Mechanism of virus-induced Ig subclass shifts.
Infection of mice with live viruses leads to a dramatic increase in the amount of IgG2a Ig with a consequent shift in the ratio of IgG1/IgG2a. To examine the Ig subclass shift induced by viral infection, we challenged mice with live virus, inactivated virus, or replication-defective mutant viruses that were able to infect cells and produce some viral proteins but were not able to complete a replicative cycle. While killed (or inactivated) virus was capable of inducing HSV-specific antibody, it did not stimulate a shift in the subclass of the total Ig. Replication-defective mutant viruses that fail to express a functional ICP8 or ICP27 protein, but not a mutant expressing a defective ICP4 protein, were able to stimulate the shift. Thus, only a portion of the lytic cycle is sufficient to induce the shift. At least part of the effect is mediated by IFN-gamma.
Nguyen
L
L
Laboratory of Infectious Diseases, Dana-Farber Cancer Institute, Boston, MA 02115.
Knipe
D M
DM
Finberg
R W
RW
D000818:Animals; D005363:Ficusin / Q000494:pharmacology; D018259:Herpesvirus 1, Human / Q000187:drug effects / Q000254:growth & development / Q000276:immunology*; D017578:Immunoglobulin Class Switching; D007074:Immunoglobulin G / Q000096:biosynthesis; D007371:Interferon-gamma / Q000502:physiology; D051379:Mice; D008807:Mice, Inbred BALB C; D014779:Virus Replication
D007074:Immunoglobulin G; D007371:Interferon-gamma; D005363:Ficusin