Interventions -Microbial Complement Inhibitorsmentioning

confidence: 99%

Complement evasion by human pathogens

2008

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The human immune system has developed an elaborate network of cascades for dealing with microbial intruders. Owing to its ability to rapidly recognize and eliminate microorganisms, the complement system is an essential and efficient component of this machinery. However, many pathogenic organisms have found ways to escape the attack of complement through a range of different mechanisms. Recent discoveries in this field have provided important insights into these processes on a molecular level. These vital developments could augment our knowledge of the pathology and treatment of infectious and inflammatory diseases.Evading the manifold attacks of the immune system is a key determinant for the survival of pathogens within their hosts. It is not surprising, therefore, that the coexistence and coevolution of humans and microorganisms has produced a multitude of microbial mechanisms for attenuating or escaping these attacks. As a first line of defence against pathogenic intruders, and a mediator between the innate and adaptive immune responses, the complement system is a particular focus of these evasion strategies. Although this carefully regulated cascade of enzymes, protein complexes and receptors ensures the rapid recognition and elimination of foreign structures, it also offers many sites of interference that can disrupt this balanced network of protein interactions. A detailed understanding of the individual processes and the underlying interactions on a molecular level is essential for describing the mechanisms of infectious diseases and the development of new therapies. Recent discoveries of complement-targeting proteins, the availability of complete microbial genome sequences and advances in experimental methods have propelled this area of research, and provide fascinating insights into complement attack and evasion. Many pathogens seem to have developed parallel routes for escaping complement, and several evasion principles are shared not only among members of the same genus but even among diverse organisms, such as bacteria, viruses, fungi and parasites.In this Review, we will provide a comprehensive over-view and update of the exciting recent developments in this field. After a short introduction that will discuss the diverse role of the complement system in defence, disease and infection, the emphasis will be on the functional and structural aspects of the evasion strategies of human pathogens. Rather than separating them by organism, we classify distinct and common mechanisms for all pathogens based on their mode of action. In light of recent findings, the unique evasion strategies of Staphylococcus

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“…Reactions were removed from the 37°C waterbath at specified time points (2,4,8,16, and 32 min for C3a and 32 min only for C5a), spun at 12,000 ϫ g for 10 s, and supernatants were removed for subsequent analysis by immunoblotting (C3a) or ELISA (C5a).…”

Section: Detection Of C3a and C5a Productionmentioning

confidence: 99%

Complement Inhibitor of C5 Activation from the Soft Tick Ornithodoros moubata

Nunn

Sharma

Paesen

et al. 2005

The Journal of Immunology

206

186

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Blood-feeding ticks must control C activation or be damaged by the host inflammatory response. We report the characterization and expression of a novel, relatively small, broad-acting C inhibitory protein (termed OmCI) from the soft tick Ornithodoros moubata. The native 17-kDa nonglycosylated protein inhibits both human and guinea pig classical and alternative C activation pathways. The IC50 values for each pathway were 12 and 27 nM, respectively, in hemolytic assays using human serum diluted 40-fold. The cDNA encodes a protein of 168 aa, including an 18-aa secretion signal sequence that is absent in the mature form. The inhibitor has 46% amino acid identity with moubatin, a platelet aggregation inhibitor also from O. moubata that is an outlying member of the lipocalin family. Native OmCI had no inhibitory effect on the addition of C8 and C9 to preformed C5b-C7 and C5b-C8 to form the membrane attack complex and no effect on the rate of C3a production by the C3 convertase enzymes C4bC2a, C3(H2O)Bb, or C3bBb. Both recombinant and native OmCI abolish production of C5a by human classical (C4bC3bC2a) and alternative (C3bC3bBb) C5 convertases. Addition of excess C5 but not C3 competes away the inhibitory activity of OmCI, indicating that OmCI targets C5 itself rather than inhibiting the C5 convertase C4bC3bC2a itself. Direct binding of OmCI to C5 was demonstrated by Western blotting and gel filtration chromatography using 125I-labeled proteins. OmCI is the first lipocalin family member shown to inhibit C and also the first natural inhibitor that specifically targets the C5 activation step.

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Virus complement evasion strategies

Cited by 99 publications

References 109 publications

Ruminant alphaherpesviruses related to bovine herpesvirus 1

Ruminant alphaherpesviruses related to bovine herpesvirus 1

Complement evasion by human pathogens

Complement Inhibitor of C5 Activation from the Soft Tick Ornithodoros moubata

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