Abstract:
:The rabies virus (RV) phosphoprotein P is a multifunctional protein involved in viral RNA synthesis and in counteracting host innate immune responses. We have previously shown that RV P gene expression levels can be regulated by using picornavirus internal ribosome entry site (IRES) elements. Here we exploited a particular feature of the foot-and-mouth disease virus (FMDV) IRES, namely, preferential initiation at a downstream initiation codon, to address the role of N-terminally truncated RV phosphoproteins usually generated in RV-infected cells through ribosomal leaky scanning. Recombinant RVs in which P synthesis was directed by the poliovirus or FMDV IRES produced full-length P (P1) or a truncated form (P2), as the dominant product, respectively. While the P2 overexpressing virus showed attenuated growth in interferon-incompetent cells, it was superior to the P1 overexpressing virus in preventing expression of host interferon-stimulated genes. This indicates that in RV infected cells the availability of the truncated P2 protein is critical for viral resistance to interferon.
journal_name
Eur J Cell Bioljournal_title
European journal of cell biologyauthors
Marschalek A,Drechsel L,Conzelmann KKdoi
10.1016/j.ejcb.2011.01.009subject
Has Abstractpub_date
2012-01-01 00:00:00pages
17-23issue
1eissn
0171-9335issn
1618-1298pii
S0171-9335(11)00019-7journal_volume
91pub_type
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journal_title:European journal of cell biology
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