#Classification Orthohantavirus is a genus of viruses that includes all hantaviruses (family Hantaviridae) that cause disease in humans.

Hantaviruses are transmitted mainly through aerosols and droplets that contain rodent excretions, as well as through contaminated food, bites, and scratches.

For HPS, initial symptoms are flu-like, with fever, headache, and muscle pain, followed by sudden respiratory failure.

For both HFRS and HPS, illness is the result of increased vascular permeability, decreased platelet count, and overreaction of the immune system.

They consist of the viral RNA, which is segmented into three parts and encased in helical nucleocapsids to form three ribonucleoprotein (RNP) complexes.

In 1978 in South Korea, the first hantavirus was isolated, Hantaan virus, and was shown to be responsible for the outbreak during the war.

Other symptoms include headache, lower back pain, nausea, vomiting, diarrhea, bloody stool, the appearance of spots on the skin (petechiae), and hemorrhaging in the respiratory treact.

Early symptoms include fever, headache, muscle pain, shortness of breath (dyspnea), and low platelet count (thrombocytopenia).

During the cardiopulmonary phase, there is elevated heart rate (tachycardia), irregular heartbeats (arrhythmias), and cardiogenic shock.

[16] Rodents can transmit hantaviruses to humans through aerosols or droplets from the excretions and through consumption of contaminated food.

It can also reportedly spread through human saliva, airborne droplets from coughing and sneezing, and to newborns through breast milk and the placenta.

[2] A 2021 systematic review, however, found human-to-human transmission of the Andes virus to not be strongly supported by evidence but nonetheless possible in limited circumstances, especially between close household contacts such as sexual partners.

[16] The expansion of agricultural land is associated with a decline in predator populations, which enables hantavirus host species to use farm monocultures as nesting and foraging sites.

[18][24] Sewers and stormwater drainage systems may be inhabited by rodents, especially in areas with poor solid waste management.

[24] Seroprevalence, which shows past infection to hantavirus, is consistently higher in occupations and areas that have greater exposure to rodents.

[20] Rodent species that carry hantaviruses inhabit a diverse range of habitats, including desert-like biomes, equatorial and tropical forests, swamps, savannas, fields, and salt marshes.

[18] The seroprevalence of hantaviruses in their host species has been observed to range from 5.9% to 38% in the Americas, and 3% to about 19% worldwide, depending on testing method and location.

[19][25] In some places, such as South Korea, routine trapping of wild rodents is performed to surveil hantavirus circulation.

[4] High humidity can benefit rodent populations in warm climates, where it may positively impact plant growth and thus food availability.

An example of this was the 1993 Four Corners outbreak in the United States, which was immediately preceded by elevated rainfall from the 1992-1993 El Niño warming period.

Heavy rainfall is a risk factor for outbreaks in the following months,[10] but may negatively affect incidence by flooding rodent burrows and nests.

Gn and Gc bind to cell receptors, regulate immune responses, and induce protective antibodies.

An open reading frame in the N gene on the S segment[28] of some orthohantaviruses also encodes the non-structural protein NS that inhibits interferon production in host cells.

[19] Each surface spike is composed of a tetramer of Gn and Gc (four units each) that has four-fold rotational symmetry, and extends about 10 nm out from the envelope.

Decay acceleration factors, complement receptors, and, for New World hantaviruses, protocadherin-1 have also been proposed to be involved in attachment.

[19][22][31] This fusion releases viral ribonucleoprotein complexes into the cell cytoplasm, which initiates transcription and replication by RdRp.

[16][19][22] The most common form of evolution for hantaviruses is mutations through single nucleotide substitutions, insertions, and deletions.

The exact evolutionary history of hantaviruses is likely obscured by many instances of genome reassortment, host spillover, and host-switching.

During the Second World War in 1942, an outbreak of disease with symptoms characteristic of hantavirus infection occurred in Salla, Eastern Lapland, Finland among German and Finnish soldiers.

[1] In 1993, an outbreak of highly lethal acute respiratory distress syndrome occurred in the Four Corners region of the United States.