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Infectious bursal disease (IBD) viruses detected in commercial flocks of different regions of Argentina were analyzed by reverse transcription-polymerase chain reaction-restriction fragment length polymorphism (RFLP) of a VP2 gene fragment, followed by sequence analysis. Two out of eight IBD viruses presented an SspI restriction site, typical of the very virulent phenotype. Three IBD viruses presented a SacI restriction site, typical of classic virulent strains, and one isolate presented restriction sites for both enzymes. The Argentine IBD viruses showed three different molecular patterns by RFLP with the restriction endonuclease BstNI and five different patterns with MboI. By comparison of nucleotide and deduced amino acid sequences of the hypervariable region of the VP2 protein, four Argentine viruses were found to be closely related to Brazilian subclinical strains and two isolates were found to be related to vaccine IBDV strains in use in Argentina. Strain LD9569 was genetically characterized as a very virulent strain and was found to be closely related to international and regional vvIBDV strains. This is the first report on variability of IBDV strains circulating in Argentina.

The aim of this study was to determine if Junin virus inactivated with formalin (FA) was immunogenic and able to elicit a protective response in the guinea pig. The XJ-Clone 3 strain of Junin virus grown in Vero cells was exposed to FA at 0 degrees C. The following inactivated antigens were prepared: A1, 0.1% FA for 50 hr; A2, 0.1% FA for 50 hr followed by concentration with polyethylene glycol (PEG); B1, 0.05% FA for 70 hr; B2, 0.05% FA for 70 hr plus PEG concentration; C, 0.1% FA for 50 hr followed by ultracentrifugation and purification by sucrose gradient. No residual infectivity was detected in any inactivated antigen either after two passages in newborn mice or by coculture with Vero cells. After immunization, high-neutralizing and low-immunofluorescent antibody titers wer obtained in adult mice and guinea pigs, thus showing that antigenicity was preserved. However, in spite of the presence of neutralizing antibodies, guinea pigs gained no protection against challenge with the highly pathogenic XJ strain. These results suggest that antibody amount and/or quality may be inadequate; alternatively, mechanisms other than humoral immunity, such as cellular response, not elicited by inactivated antigens may be essential for protection against Junin virus.