It is believed that most infections with Lassa virus never go beyond “flu-like” illness. Of all Arenaviruses only LCMV, Junin, Machupo, Guanarito, Lujo and Lassa viruses have demonstrated the ability to confer human disease ranging from the onset of neurologic diseases or hemorrhagic fevers of varying severity.

The clinical presentation of Lassa fever usually begins with insidious progression of fever and general malaise that can progress to more severe symptoms within 1-2 weeks. Hepatitis (inflammation of the liver) is frequent and moderately severe in Lassa fever. Hemorrhaging, leukopenia and thrombocytopenia as well as neurologic signs are not quite as common in Lassa fever as compared to other hemorrhagic fevers such as Ebola and Marburg. Viral particles can be found in the blood of patients up to three weeks after the onset of infection and Lassa virus can be recovered from the urine for several weeks more.

Common symptoms associated with cases of Lassa fever include fever, sore throat, headache, red eyes, weakness, facial edema, retrosternal pain, generalized abdominal pain, epistaxis and haemoptysis. Other features include low blood pressure, raised pules rate, nasal flaring and bibasal crepitations. In severe cases bleeding from mucousal membranes such as the mouth can also be observed.

Severe cases of Lassa fever are usually associated with multi organ complications with significantly raised levels of liver enzymes such as AST and ALT. The serum from these patients can turn brownish in color and a significant degree of hemolysis can be observed. Whilst it is unknown what causes Lassa fever patients to succumb from the disease, doctors within the VHFC have consistently noted signs of acute kidney failure preceding fatal outcomes.

The antibody response is generally slow in infected patients and the presence of this can be detected by enzyme-linked immunosorbent assay (ELISA), lateral flow immuno assays (LFI), complement fixation, neutralization, and fluorescent antibody techniques. However, in Lassa survivors a long-lasting and vigorous production of antibodies occurs. Complement-fixing antibodies are short-lived, diminishing 5 to 12 months after disease onset. In contrast, neutralizing antibodies remain detectable for many years and can be found in many individuals across West Africa.

Cellular immunity mediated by CD8+ T cells is important for successful recovery for Lassa fever. Transfer of early-convalescent-phase antibodies does not appear to have a protective effect, whereas late antibodies neutralize the virus and are protective. Whilst the induction of the inteferon response has shown some beneficial effect, in general, Arenaviruses are relatively resistant to the antiviral activity of these mediators. All evidence suggests that once Lassa fever has resolved in human patients, viral clearance is complete and chronic infection is not established. Reinfection with Lassa virus is possible, but data suggest that it may be uncommon.

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