INFORMATION ON LASSA FEVER

INFORMATION ON LASSA FEVER

Lassa fever is an acute viral hemorrhagic fever caused by the Lassa virus first described in 1969 in the town of Lassa, in Borno State, Nigeria, in the Yedseram river valley at the south end of Lake Chad Clinical cases of the disease had been known for over a decade but had not been connected with a viral pathogen. The infection is endemic in West Africa countries, and causes 300,000 – 500,000 cases annually, with approximately 5,000 deaths. Outbreaks of the disease have been observed in Nigeria, Liberia, Sierra Leone, Guinea, and the Central African Republic, but it is believed infections also exist in Democratic Republic of the Congo, Mali, and Senegal. The primary animal host of the Lassa virus in the Natal Multimammate Mouse (Mastomys natalensis), an animal indigenous to most of Sub-Saharan Africa. 

GENOME

Lassa fever is caused by the Lassa virus, a member of the Arenaviridae family; it is an enveloped, single-stranded, bisegmented RNA virus. Republication for Lassa virus is very rapid, while also demonstrating temporal control in replication. There are two genome segments. The first replication step is transcription of mRNA copies of the negative-or minus-sense genome. This ensures an adequate supply of viral proteins for subsequent steps of replication, as proteins known as N and L are translated from the mRNA. The positive – or plus-sense genome then makes viral complementary RNA (vcRNA) copies of itself, which are + sense. The VCRNA is a template for producing – sense progeny but mRNA is also synthesized from it. The mRNA synthesized from vcRNA are translated to make the G (spike) proteins and Z proteins. Thus, with this temporal control, the spike proteins, which are on the outside of the virus particles, are produced last, making the infection more difficult for the host immune system to detect.

RECEPTORS

The Lassa virus gains entry into the host cell by means of the cell-surface receptor the alpha-dystroglycan (alpha-DG), a versatile receptor for proteins of the extracellular matrix. It shares this receptor with the prototypic arenavirus lymphocytic choriomeningitis virus. Receptor recognition depends on a specific sugar modification of alpha-dystroglycan by a group of glycosyltransferases known as the LARGE proteins. Specific variants of the genes encoding these proteins appear to be under positive selection in West Africa where Lassa is endemic. Alpha-dystroglycan is also used as a receptor by viruses of the New World clade C arenaviruses (Oilveros and Latino viruses). In contrast, the New World areanviruses of clades A and B, which include the important viruses Machupo, Guanarito, Junin, and Sabia.

VECTORS

Lassa virus is zoonotic (transmitted from animals), in that it spreads to man from rodents, specifically multi-mammate rats (mastomys natalensis). This is probably the most common rodent in equatorial Africa, ubiquitous in human households and eaten as a delicacy in some area. In these rata infection is in a persistent asymptomatic state.

PREVENTION

Control of the Mastomys rodent population is impractical, so measures are limited to keeping rodents out of homes and food supplies, as well as maintaining effective personal hygiene. Gloves, masks, laboratory coats, and goggles are advised while in contact with an infected person.

SYMPTOMS

After an incubation period of six to twenty-one days, and acute illness with multiorgan involvement develops. Non-specific symptoms include fever, facial swelling, and muscle fatigue, as well as conjunctivitis and mucosal bleeding.

TREATMENT

In the treatment of Lassa fever using Ribavirin was pioneered by Joe McCormick in 1979.