Neuropathogenic and non-neuropathogenic EHV-1 strains induce the accumulation of hyperphosphorylated Tau in primary murine neurons.

The research paper investigates how both neuropathogenic and non-neuropathogenic strains of Equid Herpesvirus 1 (EHV-1) cause the buildup of hyperphosphorylated Tau protein in primary murine neurons.

Background

• The study is centered around Equid Herpesvirus 1 (EHV-1), a virus causing respiratory disease, abortion, and neurological disorders in horses.
• This virus belongs to the category of alphaherpesviruses that settles into a dormant state in the neurons of the inflicted organisms.
• Although there have been ample studies on the clinical effects of EHV-1, the mechanisms causing neuronal damage are still unclear.

Aim of the Study

• This study aimed to determine the phosphorylation status of Tau, a protein that plays a key role in maintaining neuron structure, in neuronal cultures infected with EHV-1.
• The researchers focused on various specific phosphorylation sites of tau such as tau-ser199/ser202, tau-ser404, tau-ser262, tau-thr181, tau-thr217, and tau-thr205.

Research Findings

• From their research, they concluded that both primary murine neurons contracted with neuropathogenic and non-neuropathogenic EHV-1 strains, led to the accumulation of an overabundance of phosphorylated Tau, known as hyperphosphorylated Tau.
• This build-up specifically occurred on tau-ser199/ser202, tau-ser404 and tau-thr205 during persistent infection and triggered a productive infection.
• This is the first study that discovered EHV-1 infection can lead to hyperphosphorylated Tau accumulation in primary murine neurons, shedding new light on the role of this virus in neurodegeneration.