Unlabelled: Like varicella-zoster virus (VZV), simian varicella virus (SVV) reactivates to produce zoster. In the present study, 5 rhesus macaques were inoculated intrabronchially with SVV, and 5 months later, 4 monkeys were immunosuppressed; 1 monkey was not immunosuppressed but was subjected to the stress of transportation. In 4 monkeys, a zoster rash developed 7 to 12 weeks after immunosuppression, and a rash also developed in the monkey that was not immunosuppressed.
View Article and Find Full Text PDFLike varicella zoster virus in humans, simian varicella virus (SVV) becomes latent in ganglionic neurons along the entire neuraxis and reactivates in immunosuppressed monkeys. Five rhesus macaques were inoculated with SVV; 142 days later (latency), four monkeys were immunosuppressed, and T cells were analyzed for naïve, memory, and effector phenotypes and expression of programmed death receptor-1 (PD-1; T cell exhaustion). All T cell subsets decreased during immunosuppression and except for CD8 effectors, peaked 2 weeks before zoster.
View Article and Find Full Text PDFBackground: An effective AIDS vaccine remains one of the highest priorities in HIV-research. Our recent study showed that vaccination of rhesus macaques with recombinant simian varicella virus (rSVV) vector - simian immunodeficiency virus (SIV) envelope and gag genes, induced neutralizing antibodies and cellular immune responses to SIV and also significantly reduced plasma viral loads following intravenous pathogenic challenge with SIVMAC251/CX1.
Findings: The purpose of this study was to define cellular immunological correlates of protection in rSVV-SIV vaccinated and SIV challenged animals.
Studies of varicella-zoster virus gene expression during latency require the acquisition of human ganglia at autopsy. Concerns have been raised that the virus might reactivate immediately after death. Because features of varicella-zoster virus latency are similar in primate and human ganglia, we examined virus gene expression in tissues either processed immediately or kept at 4°C for 30 h before necropsy of two monkeys inoculated with simian varicella-zoster virus and euthanized 117 days later.
View Article and Find Full Text PDFSimian varicella virus (SVV) infection of primates resembles human varicella-zoster virus (VZV) infection. After primary infection, SVV becomes latent in ganglia and reactivates after immunosuppression or social and environmental stress. Herein, natural SVV infection was established in 5 cynomolgus macaques (cynos) and 10 African green (AG) monkeys.
View Article and Find Full Text PDFBackground: Dual epidemics of the malaria parasite Plasmodium and HIV-1 in sub-Saharan Africa and Asia present a significant risk for co-infection in these overlapping endemic regions. Recent studies of HIV/Plasmodium falciparum co-infection have reported significant interactions of these pathogens, including more rapid CD4+ T cell loss, increased viral load, increased immunosuppression, and increased episodes of clinical malaria. Here, we describe a novel rhesus macaque model for co-infection that supports and expands upon findings in human co-infection studies and can be used to identify interactions between these two pathogens.
View Article and Find Full Text PDFBackground: The rhesus macaque is a common substitute for human subjects in many disease models, including simian immunodeficiency virus, the non-human primate equivalent of the human immunodeficiency virus. Monoclonal antibodies and fluorochromes optimized for use in macaques were included in samples examined for immune responses with the use of intracellular cytokine flow cytometry (CFC).
Methods: Sample preparation was optimized based on the following comparisons: activation of peripheral blood mononuclear cells (PBMCs) versus whole blood; separation of PBMCs using BD Vacutainer cell preparation tubes versus Ficoll; and activation of samples on the day they were collected versus holding samples overnight.