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Available online at ajdhs.com 

Asian Journal of Dental and Health Sciences 
Open Access to Pharmaceutical and Medical Research 

Copyright  © 2022 The  Author(s): This is an open-access article distributed under the terms of the CC BY-NC 4.0 
which permits unrestricted use, distribution, and reproduction in any medium for non-commercial use provided the 

original author and source are credited 
 

 

 

An Overview of Lassa fever, an Rising Old World Haemorrhagic Viral 
Disease 

Basant Khare1, Dolly Jain1, Sameeksha Jain1, Monika Jain1, Pushpendra Kumar Khangar2, Deepak Kumar 
Jain3* 

1 Adina College of Pharmacy, ADINA Campus Rd, Lahdara, Sagar, MP, 470001 

2 Adina Institute of Pharmaceutical Sciences, NH86A, Lahdara, Sagar, MP, 470001  

3 Sun Institute of Pharmaceutical Education & Research (SIPER), Bhatpura Road, Lahar, Bhind, MP, 477445 

Article Info: 
_________________________________________ 
Article History: 

Received 10 Jan 2022      
Reviewed 22 Feb 2022 
Accepted 06 March 2022 
Published 15 March 2022 

_________________________________________ 
Cite this article as:  

Khare B, Jain D, Jain S, Jain M, Khangar PK, Jain DK, 
An Overview of Lassa fever, an Rising Old World 
Haemorrhagic Viral Disease, Asian Journal of 
Dental and Health Sciences. 2022; 2(1):20-26 

DOI: http://dx.doi.org/10.22270/ajdhs.v2i1.12                                 

_________________________________________ 

*Address for Correspondence:   

Deepak Kumar Jain, Sun Institute of 
Pharmaceutical Education & Research (SIPER), 
Bhatpura Road, Lahar, Bhind, MP, 477445 

Abstract 
___________________________________________________________________________________________________________________ 

Lassa fever is an acute immunosuppressive illness of increasing public health concern causing severe 
morbidity and significant mortality especially in epidemic cases. Lassa fever is an acute viral zoonotic 
illness caused by Lassa virus, an arenavirus known to be responsible for a severe haemorrhagic fever 
characterised by fever, muscle aches, sore throat, nausea, vomiting, chest and abdominal pain. The 
virus exhibits persistent, asymptomatic infection with profuse urinary virus excretion in the 
ubiquitous rodent vector, Mastomys natalensis. Lassa fever is endemic in West Africa and has been 
reported from Sierra Leone, Guinea, Liberia, and Nigeria. The virus replicates through a strategy 
known as the Ambisense, where two RNA strands code for genes in both the sense and antisense 
direction that is rapid and demonstrate temporal control in replication. Different diagnostic tests for 
the virus are available, which range from viral culture to serological and molecular diagnostic tests. 
There is an urgent need to develop drugs and vaccines against the virus because the World Health 
Organization (WHO) has identified Lassa virus as one of the viruses that is likely to cause a future 
epidemic, although a research is ongoing to evaluate Lassa virus vaccine immunogenicity in the 
CBA/J-ML29 mouse model. This review gives an overview on the structure, replication cycle, 
pathogenesis and diagnosis of the virus. 

Keywords: Lassa fever, Lassa virus, Arenavirus, Replication, Pathogenesis, Diagnosis 

Email: jaindeepak2022@gmail.com  

Introduction 

Lassa virus (LASV) is first described in the 1950s1 but not 
identified until 1969 in Jos, Nigeria2, 3. The virus causes Lassa 
fever that is hemorrhagic in nature, which is severe and fatal. 
It affects 2-3 million people annually4,5 and has been known to 
be endemic in Benin Republic in 2014, Ghana in 2011, Guinea, 
Liberia, and Mali in 2009, Sierra Leone, and Nigeria3,4,6, but 
probably exists in other West African countries as well4. It is a 
reemerging virus with a select agent, which requires Biosafety 
Level 4-equivalent containment7. It is endemic in West African 
countries including Sierra Leone, the Republic of Guinea, 
Nigeria, and Liberia, where cases of the infection is between 
300,000 and 500,000 yearly resulting in 5000 deaths 
annually4,8,9. About 80% infected with the virus are 
asymptomatic and 1 in 5 infection results in severe disease, 
where the virus affects several organs such as the liver, spleen, 
and kidneys10. The virus is harbored by the multimammate 
rats of the genus Mastomys and transmitted to Mans through 
primary aerosols of the rat’s urine, close contact with urine, 
feces, saliva, or ingestion of contaminated foods of the rat11. 
LASV is also spread through contaminated hospital equipment 
but interestingly, it cannot be contracted by humans to 
humans only via bodily fluids contacts12. Findings have 

reported the presence of the virus in seminal fluids up to 3 
months after infection of the virus. Research to show that 
Lassa virus can be gotten via sexual intercourse has not been 
reported but there are speculations that LASV might possibly 
be used for bioterrorism, so it is now being studied at greater 
lengths13,14. Due to the variability of the clinical course of the 
disease, detection of the disease in affected patients has been 
challenging. When presence of the virus is confirmed in a 
locality, quick isolation of infected patients, good infection 
prevention and control practices, and rigorous contact tracing 
can help halt epidemicity15. 

Epidemiology 

LASV is a single-stranded RNA virus of the Arenaviridae family. 
First identified in 1969 in Nigeria, Lassa fever is now endemic 
in West Africa including Nigeria, Sierra Leone, Guinea, Liberia, 
Benin, Ghana and Mali and has spread to neighboring 
countries (Figure 1). In some areas, 10%-16% of people 
admitted to hospitals every year have LASV. Cases have also 
been identified in Germany, the Netherlands, Sweden, the USA, 
the UK and Japan, largely imported after travel in West Africa. 
The long incubation period of LASV (~7–10 days) makes it one 
of the most commonly exported VHFs to countries outside its 
endemic range16. 

  

                       Open Access                                                                                                                                                                                                            Review  Article 

http://jddtonline.info/
http://dx.doi.org/10.22270/ajdhs.v2i1.12
mailto:jaindeepak2022@gmail.com


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Figure 1 Geographic distribution of Lassa fever in West Africa, Adapted from Emergencies-Lassa fever, WHO, Geographic 
distribution of Lassa fever in West African affected countries, 1969-2018 

 

Lassa virus structure 

Lassa virus is an envelope, single-stranded, bisegmented RNA 
virus belonging to the Arenaviridae family. Like other 
arenaviruses, Lassa virus lacks a conventional negative-strand 
coding arrangement and the isolates of the virus differ in their 
genetic, serologic and pathogenic characteristics17-19. Lassa 
virus is spherical in shape and measures between 70 and 150 
nm in diameter (Figure. 2). It has a smooth surface envelope 
with T-shaped spikes measuring 7-10 nm and built with 
glycoprotein. The envelope encloses the genome which has 
helical nucleocapsid measuring between 400 and 1300 nm in 
length20,21. Often the interior contains electron dense granule 
identified as the host cell ribosome from where the name 
“arena” was derived meaning sandy22. Lassa virus can be 
inactivated in ultraviolet, gamma irradiation, heating from 56-
100oC and pH range between 5.5 and 8.5. Chemical agents like 
0.5% sodium hypocorite, 0.5% phenol and 10% formalin are 
good inactivants against the virus23,24. The single-stranded 

arenavirus genome consists of a small (s) and a large (l) RNA 
fragment, sizes 3.4 and 7 kb, respectively and the sRNA 
encodes the viral glycoprotein precursor protein (GPC) and 
the nucleoprotein (NP), while the lRNA encodes the viral 
polymerase and a small, zinc-binding (Z) protein25. New 
methods for full-length sRNA amplification are facilitating 
research efforts on the identification and molecular analysis of 
new arenaviruses or arenavirus strains26. The sequencing of 
Lassa virus sRNA has enabled the identification and molecular 
characterization of four Lassa virus strains. These include: the 
strain Josiah, originating from Sierra Leone, the strain Nigeria 
and strain LP27,28, both from Nigeria and the strain AV 
imported into Germany by a traveler who had visited Ghana, 
Côte D’Ivoire, and Burkina Faso. Sequencing of sRNA of Lassa 
virus indicated a considerable genetic variation among the 
strains of the virus, however, phylogenetically, strain AV 
appears to be the most closely related to strain Josiah from 
Sierra Leone. 

 

 

Figure 2 Structure of Lassa virus 

Replication of Lassa virus 

The first step in viral replication is adsorption on cell surface 
receptors that are found to be widely distributed and highly 
conserved molecules29. The glycoprotein of the spikes is 
responsible for the interactions with cell surface receptors30. 
The next step is the penetration of the virus, then 
deproteinisation, and finally liberation of RNA genome into the 

infected host cytoplasm where both replication and 
transcription take place. During the process, the cell nucleus 
provides capped cellular mRNA for priming transcription, and 
the nuclear membranes provide structural support. It has 
been observed that the 5’ end of the S derived subgenomic 
mRNAs extend beyond the end of the genomic RNA template 
and thelength of such an extension varies between 1 and 7 
nucleotides and terminate at 5’ cap structure31. The initiation 



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of replication and transcription starts from the terminus of the 
template. As the RNA polymerase rails on the template to add 
new nucleotides that will form polynucleotide of the new 
strand, the first two slip back on the template to create 
nontemplated nucleus, a process peculiar to arenaviruses. 
After biosynthesis of macro-molecules, the virions are 
assembled through a process not yet understood. Matured 
virions are released through budding from the plasma 
membrane of acutely infected cells. 

Reservoir 

Mastomys natalensis multimammate rodents are the most 
common rodent across the African continent, found 
predominantly in rural areas and human dwellings. These 
rodents show persistent LASV infection but are largely 
unaffected by the disease and shed the virus in their 
excrement. Seroprevalence has been reported to be as high as 
60%-80% in M. natalensis populations. More recently, other 
rodent species including Hylomyscus pamfi and Mastomys 
erythroleucus have been shown to host LASV. Transmission to 
humans occurs primarily through contact with infected rodent 
urine or faeces; handling and consumption of infected rodents 
is also a pathway to infection. Airborne transmission may 
occur from aerosolised rodent excretions (dust) during 
cleaning activities.  M. natalensis rodents readily colonise 
human areas where food is stored, contributing a significant 
risk for spillover, especially in communities with poor 
sanitation or crowded living conditions. Human-to-human 
transmission is less common, but LASV can be spread through 
direct contact with bodily secretions of persons infected with 
Lassa fever, presenting a higher risk for healthcare and 
humanitarian personnel, who increases with progression of 
disease and increasing viral load. There are suspected sexual 
transmission risks, as LASV can be detected in semen for 3 
months past symptomatic infection16. 

Pathogenesis 

The Lassa virus is well-known to cause Lassa fever32. Its 
symptoms include flu-like illness characterized by fever, 
general body weakness, cough, tonsillitis, headache and 
gastrointestinal disorders. Hemorrhagic manifestations are 
other features of Lassa fever, which include vascular 
permeability10. The virus pathogenesis is still unclear, but it 
has been shown that the virus chiefly target the antigen-
presenting cells (mainly dendritic cells) and endothelial 
cells33. Lassa virus infects most tissues in the human body 
when gained entry. It starts with the mucosa, intestine, lungs, 
and urinary system, and then moves to the vascular system. 
There are findings that the viral agent can prevent a host’s 
innate immune system by NP activity34. Usually, when a 
microbe penetrates a host, the innate defense system detects 
the pathogen-associated molecular patterns (PAMPs) and 
aggravates the response of the immune system. One of 
themechanisms identifies double-stranded RNA that is only 
produced by negative-sense viral agents35. In the cytoplasm, 
dsRNA receptors, such as melanoma differentiation-associated 
gene 5 (MDA-5) and retinoic acid-inducible gene I (RIG-I), 
detects dsRNAs and facilitates ignaling pathways that results 
in the translocation of interferon regulatory factor 3 (IRF-3) 
and other transcription factors to the nuclear material9. 
Translocated transcription factors enhance expression of 
interferons 𝛂 and 𝛃, and secreted interferons facilitate 
antiviral responses including adaptive immunity. NP encoded 
in the viral agent is important in the replication and 
transcription of the virus, but it also stops host innate IFN 
response by inhibiting translocation of IRF-3. NP of the virus is 
reported to have an exonuclease activity to only dsRNAs12. 
Double-stranded RNA exonuclease activity of the NP leads to 
counteract IFN responses by digesting the PAMP that leads to 

the evasion of host immune responses. The recent 
understanding of the pathogenesis of the viral fever does not 
involve the chain of functions that take place during 
development of the disease state and leads to mortality of 
severed ill patients36. The high death and truly dramatic 
course of the disease state, the pathological findings do not 
give the bench that would explain the mechanism of disease 
progression and the cause of mortality by the viral agent5,8. 
Development of the cellular immune response failure, which 
would control dissemination of LASV is indicated by high 
serum titers of the virus, together with dispersed replication 
in tissues and lack of neutralizing antibodies that could lead to 
the fatal Lassa fever development6,37. Patientscheck physically 
after fever onset usually depicts facial oedema, bilateral 
conjunctival hemorrhages, purulent pharyngitis, and 
abdominal disorders5. Pathological changes physically may 
include pulmonary oedema, ascites, pleural effusions, and 
hemorrhagic signs in the gastrointestinal mucosa while 
examination under the microscope reveals splenic necrosis, 
hepatocellular necrosis, adrenocortical necrosis and 
apoptosis, mild mononuclear interstitial myocarditis without 
myocardial fiber necrosis, alveolar oedema with capillary 
blockage and mild interstitial pneumonitis, lymph nodal sinus 
histiocytosis with mitoses, gastrointestinal mucosal petechiae, 
renal tubular injury, lymph nodal sinus histiocytosis with 
mitoses, and interstitial nephri. More often, lesions of Lassa 
fever in man happen in the hepatic cells5,8. There are four 
major characteristic hepatitis of LASV, which is derived: 

 i. Focal cytoplasmic degeneration of hepatocytes related to 
phagocytosed apoptotic fragments. ii. Distribution of 
multifocal hepatocellular necrosis randomly. 

iii. Monocytic reaction to necrotic hepatocytes. 

iv. Hepatocellular mitoses. 

The physical impacts do not happen uniformly in all cases, 
rather in some instances can be observed simultaneously. The 
virus fever is not associated with coagulation dysfunction, for 
example, decrease in the coagulation factors and disseminated 
intravascular coagulation (DIC) have been revealed in infected 
subjects. More so, moderate thrombocytopenia with 
importantly damaged functionality of thrombocytes is 
reported in severe Lassa fever subjects7,37. One significant 
mechanism involved in the pathogenesis of Lassa fever is 
infection-triggered induction of uncontrolled cytokine 
expression, which looks like what is seen in sepsis9. In this 
subject that died from hemorrhagic shock and multi-organ 
failure, the proinflammatory cytokines, tumor necrosis factor 
α (TNF-α), and interferon γ (IFN-γ) rises to extremely high 
level just before death. In a related study, no increase of both 
cytokine levels was reported in the checked fatal cases of the 
virus fever, and it is suggestive that the levels of IFN-γ and 
TNF-α are either elevated only in a fraction of patients or 
during a limited period that would involve frequent sampling 
for assay12,35. Virus-induced immunosuppression may be 
involved in a severe Lassa fever pathogenesis where the LASV 
infection fails to trigger macrophages (MP) and monocyte-
derived dendritic cells (DC) of human. Human-infected DC 
with the naturally nonpathogenic mopeia virus induces 
stronger CD4 and CD8 T-cell responses when compared with 
those infected with LASV5,8. Infected DC fail to secrete 
proinflammatory cytokines, do not upregulate costimulatory 
molecules, such as CD40, CD80, and CD86, and poorly induce 
proliferation of T cells. Downregulation of immune responses 
due to infection by LASV has been depicted in vitro, and it is 
also in consonance with findings of clinical reports 
demonstrating that the virus fever fatal outcome relates with 
low levels interleukin (IL) 8 and IFN inducible protein 10 (IP-
10) in the system14. 



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Diagnosis 

The signs and symptoms of Lassa fever may be difficult to 
distinguish from diseases that are common in the tropics such 
as severe malaria, typhoid fever, yellow fever and other viral 
haemorrhagic fevers38-40, but diagnosis can be assisted with 
simple laboratory support but definitive diagnosis requires 
testing that is available only in highly specialized 
laboratories42. As the symptoms of Lassa fever are so varied 
and nonspecific, clinical diagnosis is often difficult especially 
early in the course of infection. Hence, to make accurate 
diagnosis of Lassa fever, clinical manifestation, 
epidemiological data and result of laboratory findings should 
be taken into consideration.  

Laboratory investigation: Lassa fever is diagnosed by detection 
of Lassa antigen, antibodies, or virus isolation techniques. In 
the laboratory, the virus can be isolated using laboratory 
animals such as albino mice, guinea pigs, Vero cell or African 
green mon keys. Albino mice inoculated intracerebrally die 
between 3 and 5 days. Lassa fever virus causes conspicuous 
cytopathic effect on confluent monolayer of Vero cell culture 
within 96 h. The antigens to be used for viral isolation can be 
obtained from the patients blood, urine, pleural fluid, throat 
swab and in case of death, pathological materials from liver, 
kidney, spleen and heart41. The virus can be seen under 
electron microscope using specimens obtained from infected 
persons. Although virus isolation remains the most sensitive, 
it is still uniquely a research tool. The classical method to 
detect Lassa virus is inoculation of Vero cells with serum, 
cerebrospinal fluid (CSF), throat washing, pleural fluid or 
urine of the patient. Specimen for laboratory analysis should 
be collected as soon as possible from the patient suspected of 
having the infection. Lassa virus is infectious by aerosol and 
the human and rodent specimens should be processed with 
appropriate precautions in biosafety level IV laboratories 42. 
The specific diagnosis is readily made by the isolation and 
identification of the virus. This is usually done by the 
inoculation of blood from the patient into Vero cell cultures. 
Virus antigen can be detected by enzymelinked 
immunosorbent assays (ELISA) using Lassa virus-specific 
antibodies. These tests are easy to handle and rapid, and can 
be performed with inactivated specimens, which is 
advantageous in the field if sophisticated equipment is not 
available. Results should be mentioned as soon as they are 
ready to help in monitoring the prognosis of the disease. The 
indirect fluorescent-antibody (IFA) test has traditionally been 
employed in the laboratory diagnosis of acute Lassa virus 
infection43,44. Although the interpretation of IFA results is 
complicated by the presence of IFA during both acute and 
convalescent stages of infection and by the subjective nature 
of the assay, the appearance of IFA antibody early in the 
course of Lassa infection may be useful in identifying patients 
with poor prognosis. However, due to lack of specificity in 
populations in non-endemic areas45 the technique has been 
largely replaced by ELISA for Lassa virus antigen and Lassa 
virus-specific immunoglobulin M (IgM) and G (IgG) 
antibodies46-48. A thorough evaluation of the Lassa virus ELISA 
on field-collected samples to assess its true sensitivity and 
specificity was performed in Sierra Leone and Guinea in West 
Africa49. In the study, isolation of virus as detected by 
immunofluorescent stains for viral antigen along with a 
positive reverse transcription-PCR (RT-PCR) test on the 
isolate wasemployed as the “gold standard” test of Lassa virus 
infection. The results showed that the combined ELISA Ag/IgM 
assay was highly sensitive and specific for the diagnosis of 
Lassa fever and the antigen detection assay offered a 
particular advantage in providing early diagnosis as well as 
prognostic information. From this research, the technique 
appeared to be a better diagnostic tool for Lassa virus 
infection compared to other serological techniques. Although 

the RT-PCR assays are very sensitive, their applicability in the 
West African countries where Lassa fever is endemic is limited 
by issues of strain variation, cross contamination, lack of 
qualified personnel, inadequate facilities and expense50,51. 
Another valuable diagnostic tool is the rapid diagnostic 
immunoblot assay (RDIA) for Lassa fever. Unfortunately, its 
usefulness is limited by its low capacity to provide prognostic 
information and also its low sensitivity.  

Differential diagnosis: Lassa haemorrhagic fever must be 
differentiated from other febrile diseases like Ebola (Marburg) 
haemorrhagic fever, malaria, diphtheria, legionella, yellow 
fever, Congo-haemorrhagic fever, etc. Lassa fever virus has a 
peculiar natural reservoir rodent host (M. natalensis). It is very 
imperative that clinical assessment be combined with specific 
laboratory diagnosis to adequately identify the Lassa fever 
virus in order to commence early treatment which is 
paramount to the survival of infected individual52. 

Useful prevention/control measures 

Lassa fever transmission is enhanced by cohabitation of M. 
natalensis species of rodent with humans in their residences in 
the affected areas having access to water and food items in the 
household. These rats are also prepared and consumed as 
delicacies by many inhabitants of West African region53,54. 
Therefore, any control/preventive measures to be adopted 
must take cognizance of routes and mechanism of 
transmission of Lassa fever. The following measures are 
imperative in curtailing the regular epidemic outbreak and 
spread of Lassa fever in sub-Saharan region of Africa. These 
include: 

 Observance of general hygiene including personal and 
environmental hygiene by the populace. 

 Since Lassa fever transmission is associated with infected 
mouse (M. natalensis), therefore, every household needs to 
device all means geared towards preventing rats from 
having any contact with foods, water and utensils utilized 
by the household. This may be achieved by: -Covering of 
foods and water meant for human consumption regularly. -
Foods should be kept in tightly sealed containers. -Ready-
to-eat food item (such as gari) should not be spread in the 
open or by the roadside where rats can have access to it. 

 Public enlightenment campaign about Lassa fever should 
be conducted regularly in areas where the disease is 
prevalent.  

 Every community should be counseled to avoid foods and 
other items contaminated with rat’s excretions and 
secretions.   

 People should be admonished to kill and destroy rats in 
and around the house, shops or market places. 

 Foods and water should be boiled adequately before 
consumption. 

 Encourage members of the community to always attend 
healthcare centre nearest to them for medical attention 
when they are sick or have had contact with contaminated 
environment. 

 All persons suspected of Lassa virus infection should be 
admitted to isolation facilities and promptly attended to 
with utmost care. -Hospital workers should take universal 
precautions and protective measures when attending to 
such patients. -Every body fluids and excreta produced 
bysuch patients should be handled with care and properly 
disposed of.  



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 Early detection of the disease and aggressive treatment 
(such as the use of intravenous ribavirin) 55 is important 
for the survival of infected patient. 

 Healthcare workers should be sensitized about the need to 
adopt universal preventive measures in their routine 
hospital procedures to limit the transmission and 
acquisition of Lassa virus infection and indeed all 
infectious diseases in hospital setting. 

 Governments at all levels (National, State and Local) 
should demonstrate political will in mobilizing logistics 
and necessary materials and financial support to aid 
adequate management and effective control of Lassa fever. 

 More diagnostic and treatment centres for Lassa fever 
should be established at various regions of each country 
endemic for Lassa fever. 

 Development of effective vaccine against Lassa fever 
(which has reached advanced stage with positive results in 
animal trials) 56 is crucial in checkmating the spread of 
Lassa fever. 

Treatment 

Ribavirin the antiviral drug is effective in the treat ment of 
Lassa fever, but only if administered early in the course of 
illness57. In a study of Lassa fever in Sierra Leone, West Africa, 
it was observed that patients with a high risk of death who 
were treated for 10 days with intravenous ribavirin, begun 
within the first six days after the onset of fever, had a case-
fatality rate of 5% (1 of 20) (p = 0.0002 by Fisher’s exact test), 
while patients whose treatment began seven or more days 
after the onset of fever had a case fatality rate of 26% (11 of 
43) (p = 0.01). The study confirmed the efficacy of ribavirin in 
the treatment of Lassa fever and that it should be used at any 
point in the illness, as well as for post-exposure prophylaxis. 
Because of its expense, need for intravenous administration, 
potential toxicity and teratogenicity, empiric therapy with 
ribavirin is undesirable58-60. In a remote area of eastern Sierra 
Leone, West Africa, brief episodes of rigors were reported in 
patients receiving ribavirin. However, the occurrence or 
number of rigors in an individual patient was not associated 
with sex, age, weight, volume of loading dose, cumulative dose, 
and administration of other drugs and use of intravenous lines 
or heparin traps. The report indicated slowing the infusion 
rate, generated no further episodes and concluded that 
epidemiologic techniques are important tools in rapid 
assessment of unexpected events particularly when 
conducting trials in remote locations. Supportive treatment is 
often necessary and includes fluid replacement, blood 
transfusion, administration of paracetamol, phylometadione, 
ringer lactate, haemocoel quinine and broad spectrum 
antibiotics61. 

Conclusion/recommendations 

Lassa fever has emerged as one of the most prevalent, 
immunosuppressive and highly fatal haemorrhagic fevers 
endemic in sub-Saharan Africa particularly West and Central 
Africa. Transmission of the disease is influenced by 
cohabitation of reservoir rodent (M. natalensis) with human 
population and poor environmental hygiene common in most 
parts of the region resulting in regular outbreak of the disease 
and fatality. Currently, there are no clinically certified vaccines 
against Lassa fever which limits the scope of 
control/preventive measures against Lassa fever. 

Hence, there is need to intensify public educational or 
enlightenment program in all affected areas on the useful 
control measures against Lassa fever. The stakeholders need 
to prioritize the intervention, support and deterrent program 

and speed up the process leading to production of effective 
vaccine to checkmate the menace of Lassa fever outbreak and 
associated morbidity and mortality. 

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