Open AccessVP5 and the N terminus of VP2 are not responsible for the different pathotype of serotype I and II infectious bursal disease virus
Author(s) -
AC Schröder,
A.A.W.M. van Loon,
D. Goovaerts,
Jens Peter Teifke,
Egbert Mundt
Publication year - 2001
Publication title -
journal of general virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.55
H-Index - 167
eISSN - 1465-2099
pISSN - 0022-1317
DOI - 10.1099/0022-1317-82-1-159
Subject(s) - infectious bursal disease , biology , serotype , virology , virus , chimera (genetics) , in vitro , reoviridae , gene , virulence , genetics , rotavirus
Two serotypes have been identified in infectious bursal disease virus (IBDV), a member of the family Birnaviridae . A reverse genetics system was used for generation of chimeras in genome segment A of the two serotypes, in which the complete viral VP5 gene and 3′ noncoding region (NCR), or parts thereof, were exchanged. The engineered viruses were characterized in vitro and in vivo in comparison to serotype I and II IBDV. Our results show that IBDV chimeras exhibit a different phenotype in cell culture compared to the wild-type viruses. In in vitro -cultivated bursal-derived cells, chimeric viruses infected B lymphocytes, as does serotype I IBDV. Surprisingly, serotype II virus was also able to infect in vitro -cultivated bursal cells, but these were neither B lymphocytes nor macrophages. After infection of susceptible chickens all chimeras replicated in the bursa of Fabricius (BF), and three chimeric viruses caused mild depletion of bursal cells. In contrast, after infection of chickens with a chimeric IBDV containing exchanged VP5 as well as 3′-NCR, no depletion was detectable. The serotype II strain did not replicate in the BF nor did it cause depletion of bursal cells. Thus, the origin of VP5 does not explain the different pathotype of IBDV serotype I and II.