Amplification of phage neutralization by complement, antiglobulin, and antiallotype sera

Adler, Frank L.; Walker, William S.; Fishman, Marvin A.

doi:10.1016/0042-6822(71)90081-x

Cited by 22 publications

(10 citation statements)

References 23 publications

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“…Participation of complement in the neutralization of bacteriophages has also been reported by Barlow et a2. (19581, Cowan (1962), Toussaint and Muschel (1962), Pernis et al (1963) , and Adler et al (1971). Harris et al (1962) reported the induction in humans and mice of complementdependent antibody following immunization with Bacillus megatherium bacteriophage.…”

Section: A Backgroundmentioning

confidence: 99%

Neutralization of Animal Viruses

Mandel¹

1978

Advances in Virus Research Volume 23

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Section: A Backgroundmentioning

confidence: 99%

Neutralization of Animal Viruses

Mandel¹

1978

Advances in Virus Research Volume 23

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“…With the mechanisms of neutralization of sensitized virus by anti-globulin serum, the most likely explanation is considered to be that the anti-globulin antibody molecules are attached to sensitized virus particles, resulting an increase in size of virus-antibody complexes or a bridge formation between anti-viral antibody molecules which were bound with the virus particles, thus blocking the adsorption or penetration of sensitized virus to or into the host cells (1,5,13). On the basis of such a hypothesis, the addition of ACRS to the reaction systems or pretreatment of the host cells with ACRS would be expected to facilitate the adsorption or penetration of sensitized virus by formation of a bridge between anti-viral antibody and anti-cellular antibody which had been bound to virus particles and the surface of the host cells, respectively.…”

Section: Diseussionmentioning

confidence: 99%

“…Since it was demonstrated that an infectious virus antibody complex (sensitized virus) was formed during the process of neutralization of Lactic dehydrogenase virus or herpes simplex virus and that this could be neutralized by anti-globulin serum, the anti-T-globulin method has been used as a useful tool for the analysis of the mechanisms of viral neutralization (1,2,5,7,9,12,13). Our recent studies on the interaction of Japanese encephalitis virus (JEV) with antibody showed that the neutralization reactions were potentiated by anti-globulin and differed in their patterns between early IgM and late IgG antibody (10).…”

Section: Introductionmentioning

confidence: 99%

“…Although the mechanisms of neutralization of sensitized virus by anti-y-globulin have not yet been fully explained, the most possible explanation seems to be that anti-globulin molecules act to form bridges between anti-viral antibody molecules bound to the surface of sensitized virus particles, and inhibit the adsorption of sensitized virus to the surface of the host cells by blocking the infective sites on the virus particles (1,5). If so, the enhancement of adsorption of sensitized virus to the host cells would be expected to restore the loss of infectivity occurring during the process of neutralization by anti-IgG serum.…”

Section: Introductionmentioning

confidence: 99%

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Studies on neutralization of Japanese encephalitis virus

Ozaki

Kumagai

Kawanishi

1975

Archives of Virology

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The effect of anti-cellular rabbit serum (ACRS) on the neutralization of sensitized Japanese encephalitis virus (JEV) by anti-rabbit IgG serum was examined to elucidate the interaction between virus-antibody complex and the surface of the host cells during the process of neutralization. ACRS had no effect on the adsorption of either sensitized or non-sensitized virus, but was able to restore the lost infectivity of sensitized virus which occurred during the process of neutralization by anti-rabbit IgG serum. This restoration of infectivity was found to take place not only by the addition of ACRS to the reaction mixtures (virus-antibody, anti-rabbit IgG complex) but also by pretreatment of the host cells with ACRS. Although the restoration of lost infectivity varied in magnitude with the concentration of ACRS used, it never exceeded the infectivity titer of the sensitized virus befor incubatio with anti-rabbit IgG serum. This result suggests that ACRS has no ability to reverse the neutralization by anti-viral serum. Since the ACRS reacted only with anti-rabbit IgG serum treated sensitized virus, resulting in an increase of the number of infectious centers, the restoration of lost infectivity was explained as being due to the enhancement of adsorption of sensitized virus to the host cells by bridge formation of anti-rabbit IgG antibody between them.

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“…CRN antibody has been found not only with HSV but also with a number of other viruses (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(15)(16)(17)(18)(19)(20)(21)(23)(24)(25)(28)(29)(30)(31). This was not the case, however, with poliovirus (14).…”

Section: Sensitization Kinetic Curves Differentiating Surivors With Dmentioning

confidence: 99%

Studies on the Neutralization of Herpes Simplex Virus

Yoshino

Isono

Tada

et al. 1979

Microbiology and Immunology

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A sample of late IgG from a rabbit hyperimmunized with herpes simplex virus was analyzed for neutralizing (N) and complement-requiring neutralizing (CRN) antibodies. In a usual endpoint test, N and CRN titers were 1: 40 and 1: 160, respectively, but when virus-IgG mixtures were incubated at 0 C overnight before addition of complement (C), an endpoint of 1 :1280 was obtained. Virus sensitized at 0 C overnight required more C for inactivation than did sensitized virus formed earlier. Sensitization kinetic curve experiments employing a proper initial virus concentration, which permitted differentiation of sensitized viruses requiring different amounts of C, indicated that formation of sensitized virus detectable only with a relatively large amount of C proceeded slowly at IgG dilutions where the ordinary CRN antibody requiring a smaller amount of C was negligible. The results strongly suggested that the IgG sample contained slow-reacting CRN (s-CRN) antibody in excess of the hitherto known CRN antibody. As to the mechanism of formation of s-CRN complexes, experiments failed to prove the occurrence of complexes initially insensitive to C, and it appears more likely that s-CRN antibody has a comparatively low avidity for virus.Studies with herpes simplex virus (HSV) (35,36,38) indicated the presence of complement-requiring neutralizing (CRN) antibody in early immune sera. Later it was learned that CRN antibody, usually predominant in IgM and early IgG, also coexisted with ordinary neutralizing (N) antibody in late sera, too (32). Virus retaining infectious potential after binding with CRN antibody was called sensitized virus, in the sense that subsequent addition of complement (C) could inactivate the virus (37). The amount of C needed for this inactivation differed between IgMand IgG-sensitized virus particles, and use was made of this fact to delineate the mechanism of viral neutralization in our previous work (33).Thereby, we happened to find that virus sensitized with late IgG or IgM showed unexpectedly high neutralization endpoints when sensitization proceeded at 0 C overnight. The sensitized virus so formed was named slow-reacting CRN (s-CRN) 975

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Amplification of phage neutralization by complement, antiglobulin, and antiallotype sera

Cited by 22 publications

References 23 publications

Neutralization of Animal Viruses

Neutralization of Animal Viruses

Studies on neutralization of Japanese encephalitis virus

Studies on the Neutralization of Herpes Simplex Virus

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