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From November 2018 through February 2019, person-to-person transmission of Andes virus (ANDV) hantavirus pulmonary syndrome occurred in Chubut Province, Argentina, and resulted in 34 confirmed infections and 11 deaths. Understanding the genomic, epidemiologic, and clinical characteristics of person-to-person transmission of ANDV is crucial to designing effective interventions.Clinical and epidemiologic information was obtained by means of patient report and from public health centers. Serologic testing, contact-tracing, and next-generation sequencing were used to identify ANDV infection as the cause of this outbreak of hantavirus pulmonary syndrome and to reconstruct person-to-person transmission events.After a single introduction of ANDV from a rodent reservoir into the human population, transmission was driven by 3 symptomatic persons who attended crowded social events. After 18 cases were confirmed, public health officials enforced isolation of persons with confirmed cases and self-quarantine of possible contacts; these measures most likely curtailed further spread. The median reproductive number (the number of secondary cases caused by an infected person during the infectious period) was 2.12 before the control measures were enforced and decreased to 0.96 after the measures were implemented. Full genome sequencing of the ANDV strain involved in this outbreak was performed with specimens from 27 patients and showed that the strain that was present (Epuyén/18-19) was similar to the causative strain (Epilink/96) in the first known person-to-person transmission of hantavirus pulmonary syndrome caused by ANDV, which occurred in El Bolsón, Argentina, in 1996. Clinical investigations involving patients with ANDV hantavirus pulmonary syndrome in this outbreak revealed that patients with a high viral load and liver injury were more likely than other patients to spread infection. Disease severity, genomic diversity, age, and time spent in the hospital had no clear association with secondary transmission.Among patients with ANDV hantavirus pulmonary syndrome, high viral titers in combination with attendance at massive social gatherings or extensive contact among persons were associated with a higher likelihood of transmission. (Funded by the Ministerio de Salud y Desarrollo Social de la Nación Argentina and others.).

Andes virus, one of five hantaviruses known to cause hantavirus pulmonary syndrome (HPS), emerged in 1995 in southwestern Argentina ( Lopez et al. (1996) Virology 220, 223–226). The complete nucleotide sequence of Andes virus S genome segment was determined and compared with sequences of viral RNAs in autopsy tissues of more recently reported HPS cases from southwestern Argentina and south of Chile (cases ESQ H-1/96 and CH H-1/96). Andes virus S segment was found to be 1876 nucleotides in length and to encode the nucleocapsid protein (N), 428 amino acids in length. S segment analysis also revealed a long 5′ non-coding region (547 nucleotides) which displays three copies of an octanucleotide sequence repeat. Comparisons of S segment sequences of ESQ H-1/96 and CH H-1/96 (82% of the entire genome sequence) with the corresponding sequences of Andes virus revealed identities of 97.2% and 98.5%, respectively. Sequence motifs identical and in the same positions as exhibited in Andes virus 5′ non-coding region were found in both, ESQ H-1/96 and CH H-1/96 sequences. Three genome fragments of the M segment sequence of the viruses (representing approximately 34% of the entire sequence) were also analyzed. Comparisons of S and M segment sequences of Andes virus with the corresponding sequences of ESQ H-1/96 showed S and M segment identities which differ by less than 1.4%. Andes virus and CH H-1/96 have S segments that differ by 1.5% from one another while their M segment fragments differ by 5.5–8.2%. Phylogenetic analysis showed that Andes virus along with ESQ H-1/96 and CH H-1/96 form a distinct lineage within the clade containing Bayou and Black Creek Canal viruses. It also showed that Andes virus branch of trees derived from comparisons of S or M sequences differed. It is concluded that Andes virus variants causing HPS circulate east and west of the Andes mountains.

We studied hantavirus seroprevalence and virus variability in rodent populations in Diego Gaynor, northwest of Buenos Aires province, Argentina. Rodent samplings were conducted in railroads and cropfield borders in March and July 1999, September and December 2000, and March 2001. Antibody detection was performed by an enzyme link immunosorbent assay (ELISA), using the recombinant nucleoprotein of Andes (AND) virus as antigen. Tissue samples were taken from positive antibody individuals in order to confirm the presence of hantavirus genomic material and to identify virus genotypes. Akodon azaraewas the most abundant species, followed by Oligoryzomys flavescens, while Calomys laucha and C. musculinus were rarely caught. We found a rate of seroprevalence of 9.3% for a total sample of 291 A. azaraeand 13.5% for 37 O. flavescens. After molecular analyses of hantavirus, we confirmed the presence of hantavirus genomic material in 16 individuals with ELISA (+) results and two individuals with ELISA (-). Four amplimers for each species were sequenced and compared to the corresponding sequences of representative hantaviruses. We identified the AND Cent Lec from three O. flavescens, and the Pergamino virus from four A. azaraeand from one O. flavescens. A. azaraemales had higher seroprevalence than females, and heavier individuals showed higher seroprevalence than lighter ones. We did not find seroprevalence differences according to sex in O. flavescens,although this result may have been produced by the low sample size. The lowest seroprevalence was found in a period of high rodent density, when juveniles prevailed in the population. We found higher seroprevalences than those detected in previous studies for other localities of central Argentina where cases of hantavirus pulmonary syndrome (HPS) have been reported. The presence of AND Cent Lec virus in rodent populations of the study area, which is responsible of HPS cases in central Argentina, suggests that human populations are at risk of HPS disease, although there were not reported cases of this disease until today. Fil: Suárez, Olga V. Facultad de Ciencias Exactas y Naturales. Laboratorio de Ecología de Poblaciones; Argentina. Fil: Cueto, Gerardo. Facultad de Ciencias Exactas y Naturales. Laboratorio de Ecología de Poblaciones; Argentina. Fil: Cavia, Regino. Facultad de Ciencias Exactas y Naturales. Laboratorio de Ecología de Poblaciones; Argentina. Fil: Gómez Villafañe, Isabel E. Consejo Nacional de Investigaciones Científicas y Tecnológicas; Argentina. Fil: Bilenca, David N. Consejo Nacional de Investigaciones Científicas y Tecnológicas; Argentina. Fil: Edelstein, Alexis. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas; Argentina. Fil: Martínez, Valeria Paula. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas; Argentina. Fil: Miguel, Sergio. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas; Argentina. Fil: Bellomo, Carla. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas; Argentina. Fil: Hodara, Karina. Facultad de Ciencias Exactas y Naturales. Laboratorio de Ecología de Poblaciones; Argentina. Fil: Padula, Paula. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas; Argentina. Fil: Busch, María. Consejo Nacional de Investigaciones Científicas y Tecnológicas; Argentina.

Hantavirus pulmonary syndrome (HPS) has been documented in the Salta and Jujuy provinces of northern Argentina since 1991 and 1997, respectively, accounting for almost 50% of the cases of HPS reported in this country. Andes (AND) virus, specifically the AND virus Nort lineage, was previously associated with human disease in this region. Genetic analysis of viral medium RNA segments obtained from 18 HPS cases showed the existence of three AND virus Nort sublineages co-circulating in these two provinces. They showed a nucleotide sequence diversity of up to 11.1% between the sublineages. The putative site of infection of one of these cases (Sal3/97) was determined. A 100% nucleotide sequence identity was observed between the viral sequence found in patient Sal3/97 and in two virus-positive Oligoryzomys chacoensis captured in the same place where the case lived and worked. These results indicated the putative site of infection and identified this rodent species as the source of infection.

This paper analyzed the prevalence and distribution of serological reactivity to hantavirus (antibody against ANDES virus) of human population exposed to hantavirus and rodents trapped in the studied area. This study was developed in Salta (Orán and San Martín Departments), area with the highest incidence for Hantavirus Pulmonary Syndrome (HPS) in Argentina. In December 1997, 453 healthy people were studied by serology and 39 rodents by serology and PCR. The studied individuals were distributed as: 145 farm inhabitants (FI), 212 people living in the same dwelling with healthy individuals (controls) (Cco), 87 people living in the same dwelling with persons undergoing SPH in 1997 (cases) (Cca). Moreover, 19 physicians and nurses who cared for patients with SPH in 1997 were also studied. The prevalence of hantavirus infection among the studied population was 6.3%. The prevalence was 10.3% among FI, 6.9% among Cca and 3.3% among Cco (p0.02). There was no serological reactivity among PS. The prevalence in 39 trapped rodents was 10.2%, with infection only for Oligoryzomys chacoensis, O. flavescens and Akodon varius species. The prevalence of human cases with asymptomatic infection in Salta is higher than in other regions of the country, and we are presenting a hypothesis to explain these differences. The analyzed data suggest that in this region up to the time this study was performed, there would not have been person to person transmission of hantavirus. The transmission would be from rodent contact exclusively and mainly in ongoing deforestation areas and domestic habitat surrounding rural dwellings.