Subversion of innate and adaptive immunity: Immune evasion from antibody and complement

Lauren M. Hook, Harvey M. Friedman

Research output: Chapter in Book/Report/Conference proceedingChapter

7 Citations (Scopus)

Abstract

Many herpesviruses encode immune evasion molecules that interfere with activities mediated by antibody and complement, suggesting the importance of antibody and complement in host defense against herpes infections. How does this observation reconcile with the clinical findings that severe infections develop mostly in subjects with T-cell deficiencies, such as transplant recipients or those with advanced HIV infection? An explanation that we favor is that T-cells assume a pivotal role in host defense partly because herpesviruses are very effective at limiting the activities of antibody and complement. Support for this hypothesis comes from experimental studies using mutant HSV-1 strains defective in antibody and complement immune evasion that demonstrate a marked increased in effectiveness of antibody and complement in host defense against the mutant viruses (Lubinski et al., 2002). Newborns lack mature T-cell repertoires and generally have low serum complement levels; therefore, observations in human newborns provide opportunities to assess the contributions of antibodies independent of T-cells and perhaps complement in host defense against herpesviruses. The severity of HSV and CMV infection in the fetus and newborn are greatly reduced when the infection in the mother is recurrent rather than primary. In recurrent infection, antibodies pass transplacentally to the fetus and protect against the infection. Passive transfer of VZV antibodies from mother to fetus protects the newborn from severe chickenpox when exposed days to weeks after delivery.

Original languageEnglish (US)
Title of host publicationHuman Herpesviruses: Biology, Therapy, and Immunoprophylaxis
PublisherCambridge University Press
Pages1137-1150
Number of pages14
ISBN (Print)9780511545313, 0521827140, 9780521827140
DOIs
StatePublished - Jan 1 2007
Externally publishedYes

Fingerprint

Immune Evasion
Adaptive Immunity
Innate Immunity
Antibodies
Herpesviridae
Infection
Newborn Infant
T-Lymphocytes
Fetus
Mothers
Passive Immunization
Chickenpox
Human Herpesvirus 1
HIV Infections
Viruses
Serum

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Hook, L. M., & Friedman, H. M. (2007). Subversion of innate and adaptive immunity: Immune evasion from antibody and complement. In Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis (pp. 1137-1150). Cambridge University Press. https://doi.org/10.1017/CBO9780511545313.064

Subversion of innate and adaptive immunity : Immune evasion from antibody and complement. / Hook, Lauren M.; Friedman, Harvey M.

Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis. Cambridge University Press, 2007. p. 1137-1150.

Research output: Chapter in Book/Report/Conference proceedingChapter

Hook, LM & Friedman, HM 2007, Subversion of innate and adaptive immunity: Immune evasion from antibody and complement. in Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis. Cambridge University Press, pp. 1137-1150. https://doi.org/10.1017/CBO9780511545313.064
Hook LM, Friedman HM. Subversion of innate and adaptive immunity: Immune evasion from antibody and complement. In Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis. Cambridge University Press. 2007. p. 1137-1150 https://doi.org/10.1017/CBO9780511545313.064
Hook, Lauren M. ; Friedman, Harvey M. / Subversion of innate and adaptive immunity : Immune evasion from antibody and complement. Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis. Cambridge University Press, 2007. pp. 1137-1150
@inbook{bc37c07998e94d90b800dc30ea390841,
title = "Subversion of innate and adaptive immunity: Immune evasion from antibody and complement",
abstract = "Many herpesviruses encode immune evasion molecules that interfere with activities mediated by antibody and complement, suggesting the importance of antibody and complement in host defense against herpes infections. How does this observation reconcile with the clinical findings that severe infections develop mostly in subjects with T-cell deficiencies, such as transplant recipients or those with advanced HIV infection? An explanation that we favor is that T-cells assume a pivotal role in host defense partly because herpesviruses are very effective at limiting the activities of antibody and complement. Support for this hypothesis comes from experimental studies using mutant HSV-1 strains defective in antibody and complement immune evasion that demonstrate a marked increased in effectiveness of antibody and complement in host defense against the mutant viruses (Lubinski et al., 2002). Newborns lack mature T-cell repertoires and generally have low serum complement levels; therefore, observations in human newborns provide opportunities to assess the contributions of antibodies independent of T-cells and perhaps complement in host defense against herpesviruses. The severity of HSV and CMV infection in the fetus and newborn are greatly reduced when the infection in the mother is recurrent rather than primary. In recurrent infection, antibodies pass transplacentally to the fetus and protect against the infection. Passive transfer of VZV antibodies from mother to fetus protects the newborn from severe chickenpox when exposed days to weeks after delivery.",
author = "Hook, {Lauren M.} and Friedman, {Harvey M.}",
year = "2007",
month = "1",
day = "1",
doi = "10.1017/CBO9780511545313.064",
language = "English (US)",
isbn = "9780511545313",
pages = "1137--1150",
booktitle = "Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis",
publisher = "Cambridge University Press",

}

TY - CHAP

T1 - Subversion of innate and adaptive immunity

T2 - Immune evasion from antibody and complement

AU - Hook, Lauren M.

AU - Friedman, Harvey M.

PY - 2007/1/1

Y1 - 2007/1/1

N2 - Many herpesviruses encode immune evasion molecules that interfere with activities mediated by antibody and complement, suggesting the importance of antibody and complement in host defense against herpes infections. How does this observation reconcile with the clinical findings that severe infections develop mostly in subjects with T-cell deficiencies, such as transplant recipients or those with advanced HIV infection? An explanation that we favor is that T-cells assume a pivotal role in host defense partly because herpesviruses are very effective at limiting the activities of antibody and complement. Support for this hypothesis comes from experimental studies using mutant HSV-1 strains defective in antibody and complement immune evasion that demonstrate a marked increased in effectiveness of antibody and complement in host defense against the mutant viruses (Lubinski et al., 2002). Newborns lack mature T-cell repertoires and generally have low serum complement levels; therefore, observations in human newborns provide opportunities to assess the contributions of antibodies independent of T-cells and perhaps complement in host defense against herpesviruses. The severity of HSV and CMV infection in the fetus and newborn are greatly reduced when the infection in the mother is recurrent rather than primary. In recurrent infection, antibodies pass transplacentally to the fetus and protect against the infection. Passive transfer of VZV antibodies from mother to fetus protects the newborn from severe chickenpox when exposed days to weeks after delivery.

AB - Many herpesviruses encode immune evasion molecules that interfere with activities mediated by antibody and complement, suggesting the importance of antibody and complement in host defense against herpes infections. How does this observation reconcile with the clinical findings that severe infections develop mostly in subjects with T-cell deficiencies, such as transplant recipients or those with advanced HIV infection? An explanation that we favor is that T-cells assume a pivotal role in host defense partly because herpesviruses are very effective at limiting the activities of antibody and complement. Support for this hypothesis comes from experimental studies using mutant HSV-1 strains defective in antibody and complement immune evasion that demonstrate a marked increased in effectiveness of antibody and complement in host defense against the mutant viruses (Lubinski et al., 2002). Newborns lack mature T-cell repertoires and generally have low serum complement levels; therefore, observations in human newborns provide opportunities to assess the contributions of antibodies independent of T-cells and perhaps complement in host defense against herpesviruses. The severity of HSV and CMV infection in the fetus and newborn are greatly reduced when the infection in the mother is recurrent rather than primary. In recurrent infection, antibodies pass transplacentally to the fetus and protect against the infection. Passive transfer of VZV antibodies from mother to fetus protects the newborn from severe chickenpox when exposed days to weeks after delivery.

UR - http://www.scopus.com/inward/record.url?scp=84929283881&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84929283881&partnerID=8YFLogxK

U2 - 10.1017/CBO9780511545313.064

DO - 10.1017/CBO9780511545313.064

M3 - Chapter

AN - SCOPUS:84929283881

SN - 9780511545313

SN - 0521827140

SN - 9780521827140

SP - 1137

EP - 1150

BT - Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis

PB - Cambridge University Press

ER -