Antibody and complement-dependent viral neutralization

Cooper, Neil R.; Welsh, Raymond M.

doi:10.1007/bf00198721

Cited by 26 publications

(17 citation statements)

References 63 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our studies suggest a correlation between protection and the serum antibody titres induced by vaccination, but since no other host parameters were measured the importance of the humoral immune response cannot be assessed. Previous studies have shown that humoral IgG antibodies play a role in the mechanism of protection against alphavirus encephalitis (Griffin & Johnson, 1977) but other defence mechanisms are operative as well (McFarland et al, 1972;Hirsch & Griffin, 1979;Hirsch et aL, 1980;Cooper & Welsh, 1979). The defence mechanisms of the host against microbial disease are mediated by a complex interplay of immunological and other factors which have so far been difficult to single out in each specific instance (see Smith et al, 1980).…”

Section: Discussionmentioning

confidence: 99%

Antibody Response to Spike Protein Vaccines Prepared from Semliki Forest Virus

Balcarová

Helenius

Simons

1981

Journal of General Virology

View full text Add to dashboard Cite

SUMMARYSubunit vaccines, containing the spike glycoproteins of Semliki Forest virus (SFV) in three different forms, have been prepared: detergent-solubilized monomers, detergent-and lipid-free octamers, and virosomes in which the spike proteins are reconstituted into phospholipid vesicles. Previous studies have shown that the octamers and the virosomes are very efficient in protecting mice against the encephalitis caused by virulent SFV (Morein et al., 1978). In this study we have characterized the specific antibody responses in mice vaccinated with the three SFV vaccines and correlated them with the protection against SFV encephalitis. The multimeric forms induced high humoral antibody titres; two doses of only 1 /tg protein gave rise to specific antibody titres of 0.6 mg/ml. The monomeric form was much less immunogenic.

show abstract

Section: Discussionmentioning

confidence: 99%

Antibody Response to Spike Protein Vaccines Prepared from Semliki Forest Virus

Balcarová

Helenius

Simons

1981

Journal of General Virology

View full text Add to dashboard Cite

show abstract

“…Complement-mediated functions usually considered to protect against bacterial infection include opsonization, cytolysis, and the generation of chemotactic activity for phagocytes (18). Protective functions relating to the development of inflammatory diseases are less easy to define, but should at least include mechanisms involved in elimination of immune complexes (75,103) and possibly also of certain viruses (17). A function of general interest is the influence of complement on the immune response (45).…”

Section: Mechanisms and Animal Modelsmentioning

confidence: 99%

Inherited complement deficiency states: implications for immunity and immunological disease

Sjöholm

1990

APMIS

View full text Add to dashboard Cite

The study of complement deficiency states and their influence on immune function has generated new insights and still provides a challenge to continued investigation. The association of classical pathway deficiencies (C1, C4, C2 or C3) with immunological diseases such as SLE and glomerulonephritis has contributed to current knowledge concerning complement‐dependent immune complex handling and elimination. Susceptibility to systemic infection with encapsulated bacteria is encountered in most forms of inherited complement deficiency. Recurrent neisserial infection is the only clinical manifestation clearly associated with defects of the mem‐branolytic sequence C5‐C9, while deficiency of properdin, a component of the alternative activation pathway, appears to predispose to nonrecurrent meningococcal disease. Inherited complement deficiency is rare, but the perspective is widened by the more common occurence of acquired defects in immunological diseases, and the apparent requirement for efficient complement recruitment in host defense. Another aspect is the possibility that complement deficiency might alleviate or prevent inflammatory symptoms. Notably, complement deficiency has not been reported in classical rheumatoid arthritis. Considerations of this kind would be refuted or modified by findings of complement deficiency in single patients.

show abstract

“…1). Clear-cut demonstration of immune virolysis was provided by Oroszlan and Gilden (2), who measured the release of radiolabeled RNA from mouse leukemia viruses (retroviruses).…”

mentioning

confidence: 99%

Disassembly of viral membranes by complement independent of channel formation.

Esser¹,

Bartholomew²,

Jensen³

et al. 1979

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

View full text Add to dashboard Cite

We have compared the effects of the complement membrane attack complex (MAC), nystatin, and melittin on the envelope of murine leukemia viruses to determine if channel formation alone is sufficient to cause membranolysis. Nystatin is a channel former and mellitin is not, although both are hemolytic. Whereas MAC and melittin disintegrated the viral membrane, nystatin had no effect on mo hology, integ- (2), who measured the release of radiolabeled RNA from mouse leukemia viruses (retroviruses). Later experiments with retroviruses indicated that human complement alone, without specific antibody, could lyse retroviruses (3-5). The mechanism of lysis of enveloped viruses was assumed to be similar or identical to complement-mediated lysis of mammalian cells, a more extensively studied and better understood reaction.In complement-dependent cytolysis, five complement proteins-C5b, C6, C7, C8, and C9-become physically attached to the outer membrane of a cell. Without further enzymatic modification, these proteins form a multimolecular complex, the membrane attack complex (MAC), that lyses cells by purely physicochemical means (reviewed in ref. 6). Loss of the natural impermeability of the cell membrane to small solutes leads to colloid-osmotic swelling of the cell, rupture, and release of internal proteins. Mayer (7,8) theorized that the MAC forms hydrophilic protein channels; this action is reminiscent of the channel-forming (9) and hemolytic (10) properties of the antibiotics nystatin and amphotericin B.In contrast to Mayer's channel theory, we recently proposed (11, 12) that the MAC is membranolytic not because of channel formation, but because of its strong phospholipid binding capacity, through which it is enabled to reorient the lipid bilayer structure of membranes.Examining our hypothesis, we have compared the effects of nystatin, melittin, and the MAC on the envelope of murine leukemia virus (MuLV) to determine if channel formation alone is sufficient to cause membranolysis. Nystatin is a channel former and melittin is not, although it is membranolytic. Our results show that whereas the MAC and melittin are virolytic, nystatin has no effect on the morphology and infectivity of the virus.MATERIALS AND METHODS Materials. Nystatin, amphotericin B, and melittin were purchased from Sigma. Rauscher MuLV, prepared by Electro-Nucleonics (Bethesda, MD), was supplied by the Office of Program Resources and Logistics, Viral Oncology, National Cancer Institute. Freshly harvested Moloney, xenotropic (ATS-124) murine, and (BN-p 454-9) rat leukemia viruses were propagated as described (6). Fresh human serum (Community Blood and Plasma, San Diego, CA) frozen at -70'C was used as a source of complement.Uranyl formate was prepared according to published procedures (13); all other chemicals were of the best grade commercially available. Buffer osmolarities were measured with a freezing-point depression osmometer (Osmette, Precision Systems, Sudbury, MA).Virolysis Assays. Virus samples (100,ug or approximately 1010 virions ...

show abstract

Antibody and complement-dependent viral neutralization

Cited by 26 publications

References 63 publications

Antibody Response to Spike Protein Vaccines Prepared from Semliki Forest Virus

Antibody Response to Spike Protein Vaccines Prepared from Semliki Forest Virus

Inherited complement deficiency states: implications for immunity and immunological disease

Disassembly of viral membranes by complement independent of channel formation.

Contact Info

Product

Resources

About