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Updated: Apr 3, 2026
Analysis of Simian Immunodeficiency Virus-specific CD8+ T-cells in Rhesus Macaques by Peptide-MHC-I Tetramer Staining
Published on: December 23, 2016
Durable sequence stability and bone marrow tropism in a macaque model of human pegivirus infection
Adam L Bailey1, Michael Lauck1, Mariel Mohns1
1Department of Pathology and Laboratory Medicine, University of Wisconsin-Madison, Madison, WI 53711, USA. Wisconsin National Primate Research Center, Madison, WI 53711, USA.
Abstract:
Human pegivirus (HPgV)-formerly known as GB virus C and hepatitis G virus-is a poorly characterized RNA virus that infects about one-sixth of the global human population and is transmitted frequently in the blood supply. We create an animal model of HPgV infection by infecting macaque monkeys with a new simian pegivirus (SPgV) discovered in wild baboons. Using this model, we provide a high-resolution, longitudinal picture of SPgV viremia where the dose, route, and timing of infection are known. We detail the highly variable acute phase of SPgV infection, showing that the viral load trajectory early in infection is dependent on the infecting dose, whereas the chronic-phase viremic set point is not. We also show that SPgV has an extremely low propensity for accumulating sequence variation, with no consensus-level variants detected during the acute phase of infection and an average of only 1.5 variants generated per 100 infection-days. Finally, we show that SPgV RNA is highly concentrated in only two tissues: spleen and bone marrow, with bone marrow likely producing most of the virus detected in plasma. Together, these results reconcile several paradoxical observations from cross-sectional analyses of HPgV in humans and provide an animal model for studying pegivirus biology.
Insights
Researchers developed a simian pegivirus (SPgV) macaque model to study human pegivirus (HPgV) infection. This model reveals SPgV
Area of Science:
- Virology
- Infectious Diseases
- Animal Models
Background:
- Human pegivirus (HPgV), formerly GB virus C/hepatitis G virus, infects ~16% of the global population.
- HPgV is frequently transmitted through the blood supply, but its biology remains poorly understood.
- A lack of suitable animal models has hindered in-depth study of pegivirus infection dynamics.
Purpose of the Study:
- To establish and characterize a novel animal model for studying pegivirus infection and pathogenesis.
- To elucidate the longitudinal dynamics of simian pegivirus (SPgV) viremia in a controlled setting.
- To investigate the genetic stability and tissue tropism of SPgV.
Main Methods:
- Infection of macaque monkeys with a newly discovered simian pegivirus (SPgV) from baboons.
- Longitudinal monitoring of SPgV viremia, including viral load quantification and genetic sequencing.
- Analysis of SPgV RNA distribution in various tissues post-infection.
Main Results:
- The SPgV macaque model successfully recapitulated key aspects of pegivirus infection.
- Viral load during the acute phase was dose-dependent, while the chronic phase set point was not.
- SPgV exhibited extremely low genetic variation, with minimal variant accumulation observed.
- SPgV RNA was highly concentrated in spleen and bone marrow, with bone marrow identified as a likely primary site of viral production.
Conclusions:
- The SPgV macaque model provides a valuable platform for studying HPgV biology and infection.
- Understanding SPgV viremia dynamics and tissue tropism offers insights into HPgV pathogenesis in humans.
- The low genetic variability of SPgV has implications for viral persistence and host immune response.
