Complement activation by respiratory syncytial virus-infected cells

Edwards, Kathryn M.; Snyder, Paula N.; Wright, Peter F.

doi:10.1007/bf01310889

Cited by 21 publications

(8 citation statements)

References 12 publications

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“…One would predict that the effect of C 0 in vivo would be influenced by the low C 0 levels at the site of RSV replication in the respiratory tract epithelium and the fact that IgA, the dominant antibody at that site, does not fix C 0 . However, C 0 deposition has been seen on epithelial cells in the respiratory tract [Kaul et al, 1982] and in RSV infected cells in tissue culture [Edwards et al, 1986;Kimman et al, 1989a]. Polack has suggested that antigen-antibody complexes and subsequent C 0 fixation may be a critical component in the enhanced illness seen on RSV exposure after administration of formalin-inactivated RSV vaccine [Polack et al, 2002].…”

Section: Discussionmentioning

confidence: 98%

Role of complement in neutralization of respiratory syncytial virus

Yoder

Zhu

Ikizler

et al. 2004

Journal of Medical Virology

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Serum neutralizing antibody titers to respiratory syncytial virus (RSV) are higher when assayed with guinea pig complement. A number of different mechanisms have been suggested for enhancement of neutralization by complement. The most straightforward is that complement-antibody complexes present a greater steric hindrance to viral entry than with antibody alone. To define the implications of measuring serum neutralizing antibody with and without complement, sera from adults, young children, infants, and cord bloods were run in plaque neutralization assays with representative viruses of the RSV A and B subgroups. Although titers of neutralizing antibody were higher in the presence of complement, the addition of complement did not increase the ability to detect antibody rises after natural infection. Some of the complement effect may be attributable to an inhibition of RSV replication by complement alone. While these observations do not address the role for complement in the pathogenesis of RSV infection, they suggest that neutralization assays performed without complement may be most reflective of physiologic conditions in the respiratory tract.

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Section: Discussionmentioning

confidence: 98%

Role of complement in neutralization of respiratory syncytial virus

Yoder

Zhu

Ikizler

et al. 2004

Journal of Medical Virology

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“…They include Epstein-Burr virus (McConneU et al, 1978), respiratory syncytial virus (Smith et al, 1981;Kaul et al, 1984;Edwards, K. M. et al, 1986), mumps virus (Hirsch et al, 1986), measles virus (Sissons et al, 1980), Sendal virus (Okada & Okada, 1981), influenza virus (Lambre et al, 1982), oncornaviruses (Bartholomew et al, 1978), feline leukaemia virus (Kobilinsky et al, 1980), and vesicular stomatitis virus and infectious bovine rhinotracheitis virus (Grewal & Babiuk, 1980). However such a phenomenon is not observed with HSV.…”

Section: Discussionmentioning

confidence: 99%

Glycoprotein C of herpes simplex virus type 1 is essential for the virus to evade antibody-independent complement-mediated virus inactivation and lysis of virus-infected cells

Hidaka

Sakai

Toh

et al. 1991

Journal of General Virology

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Glycoprotein C (gC) of herpes simplex virus type 1 (HSV-1) is a receptor for the complement component C3b. We have previously isolated HSV-1 gC-strains (TN1, TN2 and TN3) from a patient with recurrent keratitis at three different times. These are very rare isolates because gC was thought to be essential for the virus in vivo. To determine whether gC modifies the interaction of complement with cell-free virus or virusinfected cells, we constructed gC + recombinant viruses in which the intact gC gene of strain KOS was inserted into the TN 1 virus genome. TN 1 virus was inactivated by complement and TN1 virus-infected cells were lysed by complement; however, gC ÷ recombinant viruses became resistant to these effects of complement. These results suggest a role for gC in protection of both the virion envelope and the infected cell surface against damage by complement. TN1 virus was inactivated by complement from rats (Wistar, WKA, F344 and SD), guinea-pigs (Hartley) and humans, but not by complement from mice (C3H, DDD and BALB/c), which indicates that mice seem to be inappropriate as an experimental model for the study of HSV infection in which complement factors need to be considered.

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“…An antibody-dependent protection in hRSV infection was later confirmed in complement-deficient mice ( 34 , 35 ). HeLa cells infected with hRSV activated both CP and AP; however, anti-hRSV antibodies were required for cytolysis by complement ( 36 , 37 ). The importance of pulmonary macrophages and the CS in restricting hRSV replication suggests the significance of local complement production in limiting RNA viruses ( 34 ).…”

Section: Complement Activation and Its Effects On Rna Virusesmentioning

confidence: 99%

In the Crosshairs: RNA Viruses OR Complement?

et al. 2020

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Complement, a part of the innate arm of the immune system, is integral to the frontline defense of the host against innumerable pathogens, which includes RNA viruses. Among the major groups of viruses, RNA viruses contribute significantly to the global mortality and morbidity index associated with viral infection. Despite multiple routes of entry adopted by these viruses, facing complement is inevitable. The initial interaction with complement and the nature of this interaction play an important role in determining host resistance versus susceptibility to the viral infection. Many RNA viruses are potent activators of complement, often resulting in virus neutralization. Yet, another facet of virus-induced activation is the exacerbation in pathogenesis contributing to the overall morbidity. The severity in disease and death associated with RNA virus infections shows a tip in the scale favoring viruses. Growing evidence suggest that like their DNA counterparts, RNA viruses have co-evolved to master ingenious strategies to remarkably restrict complement. Modulation of host genes involved in antiviral responses contributed prominently to the adoption of unique strategies to keep complement at bay, which included either down regulation of activation components (C3, C4) or up regulation of complement regulatory proteins. All this hints at a possible “hijacking” of the cross-talk mechanism of the host immune system. Enveloped RNA viruses have a selective advantage of not only modulating the host responses but also recruiting membrane-associated regulators of complement activation (RCAs). This review aims to highlight the significant progress in the understanding of RNA virus–complement interactions.

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Complement activation by respiratory syncytial virus-infected cells

Cited by 21 publications

References 12 publications

Role of complement in neutralization of respiratory syncytial virus

Role of complement in neutralization of respiratory syncytial virus

Glycoprotein C of herpes simplex virus type 1 is essential for the virus to evade antibody-independent complement-mediated virus inactivation and lysis of virus-infected cells

In the Crosshairs: RNA Viruses OR Complement?

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