as na [1,2]. Moreover, EV71 has also been associated with fatal pulmonary edema, severe neurological complications, in-tiation, movement, and death [7-9]. To date, seven distinct groups of MAPKs have been characterized in mammalian Peng et al. BMC Microbiology 2014, 14:147 http://www.biomedcentral.com/1471-2180/14/147JNK1/2 and p38 MAPK activation by these virusesUniversity, No. 185 Juqian street, Changzhou, Jiangsu 213003, P. R. China Full list of author information is available at the end of the articlecluding encephalitis, meningitis, and a poliomyelitis-like syndrome [3,4]. Increasing evidences have found it to be the major etiological agent causing current outbreaks of HFMD in the Asia-Pacific region, including mainland China [2,5,6]. However, the molecular pathogenesis of EV71 infection remains obscure. cells, including extracellular regulated kinases (ERK1/2), JNK1/2/3, p38 MAPK (p38 α/β/γ/δ), ERK3/4, ERK5, ERK7/8 and Nemo-like kinase (NLK) [10-12]. Of these, the most extensive studies are ERK1/2, JNKs and p38 MAPKs. As previously reported, JNK1/2 and/or p38 MAPK pathways is required for infection and replica-tion of human immunodeficiency virus type 1, encepha-lomyocarditis virus, coxsackievirus B3, hepatitis C virus, herpes simplex virus 1, and the severe acute respiratory syndrome coronavirus [13-18]. The diverse effects of * Correspondence
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