Definition: Chapare hemorrhagic fever (CHHF) is caused by Chapare virus, a single-strand RNA virus of the Arenaviridae family. Chapare virus is certainly zoonotic, or animal-borne. The limited clinical information about CHHF comes from a small, poorly described cluster of hemorrhagic fever cases in rural Bolivia. A single fatal case yielded the only clinical description and blood specimen to date.
Symptoms and Treatment: The symptoms of CHHF, as reported in the only described patient, resemble those of other South American hemorrhagic fevers, such as Argentine HF or Bolivian HF. The incubation period is unknown, but for Argentine hemorrhagic fever (AHF) is 6 to 16 days. The CHHF clinical course included: Fever, headache, articulation and muscle pain, vomiting. These symptoms were followed by deterioration with multiple hemorrhagic signs. The only described CHHF patient died 14 days after onset of symptoms. A patient must visit a doctor once the mentioned symptoms are becoming regular, although most of the times they are ignored or many a times diagnosed as something else too. Blood, platelet, and plasma replacement may be useful for Crimean-Congo hemorrhagic fever (CCHF). High-dose corticosteroids, immune globulin intravenous, and fresh frozen plasma have also been reported to be successful in CCHF.Infusion of convalescent plasma during the first 8 days of illness with Argentine HF reduces the mortality rate from 15-30% to less that 1%.
Statistics: In Australia disease statistics resulted as there are other viral receptors that are present in cells of the immune system, such as Clec-2 and DC-SIGN that binds HIV ; DC-SIGN also shows affinity for other lentiviruses and DENV. DC-SIGN, Axl, and Tyro3 are Ebola virus and LASV receptors. Ebola virus requires the cholesterol transporter Niemann-Pick C1 (NPC1) for cell entry. This receptor is found in cells that are affected by HFV, such as gastrointestinal epithelial cells, and hepatocytes. Although all these receptors that bind HFV in target cells are also present in platelets and MKs (and, in some cases, have been shown to mediate virus internalization), it remains unknown whether they interact with platelets in vivo or if virus internalization leads to successful replication or even propagation of these viruses.