Identification of viral protease-dependent cleavage sites within the human astrovirus polyprotein.

Infection by human astrovirus (HAstV), a small, positive-strand RNA virus, is a major cause of gastroenteritis and has been implicated in an increasing number of severe, sometimes fatal, neurological diseases since 2008. Currently, there are no vaccines or antiviral treatments available to treat HAstV infection. An attractive target for antiviral therapeutics is the viral protease due to its essential functions throughout infection.

Modification of N-Linked Glycan Sites in Viral Glycoproteins.

Post-translational modification of proteins by the addition of sugar chains, or glycans, is a functionally important hallmark of proteins trafficked through the secretory system. These proteins are termed glycoproteins. Glycans are known to be important for initiating signaling through binding of cell surface receptors, facilitating protein folding, and maintaining protein stability.

Construction and Rescue of a DNA-Launched DENV2 Infectious Clone.

Flaviviruses represent a large group of globally significant, insect-borne pathogens. For many of these viruses, there is a lack of antivirals and vaccines. Thus, there is a need to continue the development of tools to further advance our efforts to combat these pathogens, including reverse genetics techniques.

Dual-fluorescent reporter for live-cell imaging of the ER during DENV infection.

Infection by flaviviruses leads to dramatic remodeling of the endoplasmic reticulum (ER). Viral replication occurs within virus-induced vesicular invaginations in the ER membrane. A hallmark of flavivirus infection is expansion of the ER membrane which can be observed at specific time points post infection.

Role of leukocyte adhesion in clinical stroke.

Activated neutrophils appear to be directly involved in potentiating central nervous system ischemic injury. After initial endothelial adherence, neutrophils can produce capillary plugging with subsequent parenchymal infiltration and resulting cytotoxic neuronal injury. We used an in vitro leukocyte adherence assay to determine if adhesion is increased in acute stroke (within 72 h) or in patients at high risk for stroke (two or more risk factors) compared to matched controls.