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Key Points Hantaviruses are negative-sense single-stranded RNA viruses that infect many species of rodents, shrews, moles and bats. Hantaviruses primarily replicate in the endothelium and might use integrins to enter cells. Following entry, the virus synthesizes viral mRNA to produce viral proteins and replicate the genome (comprising small, medium and large segments), although the exact details of these processes remain unclear. The viral genome is encapsided by nucleocapsid protein to form ribonucleoproteins, which interact with viral glycoprotein to form virus particles. The three segments of viral RNA encode nucleocapsid protein, glycoprotein and RNA-dependent RNA polymerase. Infection of reservoir hosts is asymptomatic, possibly owing to immunosuppression. Infection of humans causes either haemorrhagic fever with renal syndrome or hantavirus cardiopulmonary syndrome. Disease pathology is characterized by increased permeability of the endothelial cells lining capillaries and is also thought to be mediated by enhanced immune responses, such as increased production of cytokines and expansion of cytotoxic T cells. Vaheri and colleagues discuss the molecular and cell biology of hantavirus infection and provide an overview of the virus-induced and immune-mediated pathology caused by this virus family in humans. Hantaviruses are negative-sense single-stranded RNA viruses that infect many species of rodents, shrews, moles and bats. Infection in these reservoir hosts is almost asymptomatic, but some rodent-borne hantaviruses also infect humans, causing either haemorrhagic fever with renal syndrome (HFRS) or hantavirus cardiopulmonary syndrome (HCPS). In this Review, we discuss the basic molecular properties and cell biology of hantaviruses and offer an overview of virus-induced pathology, in particular vascular leakage and immunopathology.

Hantaviruses, members of the order Bunyavirales, family Hantaviridae, have a world-wide distribution and are responsible for greater than 150,000 cases of disease per year. The spectrum of disease associated with hantavirus infection include hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS) also known as hantavirus cardiopulmonary syndrome (HCPS). There are currently no FDA-approved vaccines or treatments for these hantavirus diseases. This review provides a summary of the status of vaccine and antiviral treatment efforts including those tested in animal models or human clinical trials.

Hantavirus cardiopulmonary syndrome (HCPS) is a severe respiratory disease caused by Sin Nombre virus in North America (SNV). As of January 1, 2020, SNV has caused 143 laboratory-confirmed cases of HCPS in Canada. We review critical aspects of SNV virus epidemiology and the ecology, biology, and genetics of HCPS in Canada.

In late 2018, Andes virus was identified as the cause of an outbreak of hantavirus pulmonary syndrome in Argentina. This outbreak was associated with 34 confirmed infections and 11 deaths. A detailed investigation identified person-to-person transmission that was driven by three symptomatic persons.

During 2020-2023, we sequenced Bayou virus from 2 patients in Louisiana, USA, with hantavirus cardiopulmonary syndrome. Direct virus sequencing demonstrated an inferred evolutionary relationship to previous cases. Our findings demonstrate that separate virus spillovers cause isolated cases and probable wide distribution of Bayou hantavirus in rodents across Louisiana.

Hantavirus Pulmonary Syndrome (HPS), characterized by its high fatality rate, poses a significant public health concern in Argentina due to the increasing evidence of person-to-person transmission of Andes virus. Several orthohantaviruses were described in the country, but their phylogenetic relationships were inferred from partial genomic sequences. The objectives of this work were to assess the viral diversity of the most prevalent orthohantaviruses associated with HPS cases in the Central-East (CE) region of Argentina, elucidate the geographic patterns of distribution of each variant and reconstruct comprehensive phylogenetic relationships utilizing complete genomic sequencing. To accomplish this, a detailed analysis was conducted of the geographic distribution of reported cases within the most impacted province of the region. A representative sample of cases was then selected to generate a geographic map illustrating the distribution of viral variants. Complete viral genomes were obtained from HPS cases reported in the region, including some from epidemiologically linked cases. The phylogenetic analysis based on complete genomes defined two separate clades in Argentina: Andes virus in the Southwestern region and Andes-like viruses in other parts of the country. In the CE region, Buenos Aires virus and Lechiguanas virus clearly segregate in two subclades. Complete genomes were useful to distinguish person-to-person transmission from environmental co-exposure to rodent population. This study enhances the understanding of the genetic diversity, geographical spread, and transmission dynamics of orthohantaviruses in Central Argentina and prompt to consider the inclusion of Buenos Aires virus and Lechiguanas virus in the species Orthohantavirus andesense , as named viruses.

Dobrava-Belgrade virus (DOBV) is a human pathogen that has evolved in, and is hosted by, mice of several species of the genus Apodemus . We propose a subdivision of the species Dobrava-Belgrade virus into four related genotypes – Dobrava, Kurkino, Saaremaa, and Sochi – that show characteristic differences in their phylogeny, specific host reservoirs, geographical distribution, and pathogenicity for humans.

Finland has the highest incidence of hantavirus infections globally, with a significant impact on public health. The large coverage of boreal forests and the cyclic dynamics of the dominant forest rodent species, the bank vole Myodes glareolus, explain most of this. We review the relationships between Puumala hantavirus (PUUV), its host rodent, and the hantavirus disease, nephropathia epidemica (NE), in Finland. We describe the history of NE and its diagnostic research in Finland, the seasonal and multiannual cyclic dynamics of PUUV in bank voles impacting human epidemiology, and we compare our northern epidemiological patterns with those in temperate Europe. The long survival of PUUV outside the host and the life-long shedding of PUUV by the bank voles are highlighted. In humans, the infection has unique features in pathobiology but rarely long-term consequences. NE is affected by specific host genetics and risk behavior (smoking), and certain biomarkers can predict the outcome. Unlike many other hantaviruses, PUUV causes a relatively mild disease and is rarely fatal. Reinfections do not exist. Antiviral therapy is complicated by the fact that when symptoms appear, the patient already has a generalized infection. Blocking vascular leakage measures counteracting pathobiology, offer a real therapeutic approach.

Hantaviruses, members of the Bunyaviridae family, can cause two patterns of disease in humans, hantavirus hemorrhagic fever with renal syndrome (HFRS) and cardiopulmonary syndrome (HCPS), being the latter hegemonic on the American continent. Andesvirus is one of the strains that can cause HCPS and is endemic in Chile. Its transmission occurs through direct or indirect contact with infected rodents' urine, saliva, or feces and inhalation of aerosol particles containing the virus. HCPS rapidly evolves into acute but reversible multiorgan dysfunction. The hemodynamic pattern of HCPS is not identical to that of cardiogenic or septic shock, being characterized by hypovolemia, systolic dysfunction, and pulmonary edema secondary to increased permeability. Given the lack of specific effective therapies to treat this viral infection, the focus of treatment lies in the timely provision of intensive care, specifically hemodynamic and respiratory support, which often requires veno-arterial extracorporeal membrane oxygenation (VA-ECMO). This narrative review aims to provide insights into specific ICU management of HCPS based on the available evidence and gathered experience in Chile and South America including perspectives of pathophysiology, organ dysfunction kinetics, timely life support provision, safe patient transportation, and key challenges for the future. •Hantavirus cardiopulmonary syndrome provokes a reversible multiorgan failure.•Different strategies of timely provision of life support (including VA ECMO) have been implemented to face this challenge.•In this narrative review, we provide key concepts of the management of these patients obtained from accrued experience in Chile and available literature from the last decades.

The zoonotic transmission of hantaviruses from their rodent hosts to humans in North and South America is associated with a severe and frequently fatal respiratory disease, hantavirus pulmonary syndrome (HPS) 1 , 2 . No specific antiviral treatments for HPS are available, and no molecular determinants of in vivo susceptibility to hantavirus infection and HPS are known. Here we identify the human asthma-associated gene protocadherin-1 ( PCDH1 ) 3 – 6 as an essential determinant of entry and infection in pulmonary endothelial cells by two hantaviruses that cause HPS, Andes virus (ANDV) and Sin Nombre virus (SNV). In vitro, we show that the surface glycoproteins of ANDV and SNV directly recognize the outermost extracellular repeat domain of PCDH1—a member of the cadherin superfamily 7 , 8 —to exploit PCDH1 for entry. In vivo, genetic ablation of PCDH1 renders Syrian golden hamsters highly resistant to a usually lethal ANDV challenge. Targeting PCDH1 could provide strategies to reduce infection and disease caused by New World hantaviruses. New World hantaviruses—which cause a severe human respiratory disease—use surface glycoproteins to bind to the human protocadherin-1 protein and enter endothelial cells in vitro; depleting protocadherin-1 in Syrian golden hamsters largely protects against disease.