Species selective interaction of Alphaherpesvirinae with the “unspecific” immune system of the host

Huemer, Hartwig P.; Larcher, Clara; Hurk, Sylvia van Drunen Littel‐van den; Babiuk, Lorne A.

doi:10.1007/bf01309666

Cited by 49 publications

(34 citation statements)

References 35 publications

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“…Here, we also investigated the effect of PRV gE-gI Fc receptor activity on the efficiency of ADCML of PRVinfected monocytes in vitro. A third potential mechanism of complement evasion, gC complement binding, has also been described for several alphaherpesviruses, including HSV and PRV (Friedman et al, 1984;Huemer et al, 1993). For HSV, it has been shown already that gC complement binding is important for evasion of the antibody-independent, alternative complement activation pathway rather than for the antibody-dependent classical pathway (ADCML) (Friedman et al, 1984(Friedman et al, , 1996Lubinski et al, 1999;Friedman et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…Our results therefore suggest that, although complement-mediated lysis of PRVinfected monocytes via the alternative pathway indeed does occur, it seems to be of rather minor importance. Efficient antibody-independent complement-mediated lysis of PRVinfected cells may perhaps be disturbed by binding of viral glycoprotein gC to complement factor C3b (Huemer et al, 1993). Activation of the alternative complement pathway by PRV-infected cells has been described before (Kimman et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

“…This may suggest that, besides the two mechanisms studied in this report, PRV may have other tools at its disposal to avoid efficient ADCML of infected cells. One such mechanism could be PRV gC complement binding (Huemer et al, 1993). The binding of gC to the C3 factor of the complement cascade was first described for HSV (Friedman et al, 1984) and has been shown to be important for immune evasion of HSV in vivo (Lubinski et al, 1999).…”

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confidence: 99%

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Antibody-induced internalization of viral glycoproteins and gE–gI Fc receptor activity protect pseudorabies virus-infected monocytes from efficient complement-mediated lysis

Walle

Favoreel

Nauwynck

et al. 2003

Journal of General Virology

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Pseudorabies virus (PRV)-infected blood monocytes are able to transport virus throughout the body of vaccination-immune pigs. PRV-infected monocytes express viral glycoproteins in their plasma membrane that can be recognized by virus-specific antibodies. Recently, it has been shown that addition of PRV-specific polyclonal immunoglobulins to PRV-infected monocytes at 37˚C induces internalization of the majority of plasma membrane-expressed viral glycoproteins. This study investigated whether this process may interfere with efficient antibody-dependent complementmediated lysis (ADCML) of infected monocytes. Therefore, an ADCML assay was set up in vitro. A significant decrease in the percentage of cells lysed by ADCML was observed when antibody-induced internalization of PRV glycoproteins occurred (P<0?005). Furthermore, it is shown (i) that the PRV gE-gI complex, which, like certain other alphaherpesvirus orthologues, possesses IgG-binding capacity, aids in avoiding efficient ADCML of PRV-infected monocytes and (ii) that the efficiency of PRV gE-gI-mediated evasion of ADCML can be decreased by the presence of gE-gI-specific antibodies. INTRODUCTIONPseudorabies virus (PRV), a member of the subfamily Alphaherpesvirinae, causes Aujeszky's disease in its natural host, the pig. Clinical signs depend on the age of the pig and are characterized by nervous signs in newborn pigs, respiratory disorders in fattening pigs and reproductive failure in sows. Abortion may be an important consequence of PRV infection in pregnant sows (Pensaert & Kluge, 1989). In the presence of a vaccination-induced immunity, PRV may still replicate in the respiratory tract and draining lymph nodes, resulting in a restricted viraemia (Wittmann et al., 1980). The limited replication in immune animals generally does not cause problems. However, abortion may occur as a result of cell-mediated transplacental spread and intrafoetus replication. It has been shown that blood monocytes are essential to transport the virus to the pregnant uterus in vaccination-immune pigs (Nauwynck & Pensaert, 1992, 1995a but little is known on exactly how these infected monocytes survive in the blood of a vaccination-immune animal.PRV-infected monocytes (and PRV-infected cells in general) express viral envelope proteins on their plasma membrane (Favoreel et al., 1999). Antibodies bind to these viral glycoproteins, which should induce antibody-dependent lysis of infected cells (Sissons & Oldstone, 1980). A major component of the antibody-dependent immune system is the complement cascade (reviewed by Sim & Dodds, 1997). Complement components bind to the Fc region of antibodies, which leads to a cascade of events and results finally in lysis of antibody-covered infected cells (antibodydependent complement-mediated cell lysis or ADCML) (reviewed by Müller-Eberhard, 1984).Recently, we described a process of how PRV-infected monocytes may avoid efficient lysis by ADCML. Addition of PRV-specific antibodies to PRV-infected monocytes in vitro results in aggregation of the majority...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Antibody-induced internalization of viral glycoproteins and gE–gI Fc receptor activity protect pseudorabies virus-infected monocytes from efficient complement-mediated lysis

Walle

Favoreel

Nauwynck

et al. 2003

Journal of General Virology

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“…BoHV-1 possesses another evasion strategy to soluble factors of the innate immune response. Conserved in related alphaherpesviruses such as PrV, EHV-1 and HSV-1, this evasion mechanism is mediated by the interaction of gC with the third complement component (C3), the key mediator of complement activation [79]. Another immunomodulatory function conserved in alphaherpesvirus has been identified through the interaction of gG with several chemokines [19,32].…”

Section: Immune Response and Immune Evasion Strategiesmentioning

confidence: 99%

Bovine herpesvirus 1 infection and infectious bovine rhinotracheitis

et al. 2007

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-Bovine herpesvirus 1 (BoHV-1), classified as an alphaherpesvirus, is a major pathogen of cattle. Primary infection is accompanied by various clinical manifestations such as infectious bovine rhinotracheitis, abortion, infectious pustular vulvovaginitis, and systemic infection in neonates. When animals survive, a life-long latent infection is established in nervous sensory ganglia. Several reactivation stimuli can lead to viral re-excretion, which is responsible for the maintenance of BoHV-1 within a cattle herd. This paper focuses on an updated pathogenesis based on a molecular characterization of BoHV-1 and the description of the virus cycle. Special emphasis is accorded to the impact of the latency and reactivation cycle on the epidemiology and the control of BoHV-1. Several European countries have initiated BoHV-1 eradication schemes because of the significant losses incurred by disease and trading restrictions. The vaccines used against BoHV-1 are described in this context where the differentiation of infected from vaccinated animals is of critical importance to achieve BoHV-1 eradication.

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“…One important antibody-independent system, acting without precedent priming with antigen, is the alternative complement pathway, a phylogenetically old system that represents a first barrier against invading microorganisms (Cooper, 1991). Its importance for complex viruses arises from the finding that several members of the Herpesviridae and also the Poxviridae express proteins on the virion and infected cell surface; these proteins are able to interact with proteins of the complement cascade at different levels (Ohmann et al, 1988;Isaacs et al, 1992;Huemer et al, 1992bHuemer et al, , 1993aRother et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Cloning and expression of the complement receptor glycoprotein C from Herpesvirus simiae (herpes B virus): protection from complement-mediated cell lysis

Huemer

Wechselberger

Bennett

et al. 2003

Journal of General Virology

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Simian herpes B virus (SHBV) is the herpes simplex virus (HSV) homologue for the speciesMacaca. Unlike in its natural host, and unlike other animal herpesviruses, SHBV causes high mortality in accidentally infected humans. SHBV-infected cells, like those infected with HSV-1 and equine herpesvirus types 1 and 4, express complement C3 receptor activity. To study immunoregulatory functions involved in susceptibility/resistance against interspecies transmission, the SHBV glycoprotein C (gC SHBV ) gene (encoding 467 aa) was isolated. Sequence analysis revealed amino acid identity with gC proteins from HSV-2 (46?9 %), HSV-1 (44?5 %) and pseudorabies virus (21?2 %). Highly conserved cysteine residues were also noted. Similar to gC HSV-2 , gC SHBV is less glycosylated than gC HSV-1 , resulting in a molecular mass of 65 kDa if expressed in replication-deficient vaccinia virus Ankara. Stable transfectants expressing full-length gC SHBV on the cell surface induced C3 receptor activity and were substantially protected from complement-mediated lysis; no protection was observed with control constructs. This suggests that expression of the gC homologues on infected cell surfaces might also contribute to the survival of infected cells in addition to decreased virion inactivation. Interestingly, soluble gC SHBV isolated from protein-free culture supernatants did not interfere with the binding of the alternative complement pathway activator properdin to C3b, which is similar to our findings with gC HSV-2 and could be attributed to major differences in the amino-terminal portion of the protein with extended deletions in both gC SHBV and gC HSV-2 . Binding of recombinant gC SHBV to polysulphates was observed. This, together with the heparin-sensitivity of the gC SHBV -C3 interaction on the infected cell surface, suggests a role in adherence to heparan sulphate, similar to the gC proteins of other herpesviruses.

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Species selective interaction of Alphaherpesvirinae with the “unspecific” immune system of the host

Cited by 49 publications

References 35 publications

Antibody-induced internalization of viral glycoproteins and gE–gI Fc receptor activity protect pseudorabies virus-infected monocytes from efficient complement-mediated lysis

Antibody-induced internalization of viral glycoproteins and gE–gI Fc receptor activity protect pseudorabies virus-infected monocytes from efficient complement-mediated lysis

Bovine herpesvirus 1 infection and infectious bovine rhinotracheitis

Cloning and expression of the complement receptor glycoprotein C from Herpesvirus simiae (herpes B virus): protection from complement-mediated cell lysis

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