Transcriptome Analysis of Human Peripheral Blood Mononuclear Cells Exposed to Lassa Virus and to the Attenuated Mopeia/Lassa Reassortant 29 (ML29), a Vaccine Candidate

Zapata, Juan Carlos; Carrion, Ricardo; Patterson, Jean L.; Crasta, Oswald; Zhang, Yan; Mani, Sachin; Jett, Marti; Poonia, Bhawna; Djavani, Mahmoud; White, David M.; Lukashevich, Igor S.; Salvato, Maria S.

LASV-induced perturbation of the cross-talk between integrins and the extracellular matrix [67] may contribute to the functional alterations of epithelial and vascular endothelial cells that precede shock and death in LF patients [95] . It is also possible that, during high states of viremia, LASV binds directly to platelets inhibiting their function. After an arterial injury, leukocytes are recruited to the site and there is an increase in ITGAM expression allowing adhesion of platelets and fibrinogen to the vessel walls [96] . We propose that LASV induction of ITGAM could increase platelet adhesion to tissues and this may explain the decreased number of circulating platelets during hemorrhagic episodes. Platelet-derived endothelial cell growth factor (PD-ECGF) is involved in angiogenesis and wound repair [97] , [98] . The differential expression of all those genes may be contributing to the non-pathogenic phenotype of ML29 and to the pathogenic phenotype of LASV.