**5. Aspect of Lassa virus diagnosis**

mechanisms identifies double-stranded RNA that is only produced by negative-sense viral agents [34]. 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 signaling pathways that results in the translocation of interferon regulatory factor 3 (IRF-3) and other transcription factors to the nuclear material [9]. Translocated transcription factors enhance expression of interferons and , 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 dsRNAs [12]. 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.

There are four major characteristic hepatitis of LASV, which is derived:

**ii.** Distribution of multifocal hepatocellular necrosis randomly.

**iii.** Monocytic reaction to necrotic hepatocytes.

156 Current Topics in Tropical Emerging Diseases and Travel Medicine

**iv.** Hepatocellular mitoses.

observed simultaneously.

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 patients [35]. 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 agent [5, 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 development [6, 36]. Patients check physically after fever onset usually depicts facial oedema, bilateral conjunctival hemorrhages, purulent pharyngitis, and abdominal disorders [5]. 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 cells [5, 8].

**i.** Focal cytoplasmic degeneration of hepatocytes related to phagocytosed apoptotic fragments.

The physical impacts do not happen uniformly in all cases, rather in some instances can be

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 subjects [7, 36]. 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 sepsis [9]. In this subject Different diagnostic tests in the laboratory are carried out in order to check the presence of an infection and assess its course and complications. The unavailability of lab tests can compromise diagnosis confidence. The most disturbing factor is the presence of febrile illnesses in Africa that mimics the Lassa fever, such as typhoid fever especially for manifestations of nonspecific Lassa fever [31]. In illness with abdominal pain, in countries where the virus is epidemic, Lassa fever may be misdiagnosed as intussusception and appendicitis that leads to delay in treatments with the antiviral drug (ribavirin) [37]. In West Africa, where the virus is most prevalent, it is difficult for laboratory scientists to diagnose due to the absence of the right equipment to perform the tests [4].

The Federal Drug Administration (FDA) has not approved any widely validated laboratory test for the virus, but there are diagnostic tests, which have been able to provide definitive evidence of the presence of the virus [4, 14]. These tests include viral cultures, polymerase chain reaction (PCR) where the virus can be uncovered using reverse transcription PCR after first reverse transcribing the RNA of the virus into DNA, Enzyme Linked Immunosorbent Assay (ELISA) test, immunofluorescence test, and plaque neutralization. But, immunofluorescence tests give less definitive presence evidence of the viral presence. Other laboratory reports in the virus fever include thrombocytopenia, lymphopenia, and elevated aspartate aminotransferase levels in the blood. The viral agent can occasionally be present in cerebrospinal fluid [38, 39].

The following diagnostic methods are briefly discussed below.
