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Lassa Fever Virus

I. General Information

1. NCBI Taxonomy ID:

2. Disease:

Lassa fever

3. Introduction

Lassa fever is a viral haemorrhagic fever caused by an arenavirus. Arenaviruses produce mostly silent, persistent infection in rodents, and their origin is thought to date back to the evolution of different rodent species, perhaps as much as 9 million years ago. Accidental human exposure to the virus is frequent. Lassa fever begins insidiously, after an incubation period of 7–18 days, with fever, weakness, malaise, severe headache, and a very painful sore throat. Up to a third of hospitalized Lassa fever patients progress to a prostrating illness 6–8 days after onset of fever, usually with persistent vomiting and diarrhea. Bleeding is seen in only 15–20% of patients, limited primarily to the mucosal surfaces or occasionally conjunctival haemorrhages or gastrointestinal or vaginal bleeding. Severe pulmonary edema and acute respiratory distress syndrome is common in fatal cases with gross head and neck edema and hypovolemic shock. Lassa fever has considerable long-term sequelae, in that nearly 30% of patients with Lassa fever infection suffer an acute loss of hearing in one or both ears. About half of these patients show a near or complete recovery by 3–4 months after onset, but the other half continue with significant sensorineural deafness, which after about a year will be permanent (Fisher-Hoch et al., 2001).

4. Microbial Pathogenesis

Disease is associated with destruction of antigen specific cytotoxic T lymphocytes (CTLs), causing leukopenia, decreased hemoglobin concentration, elevation of liver aminotransferases, and liver lipidosis. Pathogenesis involves initial replication at the site of infection. Lymph node, lung, and other parenchymal organs are important sites of viral growth. Interstitial infiltrates and edema occur during infection, and the macrophage is early and prominently involved. Many epithelial structures contain antigen and nucleic acids, with widespread marginal zone infection and splenic lymphoid follicle necrosis are common findings (Botten et al., 2006).

5. Host Ranges and Animal Models

The natural host is a small African rat, Mastomys natalensis (Fisher-Hoch et al., 2001).

6. Host Protective Immunity

Detectable neutralizing antibodies are absent during acute Lassa virus infection. Low-titer neutralizing antibodies may appear several weeks to months after the resolution of infection. Treatment of LF patients with immune plasma does not protect against disease. These observations strongly suggest that antibody response is not important, instead, cell-mediated immunity is critical for protection against LASV infection in humans. LASV-specific CD4+ T cells have been found in convalescent patients, and CD8+ T-cell response is the main determinant responsible for providing protection against LASV infection (Botten et al., 2006).

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