An increase of Hantavirus Pulmonary Syndrome (HPS) cases around a southwestern Argentina town and in persons living 1400 km away but in contact with those cases was detected during the spring of 1996. In order to evaluate person-to-person transmission we compared the homology of PCR-amplified viral sequences of 26 Argentine and Chilean cases. Sixteen of them were epidemiologically linked cases and had the same sequence (Epilink/96) in the S segment 3' noncoding region and in the M segment partial G1 and G2 region (a total of 1075 nucleotides). Contrarily, two geographical and contemporary but nonepidemiologically related cases differed from Epilink/96 in the compared regions. No significant differences, such as glycosylation or hydrophilic pattern, were found between Epilink/96 and the other sequences. Nucleotide and deduced amino acid sequence homologies between samples from southern Argentina and Chile ranged from 90.9 to 100% and 96.4 to 100%, respectively. Phylogenetic analysis revealed that all the analyzed southwestern viruses belong to the Andes lineage. Although human infection principally occurs via inhalation of contaminated rodent excreta, our results with Andes virus show the first direct genetic evidence of person-to-person transmission of a hantavirus.

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Tacaribe virus (TV), the prototype of the New World group of arenaviruses, comprises a single phylogenetic lineage together with four South American pathogenic producers of hemorrhagic disease. The TV genome consists of two single-stranded RNA segments called S and L. A reconstituted transcription-replication system based on plasmid-supplied TV-like RNAs and TV proteins was established. Plasmid expression was driven by T7 RNA polymerase supplied by a recombinant vaccinia virus. Plasmids were constructed to produce TV S segment analogs containing the negative-sense copy of chloramphenicol acetyltransferase (CAT) flanked at the 5 and 3 termini by sequences corresponding to those of the 5 and 3 noncoding regions of the S genome (minigenome) or the S antigenome (miniantigenome). In cells expressing N and L proteins, input minigenome or miniantigenome produced, respectively, encapsidated miniantigenome or minigenome which in turn produced progeny minigenome or progeny miniantigenome. Both minigenome and miniantigenome in the presence of N and L mediated transcription, which was analyzed as CAT expression. Coexpression of the small RING finger Z (p11) protein was highly inhibitory to both transcription and replication mediated by the minigenome or the miniantigenome. The effect depended on synthesis of Z protein rather than on plasmid or the RNA and was not ascribed to decreased amounts of plasmid-supplied template or proteins (N or L). N and L proteins were sufficient to support full-cycle RNA replication of a plasmid-supplied S genome analog in which CAT replaced the N gene. Replication of this RNA was also inhibited by Z expression.

A fatal case of serologically confirmed hantavirus pulmonary syndrome (HPS) was recently reported in southwestern Argentina. Nucleotide sequence analysis of PCR fragments from conserved regions of the S and M genomic segments of the virus, amplified from RNA extracted from autopsy lung and liver tissues, showed the virus (referred as Andes virus) to be novel. Comparisons between Andes virus genome sequences with the corresponding sequences of the more closely related hantaviruses revealed differences at the amino acid level from 13.6 to 23.9% for G2 protein regions and from 8.5 to 12.5% for the amino terminal region of the nucleocapsid protein. Phylogenetic analysis using the maximum parsimony and maximum likelihood methods showed that Andes virus maps within the clade containing the HPS-associated viruses from North America. Within this group, Andes virus represents a unique lineage. This is, to our knowledge, the first report on the genetic characterization of a hantavirus from South America.