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Viruses. 2019 Aug 29;11(9). pii: E797. doi: 10.3390/v11090797.

Mayaro Virus Infects Human Chondrocytes and Induces the Expression of Arthritis-Related Genes Associated with Joint Degradation.

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MIVEGEC, IRD, Univ. Montpellier, CNRS, 34394 Montpellier, France.
Unité des virus émergents, Aix Marseille Univ-IRD 190, Inserm 1207-IHU Méditerranée Infection, 13385 Marseille, France.
Department of Clinical Microbiology and Applied Technology, Faculty of Medical Technology, Mahidol University, Nakhon Pathom 73170, Thailand.
PhyMedExp, CNRS UMR 9214, INSERM U1046, University of Montpellier, 34295 Montpellier, France.
MIVEGEC, IRD, Univ. Montpellier, CNRS, 34394 Montpellier, France.


Mayaro virus (MAYV) is an emerging arthritogenic alphavirus belonging to the Togaviridae family. Infection leads to a dengue-like illness accompanied by severe polyarthralgia. However, the molecular and cellular mechanisms of arthritis as a result of MAYV infection remain poorly understood. In the present study, we assess the susceptibility of human chondrocytes (HC), fibroblast-like synoviocytes and osteoblasts that are the major cell types involved in osteoarthritis, to infection with MAYV. We show that these cells are highly permissive to MAYV infection and that viral RNA copy number and viral titers increase over time in infected cells. Knowing that HC are the primary cells in articular cartilage and are essential for maintaining the cartilaginous matrix, gene expression studies were conducted in MAYV-infected primary HC using polymerase chain reaction (PCR) arrays. The infection of the latter cells resulted in an induction in the expression of several matrix metalloproteinases (MMP) including MMP1, MMP7, MMP8, MMP10, MMP13, MMP14 and MMP15 which could be involved in the destruction of articular cartilage. Infected HC were also found to express significantly increased levels of various IFN-stimulated genes and arthritogenic mediators such as TNF-α and IL-6. In conclusion, MAYV-infected primary HC overexpress arthritis-related genes, which may contribute to joint degradation and pathogenesis.


IL-6; Mayaro virus; TNF-α; arbovirus; chondrocyte; extracellular matrix; innate immunity; matrix metalloproteinases; osteoblast; synoviocyte

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