Intervertebral disc (IVD) degeneration has a complex multifactorial origin and it is tightly associated with changes in the secretion of proteoglycans and collagen of the Nucleus Pulposus (NP) extracellular matrix. Chronic infection by Herpes virus has been previously associated with disc degeneration after detection of Herpes Simplex Virus type-1 (HSV-1) and CMV DNA in human excised disc samples. The aim of the present study was to assess the effect of HSV-1 infection on proteoglycan synthesis employing human Nucleus Pulposus (HNPCs) cells as a model of intervertebral disc degeneration. During lytic HSV-1 infection, a significant reduction of Decorin expression was observed 8 h post infection (h.p.i) which furthered deteriorated at 24 h.p.i. Biglycan was also reduced but only 24 h.p.i. Collagen type II, although demonstrated a downward trend, it was not statistically significant, whereas both Versican and Aggrecan showed a substantial decrease at 24 h.p.i. Hyaluronan production was not significantly affected. In a non-productive HSV-1 infection, a substantial reduction of Decorin, Biglycan, Versican and Aggrecan expression was found, similarly to our findings from the lytic infection. Furthermore, collagen type II expression was completely abolished. HAS1 expression was not affected, whereas HAS 2 and 3 were found to be significantly reduced. These results indicate that HSV-1 infection of human NP cells yields a complex effect on host extracellular cell function. The viral-induced changes in proteoglycan and collagen type II concentration may affect cell-matrix interactions and lead to a dysfunctional intervertebral disc which may trigger or promote the degeneration process.
Keywords: Extracellular matrix; HSV-1; Intervertebral disc degeneration; Lytic infection; Non-productive infection; Proteoglycans.
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