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Chronic immune stimulation accelerates SIV-induced disease progression.

F Villinger¹, T Rowe, B S Parekh

¹Department of Pathology, Laboratory Medicine, Emory University, Atlanta, GA, USA. fvillin@emory.edu

Journal of Medical Primatology

|May 7, 2002

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Chronic immune stimulation, including tetanus toxoid (TT) and keyhole limpet hemocyanin (KLH), accelerated simian-lentivirus (SIV) disease progression in macaques. This shortened survival suggests potential implications for human immunodeficiency virus (HIV) patients with co-infections.

Area of Science:

Immunology
Virology
Pathogenesis

Background:

Chronic immune stimulation is a hallmark of persistent viral infections like Human Immunodeficiency Virus (HIV).
The impact of ongoing immune activation on lentivirus disease progression remains incompletely understood.
The SIVmac251 macaque model closely mimics HIV infection in humans.

Purpose of the Study:

To investigate the contribution of chronic immune stimulation to the progression of lentivirus-induced disease.
To evaluate the effect of repeated antigen exposure on survival in SIV-infected macaques.

Main Methods:

Four macaques were inoculated with SIVmac251 and subsequently received repeated immune stimulations with tetanus toxoid (TT), keyhole limpet hemocyanin (KLH), and allogeneic peripheral blood mononuclear cells (PBMC).

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Survival times of stimulated macaques were compared to those of non-immune-stimulated control macaques infected with the same SIVmac251 stock and dose.

Plasma viral loads and antibody responses to immunizing antigens were monitored.

Main Results:

Immune-stimulated macaques exhibited significantly shortened survival (median 9.5 months) compared to control groups (median 17-18 months, P = 0.010 and P = 0.003).
Accelerated disease progression was not associated with increased plasma viral loads.
Suboptimal antibody responses to TT and KLH were observed, correlating inversely with survival duration.

Conclusions:

Chronic immune stimulation significantly accelerates lentivirus-induced disease progression in the SIVmac251 macaque model.
This accelerated pathogenesis may be linked to impaired adaptive immune responses rather than increased viral replication.
Findings suggest that managing chronic infectious diseases in HIV-infected individuals could be crucial for disease control.