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PUUV
PUUV Full Name
Puumala virus
PUUV Introduction
Puumala virus (PUUV) is an Old World hantavirus belonging to the family Hantaviridae, genus Orthohantavirus, and is the most common cause of hantavirus disease in Europe. First isolated in 1980 from bank voles (Myodes glareolus) in Puumala, Finland, PUUV is endemic across a vast geographic range spanning Fennoscandia, central Europe, the Balkans, and western Russia. The virus possesses a tri-segmented negative-sense single-stranded RNA genome comprising the L, M, and S segments, encoding the RNA-dependent RNA polymerase (RdRp), the glycoprotein precursor (cleaved to Gn and Gc), and the nucleocapsid protein (NP), respectively. PUUV is genetically heterogeneous, with multiple genetic lineages that correlate with the phylogeographic history of its bank vole reservoir. Infection in humans causes nephropathia epidemica (NE), a generally milder form of hemorrhagic fever with renal syndrome (HFRS) characterized by acute kidney injury, thrombocytopenia, and capillary leakage. PUUV is not transmitted person-to-person.
Figure 1. Puumala orthohantavirus: prevalence, biology, disease, animal models and recent advances in therapeutics development and structural biology.
PUUV targets vascular endothelial cells, particularly those of the renal microvasculature, leading to increased vascular permeability, interstitial hemorrhage, and acute kidney injury. The virus enters cells via α5β1 integrin-mediated endocytosis, with Gn mediating receptor engagement and Gc driving pH-dependent membrane fusion. The pathogenesis of NE involves a complex interplay between direct viral cytopathic effects and dysregulated host immune responses. PUUV infection triggers a robust cytokine response including elevated levels of TNF-α, IL-6, IL-10, and IFN-γ, contributing to the systemic inflammatory state. The NP actively suppresses type I interferon signaling, facilitating viral replication in endothelial cells. Platelet activation and dysfunction, complement activation, and increased vascular endothelial growth factor (VEGF) production collectively contribute to the capillary leak syndrome. The host cellular immune response, particularly CD8+ cytotoxic T lymphocytes targeting NP and glycoprotein epitopes, is critical for viral clearance but may also contribute to immunopathology in the kidney. Human leukocyte antigen (HLA) type influences disease severity, with certain HLA alleles associated with more severe or milder NE.
PUUV infection causes an estimated 5,000–10,000 cases of NE annually in Europe, with the highest incidence in Finland, Sweden, and parts of central Europe. The disease typically presents with fever, headache, abdominal pain, and oliguria, progressing to acute kidney injury requiring supportive care; hemodialysis is necessary in approximately 5% of cases, and the overall case fatality rate is below 0.5%. Diagnosis relies on detection of anti-PUUV IgM antibodies by ELISA using recombinant NP antigen, complemented by RT-PCR for acute-phase viral RNA detection. There is no licensed antiviral therapy or vaccine specifically for PUUV, and management is supportive with careful fluid balance and renal replacement therapy as needed. Ribavirin has been used empirically but lacks robust evidence of efficacy in NE. Multiple vaccine candidates are under development, including DNA vaccines, recombinant adenovirus vectors, and VLP formulations. Climate change and land use modifications are expanding the geographic range of bank voles, potentially increasing PUUV exposure risk in northern and central Europe, making vaccine development an increasing public health priority.
Alternate Names for PUUV
Puumala virus; PUUV; Bunyaviridae; Hanta virus Puumala strain; Hantaan virus Puumala strain; Andes virus; Amur virus; Azagny virus; Bayou virus; Black Creek Canal virus; Cano Delgadito virus; Calabazo virus; Carrizal virus; Dobrava-Belgrade virus; El Moro
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