Diversity of heparan sulfate and HSV entry: basic understanding and treatment strategies.

A modified form of heparan sulfate (HS) known as 3-O-sulfated heparan sulfate (3-OS HS) generates fusion receptor for herpes simplex virus (HSV) entry and spread. Primary cultures of corneal fibroblasts derived from human eye donors have shown the clinical significance of this receptor during HSV corneal infection. 3-OS HS- is a product of a rare enzymatic modification at C3 position of glucosamine residue which is catalyzed by 3-O-sulfotransferases (3-OSTs) enzymes. From humans to zebrafish, the 3-OST enzymes are highly conserved and widely expressed in cells and tissues. There are multiple forms of 3-OSTs each producing unique subset of sulfated HS making it chemically diverse and heterogeneous. HSV infection of cells or zebrafish can be used as a unique tool to understand the structural-functional activities of HS and 3-OS HS and likewise, the infection can be used as a functional assay to screen phage display libraries for identifying HS and 3-OS HS binding peptides or small molecule inhibitors. Using this approach over 200 unique 12-mer HS and 3-OS HS recognizing peptides were isolated and characterized against HSV corneal infection where 3-OS HS is known to be a key receptor. In this review we discuss emerging role of 3-OS HS based therapeutic strategies in preventing viral infection and tissue damage.

Statins and Incidence of Contrast-Induced Acute Kidney Injury Following Coronary Angiography - Five Year Experience at a Tertiary Care Center.

BACKGROUND: Role of statins in prevention of contrast-induced acute kidney injury (CI-AKI) in patients undergoing coronary angiography remains controversial. We studied the use of statins in decreasing CI-AKI following coronary angiography. METHODS: We reviewed all patients who underwent coronary angiography with or without PCI and had a follow-up creatinine from January 2012 to December 2016 at a single tertiary care center in the United States. CI-AKI was defined as 0.3 mg/dL absolute rise in creatinine. Patients who were on moderate to high-intensity statins or received moderate to high-intensity statins prior to coronary angiography were included in the statin group. Crude and adjusted odds ratios (AOR) were calculated using univariate multiple logistic regression analysis. RESULTS: Out of 2055 patients (females = 30.7%, mean age 58.0 ±â€¯12.5 years, statin group = 886, non-statin group = 1169), 293 (14.3%) developed CI-AKI. Mean estimated glomerular filtration rate (eGFR) was not significantly different between the statin and the non-statin group (86.5 mL/min/1.73 m2 vs 87.1 mL/min/1.73 m2, p = 0.65). There was no significant difference in the incidence of CI-AKI between statin and non-statin group (14.4% vs 14.1%, p = 0.83). When adjusted for other risk factors, statin use was not significantly associated with decreased risk of CI-AKI (AOR) = 0.8, [95% confidence interval (CI) = 0.6-1.1, p = 0.19]. Results remained statistically non-significant on subgroup analysis of patients with acute coronary syndrome (ACS) (OR = 0.8, 95% CI = 0.6-1.2, p = 0.27), patients who had percutaneous coronary intervention (PCI) (OR = 1.1, 95% CI = 0.6-1.7, p = 0.81) and patients with eGFR < 60 mL/min/1.73 m2 (OR = 0.9, 95% CI = 0.6-1.5, p = 0.9). CONCLUSION: Statin use prior to coronary angiography is not associated with decreased incidence of CI-AKI.