by Okeke MI, Adekoya OA, Moens U, Tryland M, Traavik T, Nilssen O.
Hopp over seksjon - Til hovedinnhold - Topp
2004 | 2005 | 2006 | 2007 | 2008 | 2009 | 2010 | January - February - March - April - May - June - July - September - October - November - December
19.06.2009
Okeke MI, Adekoya OA, Moens U, Tryland M, Traavik T, Nilssen O. Comparative sequence analysis of A-type inclusion (ATI) and P4c proteins of orthopoxviruses that produce typical and atypical ATI phenotypes. Virus Genes. 2009 Jun 16. [Epub ahead of print]. DOI10.1007/s11262-009-0376-8 PMID: 19533319
Abstract
Some orthopoxviruses produce large proteinaceous intracellular bodies, known as A-type inclusions (ATIs) during infection of host cells. Virions associate with ATIs resulting in distinct phenotypes referred to as V(+), V(+/) and V(-). The phenotype V(+) has the virions embedded in the ATI matrix; V(-) has no virions embedded within or on the surface of the ATI matrix, whereas an aberrant phenotype, the V(+/) has virions only on the surface of ATIs. Viruses that do not produce ATI are designated as V(0). Recombinant viruses generated from a V(+) cowpox virus (CPXV) and a V(0) transgenic vaccinia virus (VACV) produced aberrant V(+/) ATIs. ATI phenotype is dependent on the A-type inclusion protein (Atip) and the P4c protein. We sequenced the atip and p4c genes of parental and progeny recombinant viruses as well as their flanking sequences. The atip and p4c open reading frames were identical in parental V(+) CPXV and hybrid V(+/) progenies. Our results suggest that additional viral gene(s) are required for the formation of wild type V(+) ATI.