eCite Digital Repository

Poxvirus-encoded gamma interferon binding protein dampens the host immune response to infection

Citation

Sakala, IG and Chaudhri, G and Buller, RM and Nuara, AA and Bai, H and Chen, N and Karupiah, G, Poxvirus-encoded gamma interferon binding protein dampens the host immune response to infection, Journal of Virology, 81, (7) pp. 3346-3353. ISSN 0022-538X (2007) [Refereed Article]

Copyright Statement

Copyright © 2007, American Society for Microbiology

DOI: doi:10.1128/JVI.01927-06

Abstract

Ectromelia virus (ECTV), a natural mouse pathogen and the causative agent of mousepox, is closely related to variola virus (VARV), which causes smallpox in humans. Mousepox is an excellent surrogate small-animal model for smallpox. Both ECTV and VARV encode a multitude of host response modifiers that target components of the immune system and that are thought to contribute to the high mortality rates associated with infection. Like VARV, ECTV encodes a protein homologous to the ectodomain of the host gamma interferon (IFN-) receptor 1. We generated an IFN- binding protein (IFN-bp) deletion mutant of ECTV to study the role of viral IFN-bp (vIFN-bp) in host-virus interaction and also to elucidate the contribution of this molecule to the outcome of infection. Our data show that the absence of vIFN-bp does not affect virus replication per se but does have a profound effect on virus replication and pathogenesis in mice. BALB/c mice, which are normally susceptible to infection with ECTV, were able to control replication of the mutant virus and survive infection. Absence of vIFN-bp from ECTV allowed the generation of an effective host immune response that was otherwise diminished by this viral protein. Mice infected with a vIFN-bp deletion mutant virus, designated ECTV-IFN-bp, produced increased levels of IFN- and generated robust cell-mediated and antibody responses. Using several strains of mice that exhibit differential degrees of resistance to mousepox, we show that recovery or death from ECTV infection is determined by a balance between the hostís ability to produce IFN- and the virusí ability to dampen its effects.

Item Details

Item Type:Refereed Article
Keywords:Poxvirus; immune evasion;IFN-g; virus-binding protein; cytotoxic T lymphocytes.; NK cells
Research Division:Biomedical and Clinical Sciences
Research Group:Immunology
Research Field:Cellular immunology
Objective Division:Health
Objective Group:Clinical health
Objective Field:Prevention of human diseases and conditions
UTAS Author:Karupiah, G (Associate Professor Guna Karupiah)
ID Code:142820
Year Published:2007
Web of Science® Times Cited:30
Deposited By:Medicine
Deposited On:2021-02-12
Last Modified:2021-03-31
Downloads:0

Repository Staff Only: item control page