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
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 host’s ability to
produce IFN- and the virus’ 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