Andes Virus: Neither “Just a Rodent Virus” Nor the Next Pandemic Virus

As infectious disease epidemiologists, we would frame Andes virus with two cautions at once: do not sensationalize it, and do not dismiss it.

While most hantaviruses are dead-end zoonoses in humans, Andes virus is different. It is a rodent-borne orthohantavirus found mainly in Argentina and Chile, but unlike other hantaviruses it has repeatedly been shown to transmit person-to-person, especially in close-contact settings. In the Chilean household-contact study, 16 of 476 household contacts developed hantavirus cardiopulmonary syndrome, and the risk was highest among sex partners: 17.6% versus 1.2% among other household contacts.  This does not rise to the level of casual-community spread, but it is real onwards transmission from contact with an infectious person.

The best illustration of a outbreak comes from Epuyén, Argentina, in 2018–2019. A single spillover from rodents led to 34 confirmed infections and 11 deaths. Three symptomatic people drove most of the spread, accounting for 21 of 33 secondary cases. The estimated reproductive number across the outbreak was 1.19, before control measures it was 2.1 and after isolation and quarantine, it fell to 0.96. The practical lesson here is that Andes virus can sustain chains of transmission under the ideal  social conditions favoring its spread, more importantly, this  transmission chains are interruptible with classic public-health measures. 

Superspreading is central to the Andes story. In Epuyén, transmission clustered around crowded social events: a birthday party, a socially active prodromal case, and a wake. The study’s investigators defined superspreaders as people causing four or more secondary infections; three patients met that threshold. Importantly, superspreading did not appear to require significant viral mutation and rather the  evidence pointed to high viral load,  elevated liver injury markers in the cases, and high-contact settings as risk factors. 

The timing of infectiousness is more nuanced than public messaging often allows. The strongest evidence points to symptomatic and early symptomatic transmission. In Epuyén, 17 of 33 secondary transmission events could be linked to the first day of fever in the primary case. But framing this as “only after obvious illness” is too categorical. A Chilean prospective study detected Andes viral RNA in peripheral blood cells 5–15 days before symptoms or antibody appearance among contacts who later became ill. That proves presymptomatic viremia but how this translates to plausible presymptomatic transmission remains unclear.

Asymptomatic transmission is even less certain. There is no strong evidence in humans that fully asymptomatic people are major drivers of Andes virus spread. However, the uncertainty has implications for quarantine and contact-tracing policies because incubation can be long, PCR testing can be negative early, and viral RNA may appear before symptoms. Animal data add biological plausibility to why this is more nuanced. In a study of experimentally infected Syrian hamsters shed Andes virus through oral, rectal, and urine routes, horizontal transmission occurred in 45% of naïve contacts, and infectious virus was shed by more than four inoculated animals. Still, the authors  rightly cautioned that virus infectious shedding kinetics in humans remain unresolved. 

Viral shedding studies support why close contact is the biggest concern. Andes viral RNA and antigens have been detected in blood and body fluids, including saliva, gingival crevicular fluid, urine, and respiratory or salivary pathways in multiple studies. A 2024 prospective Lancet Infectious Diseases study found persistent RNA detection in blood compartments and detectable RNA in saliva and gingival crevicular fluid during acute and convalescent phases, while earlier work reported Andes antigens and infectious virus in urine of acute patients. These findings support plausibility for close-contact, droplet/saliva, and possibly aerosolized-fluid transmission, but they do not mean Andes behaves like influenza, SARS-CoV-2, or measles. 

Considering the many unknowns on this virus the right public-health posture is proportional vigilance. Andes virus has a high case-fatality rate, often reported around 20–50% depending on setting and the available care. As such outbreaks demand rapid isolation of suspected cases, monitoring of close contacts through the incubation window, serial testing when indicated, respiratory protection for healthcare workers, and careful environmental rodent control. The current evidence says Andes virus spreads inefficiently in the community, efficiently enough in close-contact clusters to matter, and most dangerously when high viral burden meets crowded social behavior.

The virus is rare but the consequences of an outbreak that is not rapidly contained can be very real. That is what makes Andes virus exactly the kind of pathogen public health systems should take seriously before it has an opportunity to spread more widely.

Statements and views expressed in this commentary are solely those of the authors and do not imply endorsement by Harvard University, the Harvard Kennedy School, or the Belfer Center for Science and International Affairs.