Abstract
Enterovirus 70 (EV70), an etiological agent of acute hemorrhagic conjunctivitis (AHC), induces apoptosis in human Chang’s conjunctival (HCC) cells. EV70 is also able to infect and replicate in some other human cells such as human lens epithelial SRA01/04 cells and U937 cells. EV70 infection was found to induce apoptosis in SRA01/04 cells. During EV70-induced apoptosis of SRA01/04 cells, the expression levels of procaspase-3, 6 and 7 (all 32kD) were not increased, but procaspase-3 and 7 were activated (cleaved) while the constitutively activated caspase-6 decreased. Z-VD-FMK inhibited EV70-induced apoptosis and extracellular EV70 release, but not intracellular viral production. UV- or heat-inactivated EV70 did not induce apoptosis. Guanidine⋅HCl inhibited EV70 induced apoptosis in a multiple-step viral growth experiment but not in a one-step viral growth experiment. Cycloheximide and high concentration of methoxysuccinyl-Ala-Ala-Pro-Val-chloromethylketone (MPCMK) (0.5 mM) or elastatinal (Ela) (125 mM) also inhibited EV70-induced apoptosis. The results suggest that infectious EV70 is capable of inducing caspase-dependent (especially caspases-3 and 7-dependent) apoptosis in human lens SRA01/04 cells that requires the syntheses of viral proteins, but not viral genome RNA. The results suggest that (a) EV70 protease(s) (2A protease and probably 3C protease) produced during viral replication initiates EV70 induced apoptosis of SRA01/04 cells and (b) EV70 may use similar or same mechanism(s) to induce apoptosis in different human cells such as SRA01/04 and HCC cells.
Highlights
Enterovirus 70 (EV70) and coxsackievirus 24 variant (CA24v) are the etiological agents of acute hemorrhagic conjunctivitis (AHC), a highly contagious ocular disease that can affect individuals of all ages and both sexes[1,2]
We demonstrate that EV70 infection induced caspase-dependent apoptosis in SRA01/04 cells by a mechanism similar to the one for EV70 induced apoptosis in human Chang’s conjunctival (HCC) cells there exist some differences in the virus induced apoptosis in both cells
HCC and SRA01/04 cells, may suggest that the virus may use apoptosis to damage human conjunctival and corneal cells and other permissive human cells such as lens epithelial cells whenever these cells are accessible to this virus
Summary
EV70 and coxsackievirus 24 variant (CA24v) are the etiological agents of acute hemorrhagic conjunctivitis (AHC), a highly contagious ocular disease that can affect individuals of all ages and both sexes[1,2]. Natural and experimental EV70 infection is generally localized to the superficial conjunctival epithelial cell layer (i.e., conjunctivitis) and corneal epithelium (i.e., keratitis)[9,10] and results in AHC. It cannot infect and replicate in all kinds of human cells, EV70 has been found to be able to infect and replicate in a broad range of human cells including leukocyte cells (A2.01, Daudi, HL60, Jurkat, Raji, THP-1 and U937)[11] and human eye cells such as HCC cell[12], SRA01/04 cells[13], human retina and retina pigment epithelial cells (unpublished). We demonstrate that EV70 infection induced caspase-dependent apoptosis in SRA01/04 cells by a mechanism similar to the one for EV70 induced apoptosis in HCC cells there exist some differences in the virus induced apoptosis in both cells
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