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February 9, 2000

Immunologic Strategies for Herpes Vaccination—Reply

Author Affiliations

Phil B.FontanarosaMD, Deputy EditorIndividualAuthorStephen J.LurieMD, PhD, Fishbein FellowIndividualAuthor

JAMA. 2000;283(6):746. doi:10.1001/jama.283.6.741

In Reply: Dr Friedman raises 2 interesting concepts related to the development of viral vaccines. Viruses use several mechanisms to evade the host immune response and the rational design of future vaccines should consider this virus-host interaction. In the case of HSV-2, the glycoprotein gC appears to inhibit the complement-mediated attack on the virus. Thus, it is possible that inducing an antibody response against gC could block this protective mechanism and allow the host to more effectively eradicate HSV-2. Of interest, human pathogenic viruses use several other strategies that appear to permit immune evasion. Perhaps the best documented example is that viruses such as adenovirus, HSV, cytomegalovirus, Epstein-Barr virus, and human immunodeficiency virus (HIV) encode genes that inhibit the processing and subsequent presentation of major histocompatibility complex (MHC) I–associated viral proteins on the surface of infected cells.1,2 Since cytotoxic T-cell recognition of virus-infected host cells requires the presentation of foreign peptide antigens by MHC I proteins, this impairs the ability of the host to eradicate infected cells. Viruses also may encode genes for chemokines (chemoattractant cytokines) that modulate the host immune response in a way that favors viral replication. This could occur by recruiting susceptible cells to the site of virus replication3 or by blocking the production of host antiviral cytokines such as interferons.4