Hantaviruses — Questions

Because hantavirus species cross-react serologically, a positive screen is confirmed with a species-specific or neutralisation assay.

The screen alone cannot identify the species, and culture, marrow biopsy and simply repeating the screen do not resolve it.

Despite profound capillary leak, true haemorrhage is uncommon in cardiopulmonary syndrome, which is dominated instead by pulmonary oedema and shock.

It does not spare the lungs, its case-fatality (~35 to 40%) is higher than most HFRS, and ribavirin has no proven benefit in it.

The virus infects endothelium without killing it, and disease follows from an immune-mediated rise in capillary permeability, so recovery leaves no vascular scarring.

It is not directly cytopathic, does not act through thrombosis or a toxin, and antibody-dependent enhancement is a dengue mechanism.

Like other members of the order Bunyavirales, hantaviruses prime their messenger RNA by cap-snatching, stealing capped fragments from host transcripts, entirely in the cytoplasm.

They do not use a poly-A primer, reverse transcription, ribozymes or nuclear splicing.

A vigorous cytotoxic CD8 T-cell response is closely associated with severe disease, its intensity tracking the degree of capillary leak, which is why the disease is largely immunopathological.

Conversely, a high early neutralising-antibody titre predicts a better outcome; low cytokines, rapid clearance and an absent response are not markers of severity.

Pathogenic hantaviruses use beta-3 integrins, receptors that also regulate vascular permeability and platelet function, linking entry to disease; non-pathogenic species use beta-1 integrins.

CD4 and CCR5 are HIV receptors, ACE2 is used by SARS-CoV-2, and sialic acid is an influenza receptor.

An El Nino-driven drought-then-rainfall sequence produced a boom in deer-mouse numbers, raising human exposure to Sin Nombre virus and causing the outbreak. It illustrates how climate cycles drive reservoir population dynamics and spillover.

HFRS runs through febrile, hypotensive, oliguric, diuretic and convalescent phases, with the greatest danger in the hypotensive and oliguric stages.

The other sequences are invented or belong to other diseases.

The genus is named after the Hantaan River in South Korea, near where Ho-Wang Lee isolated Hantaan virus from the striped field mouse in the 1970s.

It is not named for a scientist, a rodent, a Greek root or a patient.

Hantaviruses carry three negative-sense RNA segments, large, medium and small, encoding the polymerase, the glycoproteins and the nucleocapsid respectively.

The genome is not a single positive-sense strand, DNA of any kind, or an eight-segment genome (that is influenza).

The M segment encodes a precursor cleaved into the Gn and Gc envelope glycoproteins, which mediate receptor binding and fusion.

The S segment encodes the nucleocapsid, the L segment the polymerase; hantaviruses have no matrix protein and no reverse transcriptase.

Platelets are consumed at the damaged, activated endothelium rather than failing to be produced, and the fall is an early diagnostic clue.

Marrow production is preserved, and sequestration, vitamin deficiency and anti-megakaryocyte autoantibodies are not the mechanism.

Both syndromes typically begin about two to three weeks after exposure, after which a febrile prodrome opens the illness.

An interval of days, hours, months or a year does not fit the usual incubation.

The area should be ventilated and then wetted before cleaning, so the virus is not aerosolised.

Dry sweeping or vacuuming does exactly the opposite; there is no routine vaccine and no role for prophylactic ribavirin.

Severe cardiopulmonary syndrome may require extracorporeal membrane oxygenation, and corticosteroids have not been shown to help; care is otherwise supportive.

HFRS often needs dialysis, ribavirin does not cure cardiopulmonary disease, and antibiotics treat a viral illness only if bacterial co-infection arises.

Hantaviruses lack a matrix protein and assemble by budding at the Golgi, a shared bunyavirus feature.

They are enveloped, do not assemble at the plasma membrane, and do not integrate into host DNA.