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CIDRAP NEWS SCAN: Saudi MERS case; West Nile neurologic damage

Shiloh

Editor, Senior Moderator
Source: http://www.cidrap.umn.edu/news-perspective/2016/06/news-scan-jun-23-2016


News Scan for Jun 23, 2016
Saudi MERS case; West Nile neurologic damage

Filed Under:
MERS-CoV; West Nile

[h=3]New MERS case and death reported in Saudi Arabia[/h] The Saudi Ministry of Health (MOH) reported a new MERS-CoV case today, bringing the country's total to 1,400, as well as a death in a previously reported MERS patient.
A 55-year-old Bangladeshi man living in Jeddah tested positive for MERS-CoV (Middle East respiratory syndrome coronavirus). He had primary exposure to the virus, the MOH said, adding that he's currently in stable condition.
The agency also noted that a patient in Najran died from MERS-CoV. The 82-year-old Saudi man had primary exposure to the virus and co-morbidities.
MERS-CoV was first detected in Saudi Arabia in 2012. To date the MOH reports 1,400 confirmed cases, 28 asymptomatic cases, and 595 deaths from the virus.
Jun 23 MOH update

[h=3]Study: Cognitive problems with West Nile linked to synapse loss[/h] Memory loss experienced by survivors of neuroinvasive West Nile virus (WNV) infection is associated not with cell death, as previously thought, but instead with neuronal synapse destruction in the brain, according to a study today in Nature.
Researchers led by the Washington University School of Medicine found that mice who survived severe WNV disease experienced difficulty in navigating a maze, with minimal improvement in memory after 5 days. Issues with spatial learning were traced to the hippocampus, where an increase in 747 genes that regulate remodeling of the synapses that connect and communicate between neurons was observed.
Neuroinvasive WNV disease appeared to activate microglial cells, which act as macrophages in the brain and spinal cord and which engulfed and destroyed synaptic connections while leaving the neurons themselves intact, the authors said. Synaptic destruction was found in areas of the brain where viral antigen was absent, suggesting the infection's widespread effect on synapses.
Microglia were activated by complement proteins, leading to a 40% decrease in the number of presynaptic terminals 7 days after infection and marking the first time that complement expression in the brain has been observed in severe WNV disease, the authors said.
The study also marks the first time that viral infection has been shown to cause cognitive dysfunction in the absence of neuron death, claimed the researchers. Though WNV infection is rare, 1 in 100 case-patients will develop neuroinvasive disease, and survivors of severe disease are often plagued by memory loss, spatial navigation problems, and irritability.
Synaptic damage in murine survivors similar to that observed in WNV human fatalities presents an opportunity to test new therapies on mice and examine the potential for synapse loss in other diseases that affect cognition, noted the authors.
Jun 23 Nature study
 
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