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Recombinant human parainfluenza virus type 2 with mutations in V that permit cellular interferon signaling are not attenuated in non-human primates.

Abstract：

:The HPIV2 V protein inhibits type I interferon (IFN) induction and signaling. To manipulate the V protein, whose coding sequence overlaps that of the polymerase-associated phosphoprotein (P), without altering the P protein, we generated an HPIV2 virus in which P and V are expressed from separate genes (rHPIV2-P+V). rHPIV2-P+V replicated like HPIV2-WT in vitro and in non-human primates. HPIV2-P+V was modified by introducing two separate mutations into the V protein to create rHPIV2-L101E/L102E and rHPIV2-Delta122-127. In contrast to HPIV2-WT, both mutant viruses were unable to degrade STAT2, leaving virus-infected cells susceptible to IFN. Neither mutant, nor HPIV2-WT, induced significant amounts of IFN-beta in infected cells. Surprisingly, neither rHPIV2-L101E/L102E nor rHPIV2-Delta122-127 was attenuated in two species of non-human primates. This indicates that loss of HPIV2's ability to inhibit IFN signaling is insufficient to attenuate virus replication in vivo as long as IFN induction is still inhibited.

journal_name

Virology

journal_title

Virology

authors

Schaap-Nutt A,D'Angelo C,Amaro-Carambot E,Nolan SM,Davis S,Wise SM,Higgins C,Bradley K,Kim O,Mayor R,Skiadopoulos MH,Collins PL,Murphy BR,Schmidt AC

doi

10.1016/j.virol.2010.07.011

subject

Has Abstract

pub_date

2010-10-10 00:00:00

pages

65-79

issue

1

eissn

0042-6822

issn

1096-0341

pii

S0042-6822(10)00451-4

journal_volume

406

pub_type

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