|
|
|
|
|
|
|
||
J. Exp. Med.,
Volume 188, Number 9, November 2, 1998 1705-1715
By
From the Department of Pathology, University of Massachusetts Medical Center, Worcester,
Massachusetts 01655
A basic principle of immunology is that prior immunity results in complete protection against a
homologous agent. In this study, we show that memory T cells specific to unrelated viruses may alter the host's primary immune response to a second virus. Studies with a panel of heterologous viruses, including lymphocytic choriomeningitis (LCMV), Pichinde (PV), vaccinia
(VV), and murine cytomegalo (MCMV) viruses showed that prior immunity with one of these
viruses in many cases enhanced clearance of a second unrelated virus early in infection. Such
protective immunity was common, but it depended on the virus sequence and was not necessarily reciprocal. Cell transfer studies showed that both CD4 and CD8 T cell populations from
LCMV-immune mice were required to transfer protective immunity to naive hosts challenged
with PV or VV. In the case of LCMV-immune versus naive mice challenged with VV, there
was an enhanced early recruitment of memory phenotype interferon (IFN) 
-secreting CD4+
and CD8+ cells into the peritoneal cavity and increased IFN- levels in this initial site of virus
replication. Studies with IFN- receptor knockout mice confirmed a role for IFN- in mediating the protective effect by LCMV-immune T cell populations when mice were challenged with VV but not PV. In some virus sequences memory cell populations, although clearing the
challenge virus more rapidly, elicited enhanced IFN--dependent immunopathogenesis in the
form of acute fatty necrosis. These results indicate that how a host responds to an infectious
agent is a function of its history of previous infections and their influence on the memory T cell
pool.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
| TABLE OF CONTENTS |
|
