E. R. Mackow

Age-dependent Powassan Virus Lethality is Directed by Glial Cell Activation and Divergent Neuroinflammatory Cytokine Responses in a Murine Model

This study establishes a murine model of age-dependent Powassan virus (POWV) lethality, revealing divergent neuroinflammatory cytokine responses in young and old mice that correlate with CNS viral clearance and disease severity.

Age-dependent Powassan Virus Lethality and Neuropathogenesis in Mice

This study shows that older mice are more susceptible to lethal Powassan virus infection, with increased viral load and severe brain damage compared to younger mice.

ZIKV Induction of Tristetraprolin in Endothelial and Sertoli Cells Post-Transcriptionally Inhibits IFNβ/{lambda} Expression and Promotes ZIKV Persistence

This study shows ZIKV induces TTP in endothelial and Sertoli cells, which post-transcriptionally inhibits IFNβ/λ secretion, promoting viral persistence.

Establishment of a CPER Reverse Genetics System for Powassan Virus Defines Attenuating NS1 Glycosylation Sites and an Infectious NS1-GFP11 Reporter Virus

This paper establishes a reverse genetics system for Powassan virus, identifies attenuating NS1 glycosylation sites, and creates an infectious NS1-GFP11 reporter virus to study viral functions.

Powassan Viruses Spread Cell to Cell During Direct Isolation from IxodesTicks and Persistently Infect Human Brain Endothelial Cells and Pericytes

This study isolates and characterizes POWVs from ticks, showing they spread cell-to-cell in culture and infect human brain endothelial cells and pericytes, leading to persistent infection and inflammatory responses.

Binding of the Andes Virus Nucleocapsid Protein to RhoGDI Induces the Release and Activation of the Permeability Factor RhoA

This study identifies how the Andes virus N protein interacts with RhoGDI to release and activate RhoA, increasing PMEC permeability and contributing to hantavirus pulmonary syndrome.

Recombinant ACE2 Expression is Required for SARS-CoV-2 to Infect Primary Human Endothelial Cells and Induce Inflammatory and Procoagulative Responses

This study shows that SARS-CoV-2 cannot directly infect primary human endothelial cells without recombinant ACE2 expression, but infection of ACE2-expressing endothelial cells induces inflammatory and procoagulative responses seen in COVID-19.