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Updated: Aug 9, 2026
Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
Cytokine production by cats infected with feline immunodeficiency virus: a longitudinal study
C E Lawrence1, J J Callanan, B J Willett
1Department of Veterinary Pathology, University of Glasgow, Bearsden, UK.
Insights
Feline immunodeficiency virus (FIV) infection in cats significantly impairs immune responses, similar to HIV in humans. This study details the immune cell dysfunction and cytokine changes associated with FIV progression.
Area of Science:
- Veterinary Immunology
- Virology
- Immunopathology
Background:
- Feline immunodeficiency virus (FIV) is an important pathogen affecting domestic cats.
- Understanding FIV's impact on the immune system is crucial for managing feline AIDS.
Purpose of the Study:
- To investigate the immune responsiveness in cats naturally or experimentally infected with FIV.
- To characterize the changes in immune cell function and cytokine production during FIV infection.
Main Methods:
- Studied peripheral blood mononuclear cells (PBMC) from naturally and experimentally infected cats.
- Assessed cell proliferation and cytokine (IL-1, IL-6, TNF, IL-2) production in response to mitogens (Con A, PWM).
- Monitored feline CD4+ cell counts and CD4:CD8 ratios over a 4-year period.
Main Results:
- FIV-infected cats showed depressed PBMC proliferation and IL-2 production.
- Increased levels of pro-inflammatory cytokines (IL-1, IL-6, TNF) were observed, coinciding with disease progression.
- PWM responses declined progressively and correlated with disease progression, unlike Con A responses.
Conclusions:
- FIV infection causes significant immune perturbation in cats, mirroring human immunodeficiency virus (HIV) effects.
- PWM response decline suggests early involvement of the CD3 pathway, with CD2 pathway affected later in acquired immune deficient syndrome (AIDS).
Abstract:
The immune responsiveness of cats naturally or experimentally infected with feline immunodeficiency virus (FIV) was studied. Peripheral blood mononuclear cells (PBMC) from naturally infected, symptomatic animals displayed depressed proliferation and interleukin-2 (IL-2) production in response to mitogens, which was accompanied by a significant increase in IL-1, IL-6 and tumour necrosis factor (TNF) production. Longitudinal studies were performed over a period of 4 years in experimentally infected animals. The responses of cells from these cats to concanavalin A (Con A) were consistently less than those from uninfected cats throughout the period but, owing to variation between cats, were significantly lower on only a few occasions. By contrast, the responses of cells to pokeweed mitogen (PWM) were severely affected and declined progressively throughout the 4-year period. In general, responses to Con A but not PWM could be restored by the addition of exogenous IL-2. The decline in immune responsiveness was concurrent with a decline in feline (f)CD4+ cells and an inversion in the CD4:CD8 ratio. Peak production of IL-1, IL-6 and TNF coincided with periods of depressed immune responses. Additionally, immunodeficient responses and elevated levels of proinflammatory cytokines were concurrent with the presence of clinical signs. We conclude that, like human immunodeficiency virus (HIV), FIV infection results in significant perturbation of the immune response. Responses to PWM appear to correlate with disease progression which suggests that the CD3 pathway is affected in the earlier stages of the disease and that additional activation pathways such as CD2 may not be affected until the animal enters the acquired immune deficient syndrome (AIDS) stage of the disease.
