Primate Simplexviruses Differ in Tropism for Macaque Cells
Related Experiment Video
Updated: Jun 16, 2026
Transduction and Expansion of Primary T Cells in Nine Days with Maintenance of Central Memory Phenotype
Published on: March 18, 2020
Heike Hofmann-Winkler1, Abdul Rahman Siregar1,2,3, Nesil Esiyok4
1Infection Biology Unit, German Primate Center-Leibniz Institute for Primate Research, 37077 Göttingen, Germany.
Abstract:
Primate simplexviruses are closely related neurotropic herpesviruses, which are largely apathogenic in their respective host species. However, cross-species transmission of Macacine alphaherpesvirus 1 (McHV1, also termed herpes B virus) from rhesus macaques to humans can cause fatal encephalomyelitis. In contrast, closely related viruses, such as Cercopithecine alphaherpesvirus 2 (CeHV2, also termed simian agent 8) or Papiine alphaherpesvirus 2 (PaHV2, also termed herpesvirus papio 2), have not been linked to human disease and are believed to be largely apathogenic in humans. Here, we investigated whether McHV1, PaHV2 and CeHV2 differ in their capacity to infect human and non-human primate (NHP) cells. For comparison, we included the human simplexviruses HSV1 and HSV2 in our analyses. All five viruses replicated efficiently in cell lines of human and African green monkey origin, and McHV1 and PaHV2 also showed robust replication in rhesus macaque cell lines. In contrast, the replication of CeHV2 and particularly HSV1 and HSV2 in cell lines of rhesus macaque origin were reduced or inefficient. Similarly, McHV1, but not CeHV2, efficiently infected rhesus macaque brain organoids. These results point towards the previously unappreciated partial resistance of certain rhesus macaque cells to HSV1/HSV2/CeHV2 infection and reveal similarities between the cell tropism of McHV1 and PaHV2 that might be relevant for risk assessment.
Insights
Macacine alphaherpesvirus 1 (McHV1) and Papiine alphaherpesvirus 2 (PaHV2) efficiently infect rhesus macaque cells, unlike HSV1, HSV2, and Cercopithecine alphaherpesvirus 2 (CeHV2). This reveals partial resistance in some macaque cells to certain primate simplexviruses.
Area of Science:
- Virology
- Cell Biology
- Infectious Diseases
Background:
- Primate simplexviruses, neurotropic herpesviruses, are typically host-specific.
- Macacine alphaherpesvirus 1 (McHV1) poses a fatal risk to humans via cross-species transmission.
- Cercopithecine alphaherpesvirus 2 (CeHV2) and Papiine alphaherpesvirus 2 (PaHV2) are considered largely apathogenic in humans.
Purpose of the Study:
- To investigate differential infection capacities of McHV1, PaHV2, and CeHV2 in human and non-human primate (NHP) cells.
- To compare the tropism of these primate simplexviruses with human simplexviruses HSV1 and HSV2.
- To assess the relevance of cell tropism for risk assessment of primate simplexvirus infections.
Main Methods:
- Virus replication assays in human, African green monkey, and rhesus macaque cell lines.
- Infection studies using human simplexviruses (HSV1, HSV2) and primate simplexviruses (McHV1, PaHV2, CeHV2).
- Infection experiments with rhesus macaque brain organoids.
Main Results:
- All five viruses efficiently replicated in human and African green monkey cells.
- McHV1 and PaHV2 showed robust replication in rhesus macaque cell lines.
- CeHV2, HSV1, and HSV2 exhibited reduced or inefficient replication in rhesus macaque cells, with McHV1, but not CeHV2, infecting macaque brain organoids.
Conclusions:
- Certain rhesus macaque cells display partial resistance to HSV1, HSV2, and CeHV2.
- McHV1 and PaHV2 share similar cell tropism, potentially impacting risk assessment.
- Understanding differential cell tropism is crucial for evaluating primate simplexvirus risks.
More Related Videos
13:13Single-cell Quantitation of mRNA and Surface Protein Expression in Simian Immunodeficiency Virus-infected CD4+ T Cells Isolated from Rhesus macaques
Published on: September 25, 2018
06:25Analysis of Simian Immunodeficiency Virus-specific CD8+ T-cells in Rhesus Macaques by Peptide-MHC-I Tetramer Staining
Published on: December 23, 2016
