ArticleClinical and vaccine immunology : CVI2009
Natural killer cell dysfunction during acute infection with foot-and-mouth disease virus.
Article in Clinical and vaccine immunology : CVI, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 41 citations in OpenAlex.
- The pathogenesis of foot-and-mouth disease virus: current understandings and knowledge gaps.Veterinary research · 2025Review
- Review
- Foot-and-mouth disease virus VP1 promotes viral replication by regulating the expression of chemokines and GBP1.Frontiers in veterinary science · 2022Article
- Foot and Mouth Disease Vaccine Development and Challenges in Inducing Long-Lasting Immunity: Trends and Current Perspectives.Veterinary medicine (Auckland, N.Z.) · 2021Review
- Virus-Host Interactions in Foot-and-Mouth Disease Virus Infection.Frontiers in immunology · 2021Review
- Molecular Mechanisms of Immune Escape for Foot-and-Mouth Disease Virus.Pathogens (Basel, Switzerland) · 2020Review
- The Carrier Conundrum; A Review of Recent Advances and Persistent Gaps Regarding the Carrier State of Foot-and-Mouth Disease Virus.Pathogens (Basel, Switzerland) · 2020Review
- Use of IFN-Based Biotherapeutics to Harness the Host Against Foot-And-Mouth Disease.Frontiers in veterinary science · 2020Review
- The Different Tactics of Foot-and-Mouth Disease Virus to Evade Innate Immunity.Frontiers in microbiology · 2018Review
- Molecular markers for resistance against infectious diseases of economic importance.Veterinary world · 2017Review
- The Pathogenesis of Foot-and-Mouth Disease in Pigs.Frontiers in veterinary science · 2016Review
- Age-dependent variation in innate immune responses to porcine epidemic diarrhea virus infection in suckling versus weaned pigs.Veterinary immunology and immunopathology · 2015Article
- Natural killer cells in host defense against veterinary pathogens.Veterinary immunology and immunopathology · 2015Review
- Article
- Partial Activation of natural killer and γδ T cells by classical swine fever viruses is associated with type I interferon elicited from plasmacytoid dendritic cells.Clinical and vaccine immunology : CVI · 2014Article
- The porcine innate immune system: an update.Developmental and comparative immunology · 2014Review
- Assessment of the phenotype and functionality of porcine CD8 T cell responses following vaccination with live attenuated classical swine fever virus (CSFV) and virulent CSFV challenge.Clinical and vaccine immunology : CVI · 2013Article
- Characterization of cytotoxic T lymphocyte function after foot-and-mouth disease virus infection and vaccination.Viral immunology · 2013Article
- Cell mediated innate responses of cattle and swine are diverse during foot-and-mouth disease virus (FMDV) infection: a unique landscape of innate immunity.Immunology letters · 2013Review
- Porcine CD8αdim/-NKp46high NK cells are in a highly activated state.Veterinary research · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Natural killer (NK) cells provide one of the initial barriers of cellular host defense against pathogens, in particular intracellular pathogens. The role of these cells in foot-and-mouth disease virus (FMDV) infection is unknown. Previously, we characterized the phenotype and function of NK cells from swine (F. N. Toka et al., J. Interferon Cytokine Res. 29:179-192, 2009). In the present study, we report the analysis of NK cells isolated from animals infected with FMDV and tested ex vivo and show that NK-dependent cytotoxic activity against tumor cells as targets was impaired. More relevantly to this infection, the killing of target cells infected with FMDV also was inhibited. Further, the proportion of NK cells capable of producing gamma interferon and storing perforin was reduced. Peripheral blood mononuclear cells isolated from infected animals are not productively infected, but virus exposure in vivo resulted in the significant induction of NKp30 and Toll-like receptor 3 expression and the moderate activation of SOCS3 and interleukin-15 receptor mRNA. However, there was little alteration of mRNA expression from a number of other receptor genes in these cells, including SH2D1B and NKG2A (inhibitory) as well as NKp80, NKp46, and NKG2D (activating). These data indicate that this virus infection influences the ability of NK cells to recognize and eliminate FMDV-infected cells. In addition, a reduction in NK cell cytotoxicity coincided with the increase in virus titers, indicating the virus blocking of NK cell-associated innate responses, albeit temporarily. These effects likely culminate in brief but effective viral immune evasion, allowing the virus to replicate and disseminate within the host.
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