Elevated thrombopoietin and platelet indices confirm active thrombopoiesis but fail to predict clinical severity of puumala hantavirus infection

Laine, Outi; Joutsi-Korhonen, Lotta; Lassila, Riitta; Huhtala, Heini; Vaheri, Antti; Mäkelä, Satu; Mustonen, Jukka

Hantaviruses are enveloped RNA viruses belonging to the family of Bunyaviridiae. In humans, they give rise to a spectrum of illnesses called hemorrhagic fever with renal syndrome (HFRS) in Eurasia and hantavirus cardiopulmonary syndrome (HCPS) in the Americas. HCPS carries a mortality rate of 40%, whereas the mortality in HFRS is lower (0.4%-15%), but the incidence of HFRS is substantially higher. Classically, HFRS occurs in 5 distinct phases: febrile, hypotensive, oliguric, polyuric, and convalescent. Capillary leakage, thrombocytopenia, and acute kidney injury (AKI) are the key elements in the pathogenesis of HFRS. Specific treatment is not available for hantavirus infection. [1] Low platelet count is a hallmark of hantavirus disease, but the severity of bleeding symptoms varies according to the hantavirus species. Signs of bleeding can be noted in up to one-third of the patients infected with the most common European hantavirus, Puumala virus (PUUV). Hemorrhage has been documented in various organs in fatal cases, [2] and mild mucocutaneous involvement has been reported in general. However, thromboembolic complications and increased risk of acute myocardial infarction and stroke have been reported to associate with PUUVinduced HFRS in Swedish patients. [3, 4] The individual balance between enhanced and hampered coagulation prevails and remains challenging.