Articles | Volume 4, issue 1
Primate Biol., 4, 107–115, 2017

Special issue: Special diseases of nonhuman primates

Primate Biol., 4, 107–115, 2017

Research article 12 Jun 2017

Research article | 12 Jun 2017

Revisiting a quarter of a century of simian immunodeficiency virus (SIV)-associated cardiovascular diseases at the German Primate Center

Matthias Mietsch1,*, Ulrike Sauermann1,*, Kerstin Mätz-Rensing2, Antonina Klippert1, Maria Daskalaki1, Nicole Stolte-Leeb1, and Christiane Stahl-Hennig1 Matthias Mietsch et al.
  • 1Unit of Infection Models, German Primate Center, 37077 Goettingen, Germany
  • 2Pathology Unit, German Primate Center, 37077 Goettingen, Germany
  • *These authors contributed equally to this work.

Abstract. Human immunodeficiency virus (HIV) comorbidities have become clinically more important due to antiretroviral therapy. Although therapy increases life expectancy, it does not completely suppress immune activation and its associated complications. The simian immunodeficiency virus (SIV)-infected rhesus macaque (Macaca mulatta) represents a valuable model for the investigation of SIV-associated diseases. Although cardiovascular (CV) changes are common in HIV-infected patients, there are only a few reports on the incidence of CV findings in SIV-infected animals. In addition, potential associations between pathohistological findings and hematological parameters are still unclear.

We therefore conducted a retrospective analysis of 195 SIV-infected rhesus macaques that were euthanized with AIDS-related symptoms at the German Primate Center, Goettingen, over a 25-year period. Pathological findings were correlated with hematological data.

The main findings included myocarditis (12.8 %), endocarditis (9.7 %), and arteriopathy (10.3 %) in various organs. Thrombocytopenia occurred more frequently in macaques with endocarditis or arteriopathy than in macaques without CV disease (80 % in animals with endocarditis, 60 % in animals with arteriopathy, p < 0. 0001 and p = 0. 0016, respectively).

Further investigations of the interaction between coagulation markers, proinflammatory cytokines, and biomarkers associated with endothelial dysfunction (e.g., D-dimers) and histological data (vascular wall structure) may unravel the mechanisms underlying HIV/SIV-associated CV comorbidities.