RNA was purified from 39 strains of cell-cultured Junin virus (JUN) from ce
ntral Argentina, which included both human- and rodent-derived isolates (a
total of 26 and 13, respectively), as well as from 2 laboratory JUN strains
, XJ CI3 and XJ #44. JUN-specific primers were used to amplify a 511-nucleo
tide (nt) fragment of the nucleocapsid protein gene and a 495-nt fragment o
f the glycoprotein 1 (GP1) gene. Genetic diversity among JUN strains studie
d was up to 13% at the nt lever and up to 9% at the amino acid (aa) level f
or the GP1 gene and up to 9% (nt) and 4% (aa) for the NP gene. Phylogenetic
analyses of both genes revealed three distinct clades. The first clade was
composed of the JUN strains from the center of the endemic area and includ
ed the majority of JUN strains analyzed in the current study. The second cl
ade contained 4 JUN strains isolated between 1963 and 1971 from Cordoba Pro
vince, the western-most edge of the known endemic area. The third clade con
tained 4 JUN strains that originated from Calomys musculinus trapped in Zar
ate, the northeastern edge of the known endemic area. Certain JUN sequences
, which were obtained from GenBank and identified as XJ, XJ #44, and Candid
#1 strains, appeared to form a separate clade. Over 400 nt of the GP1 and
GP2 genes were additionally sequenced for 7 JUN strains derived from patien
ts with different clinical presentations and outcomes of Argentine hemorrha
gic fever. Analysis of the corresponding aa sequences did not allow us to a
ttribute any particular genetic marker to the changing severity or clinical
farm of the human disease. (C) 2000 Academic Press.