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Microbiology · Bunyaviruses (hemorrhagic fevers, hantaviruses)

Hantaviruses

Hantavirus

Hantaviruses are a group of zoonotic viruses that cause severe human disease without the involvement of insect vectors. The primary target of the pathogen is the endothelium of small blood vessels, leading to systemic hemorrhages, acute renal or cardiopulmonary failure.

Endemicity in the Russian FederationThe Ural and Volga-Vyatka regions lead in incidence rates
Ecological group«Rodent-borne viruses» (non-transmissible, transmitted exclusively by rodents)
Primary transmission routeAerogenic (inhalation of dust contaminated with excreta of infected animals)
Epidemiological featureAn infected human is a dead-end host and is not contagious to others
ImmunityLifelong, protective antibodies persist for up to 25 years
5 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Epidemiology and infection reservoirs

On the territory of the Russian Federation, hantavirus infections consistently hold a leading position among all natural focal diseases. The pathogens belong to the group of so-called «roboviruses» (from English rodent-borne). Unlike many other hemorrhagic fevers, hantaviruses are non-transmissible—their spread is in no way associated with the bites of mosquitoes, ticks, or other blood-sucking arthropods.

Wild rodents serve as the main reservoir and source of infection, in whom the disease is asymptomatic but accompanied by massive and prolonged shedding of the stable virus into the environment along with urine, feces, and saliva. Depending on the ecological niche, two groups of carriers are distinguished:

  • Rodents of the forest complex: bank vole, red-grey vole, striped field mouse, and East Asian harvest mouse.
  • Rodents of the steppe complex: deer mice and cotton rats.

Human infection occurs via three main routes:

  1. Aerogenic (airborne dust): this is the leading mechanism. The virus enters the respiratory tract upon inhaling infected dust during cleaning of old buildings, agricultural work, logging, or even sleeping on hay.
  2. Fecal-oral: alimentary infection via food and water contaminated with rodent excreta, as well as contact transmission via dirty hands.
  3. Contact: upon direct contact of infected excreta with damaged skin, during the dressing of carcasses, or from a rodent bite.

Human susceptibility to the infection is extremely high.

Pathogenesis and effects on the body

The leading mechanism of disease development is the vasotropic action of the virus. Upon entering the body, the pathogen causes systemic destructive lesions of the walls of small blood vessels. Viremia typically lasts from 4 to 7 days.

Depending on the specific serotype of the virus, various target organs are affected:

  • In HFRS (hemorrhagic fever with renal syndrome), the main pathological changes occur in the kidneys, adrenal glands, hypothalamus, myocardium, and intestines.
  • In cardiopulmonary syndrome, the virus exhibits a pronounced tropism for the endothelium of pulmonary capillaries, causing massive lung damage.
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Hemorrhagic fever with renal syndrome (HFRS)

The incubation period for HFRS can range from 7 to 45 days, but most commonly lasts 2–3 weeks. The disease begins acutely and is accompanied by pronounced fever. The clinical picture is characterized by a strict cyclicity of successive phases:

  1. Febrile phase.
  2. Oliguric phase: a sharp decrease in diuresis.
  3. Polyuric phase: a compensatory increase in the volume of excreted urine.
  4. Convalescence: gradual recovery.

The course of HFRS is often complicated by severe conditions. These include acute renal failure (uremia), kidney rupture or tearing of its capsule with massive hemorrhage into the surrounding tissue, pulmonary edema, and eclampsia. Due to systemic vascular damage, hemorrhages occur in the gastrointestinal tract, as well as hemorrhages in the brain and myocardium.

Case fatality directly depends on the strain: European variants of the virus cause death in 1–2% of cases, whereas Far Eastern strains (circulating in the Russian Federation) are more aggressive—mortality reaches 5–10%.

Hantavirus cardiopulmonary syndrome (HCPS)

This form of infection historically became widely known following a major outbreak in the USA in 1993, when the disease demonstrated an extremely high case fatality rate (over 50%). The causative agent was then identified as the Sin Nombre virus (fifth serotype), with deer mice acting as the natural reservoir. Geographically, the disease is distributed in North, Central, and South America.

The incubation period lasts about 6 weeks. The disease begins with a short prodrome featuring fever, which rapidly transitions into a phase of severe cardiopulmonary failure against the background of massive pneumonia. The prognosis for HCPS is extremely serious, with mortality rates reaching 50–60%.

Immunity and diagnostic principles

Past infection leaves behind lasting, lifelong immunity. Re-infections with a homologous viral serotype have not been registered, and protective antibodies can be detected in human blood for up to 25 years.

The following methods are used for microbiological diagnostics:

  • Virological: isolation of the pathogen from the patient's blood and urine (effective only in the acute period).
  • Serological: detection of specific antibodies in paired blood sera and urine.
  • Indication of viral antigens: allows for the rapid detection of viral proteins in the test material.

Briefly: answers to topical questions

What methods are used for laboratory diagnostics of hantavirus infection?

Laboratory diagnostics of hantavirus infection employs virological, serological, and molecular-genetic methods, as well as the indication of viral antigens.

  • Virological method — isolation of the virus from blood and urine during the acute period of the disease.
  • Serological method — detection of antibodies in paired sera and urine. This utilizes the indirect immunofluorescence assay (IFA) with mandatory assessment of the increasing titer of specific antibodies.
  • Molecular-genetic method — determination of hantavirus RNA in blood using the polymerase chain reaction (PCR).

Which hantavirus serotypes circulate in Eurasia and cause HFRS?

Hemorrhagic fever with renal syndrome (HFRS) is caused by European and Far Eastern strains of hantaviruses. HFRS pathogens include the following serotypes:

  • Hantaan — HFRS pathogen.
  • Puumala — HFRS pathogen.
  • Seoul — HFRS pathogen.
  • Dobrava/Belgrade — HFRS pathogen.

In the Russian Federation, the Ural and Volga-Vyatka regions are endemic for HFRS. The direct distribution of specific serotypes across the entire territory of Eurasia is not detailed in the texts.

How to memorize

To memorize the phases of HFRS, use the acronym LOPR: Febrile → Oliguric (low urine) → Polyuric (high urine) → Convalescence (recovery).

Class and exam questions

Can one contract a hantavirus infection from an infected person?

No, an infected person is a biological dead end for the virus and poses no epidemiological danger to others.

Are hantaviruses transmitted by mosquitoes or ticks?

No, hantaviruses belong to the group of «roboviruses» and are non-transmissible. They are transmitted exclusively by rodents (primarily through their excreta).

What is the mechanism underlying severe complications upon infection?

The main mechanism is the vasotropic action of the virus, i.e., systemic destructive damage to the walls of small blood vessels.

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What else to study on this topic

  • Morphology and antigenic structure of hantaviruses
  • Features of the Sin Nombre virus and the 1993 outbreak
  • Mechanisms of renal failure development in HFRS
  • Modern approaches to specific and non-specific prevention
  • Detailed analysis of serological reactions to confirm the diagnosis

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