Antiviral and host response studies on Junín hemorrhagic fever virus using global gene expression profiles and qRT-PCR.

GARCÍA CC; TOMNI C; SEPÚLVEDA CS; MARTIN K; DAMONTE EB; BOSCH I

Bangkok

Congreso; 15th International Congress for Infectious Diseases; 2012

International Society for Infectious Diseases

Authors: C. Garcia1, C. Tomni1, C. Sepulveda1, K. Martin2, E. Damonte1, I. Bosch3; 1School of Sciences, University of Buenos Aires, Biochemistry, Buenos Aires/AR, 2Harvard-Massachusetts Institute of Technology, Division of Health Sciences and Technology , Cambridge, MA/US, 3Harvard-Massachusetts Institute of Technology, Division of Health Sciences and Technology, Cambridge, MA/US Title: Antiviral and host response studies on Junin hemorrhagic fever virus using global gene expression profiles and qRT-PCR Body: Background Several members of the Arenavirus, such as Junin virus (JUNV) and Lassa virus, cause hemorrhagic fever in human beings. The virions contain two bisegmented single-stranded RNA genomes, large (L) and small (S), that have ambisense coding strategy. The L fragment encodes the RNA-dependent RNA polymerase and a Zn-binding protein named Z, whereas the S fragment encodes the nucleocapsid protein (NP) and the glycoprotein precursor preGPC. In previous studies we have shown that disulfides compounds have antiviral and virucidal properties against arenaviruses. The present study is focused on the modulation of gene expression in a human hepatic cell lineage, HepG2, in response to Junín virus infection and the treatment with disulfide antiviral compounds characterized in our laboratory. Methods Using microarray data analysis, we investigated the global gene expression changes in HepG2-JUNV infected cells, after 24 and 48 hs in the presence or absence of the disulfide compounds. Results The obtained profile showed that these compounds lead to an increase in the metallothionein genes. This data was validated using qRT-PCR. In addition, the innate immunity genes were monitored in order to elucidate the host response to this virus. Conclusion The results presented here comprise part of the initial steps to guide the efforts toward the elucidation of the mechanisms triggered by disulfide compounds to block JUNV infection in liver cells.