Brazilian haemorrhagic fever

Brazilian haemorrhagic fever (BHF) is caused by the Sabia virus. The Sabia virus, c and was isolated in Sao Paulo in 1990 as the causative agent of Brazilian haemorrhagic fever. Sporadic infections with the Sabia virus have only been described in the community of Sabia near Sao Paulo.

The natural reservoir for the Sabia virus is not known. It is suspected that it is a rodent that occurs in the area around the small Brazilian community of Sabia near Sao Paulo. Infections usually occur via excrements and secretions, as with the other arena viruses. Only very few infections with the Sabia virus have been reported so far. Secondary transmission from patients to medical staff has been described several times. In patients with viral haemorrhagic fever, large viral loads can often be detected in the blood and also in other secretions.

In Brazilian hemorrhagic fever, ainitial llgeneral symptoms such as malaise, headache, eye pain, conjunctivitis, hemorrhagic erythema, decreased reflexes are observed. Hemorrhagic manifestations (nosebleeds, vomiting, blood in the urine and bleeding into the oral cavity) may also be observed. The mortality rate is given as 15-30%.

Infections with the South American hemorrhagic fever viruses are mainly treated symptomatically. In many patients, light sedation (sedation) and pain treatment with opiates is recommended. Bleeding should be treated by transfusions of platelets and coagulation factors.

Control of the electrolyte and fluid balance, if necessary controlled balancing.

In individual cases, infusions of immunoplasmas (plasma from convalescent patients) have been therapeutically successful.

A commercial immunoglobulin does not yet exist.

The antiviral drug ribavirin seems to have a positive influence on the outcome of Junin and Machupo virus infections at least.

Animal experiments with the viral drug favipiravir have been successful in the treatment of arena virus infections (Gowen BB et al. 2017; Furuta Y et al. 2013), so that it can be assumed that this drug is also used in humans (see Favipiravir).

The Junin, Machupo, Guanarito and Sabia viruses belong to the New World arena virus family and occur in South America. These arena viruses are the cause of various hemorrhagic fever diseases such as:

• Argentine hemorrhagic fever
• Bolivian hemorrhagic fever
• Venezuelan hemorrhagic fever
• Brazilian haemorrhagic fever

The name arena virus is derived from a characteristic dark granulation (Latin arenosus = sandy) of the viruses in electron microscopic images. These are shown as ribosomes, which are included in the sprouting of the viruses.

The arena viruses consist of a lipid shell and are pleomorphic with an average diameter of 50-300nm. They contain 2 RNA segments, the L- and the S-segment, which contain the information for structural proteins (nucleocapsid protein and glycoproteins) and an enzyme (viral polymerase). In the finished virus, the nucleocapsid is stored protectively around the RNA. The glycoproteins G1 and G2 are anchored in the lipid envelope. They serve for the absorption and release of the L and S segments into the cytoplasm and are thus essential for recognition and penetration into the host cell. The reproduction of the viruses in the cell takes place via a viral polymerase.

1. Golden JW et al (2017) An attenuated Machupo virus with a disrupted L-segment intergenic region protects Guinea pigs against lethal Guanarito virus infection. Sci Rep 7:4679.
2. Gowen BB et al (2017) Enhanced protection against experimental Junin virus infection through the use of a modified favipiravir loading dose strategy. Antiviral Res 145:131-135.
3. Tani H et al (2018) Arenavirus research and antiviral candidate. Uirusu 68:51-62.
4. Furuta Y et al (2013) Favipiravir (T-705), a novel viral RNA polymerase inhibitor. Antiviral Res 100:446-454.