Abstract:More than 3,100 households in 27 selected villages distributed in the main geographic regions of Guinea were surveyed for the presence of Lassa virus-specific IgG antibodies (LVA), using an enzyme-linked immunosorbent assay (ELISA) with Lassa virus nucleocapsid protein expressed in insect cells infected with a recombinant baculovirus as antigen. The highest prevalence of LVA (25-55%) was found among inhabitants of tropical secondary forest (areas near Gueckedou, Yomou, and Lola) and guinea savannah (Faranah an… Show more
“…As suggested by murine experiments, ingestion of arenavirus [Rai et al, 1997] and of vectors expressing viral antigens [Djavani et al, 2000[Djavani et al, , 2001] provides immunity to lethal disease. Circumstantial evidence for mucosal immunity through virus ingestion comes from field observations: many individuals living in close contact with rodents and ingesting rodent-contaminated food are seropositive for Lassa virus but have never experienced Lassa fever disease [ter Meulen et al, 1996;Lukashevich et al, 1993;Childs and Peters, 1993]. Whether the mucosa simply serves to reduce the inoculum, to select attenuated variants, or to provide a protective immune response, it is clear that the mucosal route attenuates the infection substantially in comparison to the intravenous route.…”
Section: Subclinical Transient Mucosal Infection Of Rhesus Macaques Bmentioning
Arenaviruses can cause hemorrhagic fever and death in primates and guinea pigs, but these viruses are not highly pathogenic for most rodent carriers. In the United States, arenaviruses precipitated outbreaks of hepatitis in captive monkeys, and they present an emerging health threat in the tropical areas of Africa and South America. We describe infection of rhesus macaques with the prototype arenavirus, lymphocytic choriome-ningitis virus (LCMV), using the WE strain that has been known to cause both encephalopathy and multifocal hemorrhage. Five macaques were inoculated: two by the intravenous (i.v.) and three by the intragastric (i.g.) route. Whereas the two i.v.-inoculated monkeys developed signs and lesions consistent with fatal hemorrhagic fever, the i.g.-inoculated monkeys had an attenuated infection with no disease. Pathological signs of the primate i.v. infection differ significantly from guinea pig arenavirus infections and make this a superior model for human viral hemorrhagic disease.
“…As suggested by murine experiments, ingestion of arenavirus [Rai et al, 1997] and of vectors expressing viral antigens [Djavani et al, 2000[Djavani et al, , 2001] provides immunity to lethal disease. Circumstantial evidence for mucosal immunity through virus ingestion comes from field observations: many individuals living in close contact with rodents and ingesting rodent-contaminated food are seropositive for Lassa virus but have never experienced Lassa fever disease [ter Meulen et al, 1996;Lukashevich et al, 1993;Childs and Peters, 1993]. Whether the mucosa simply serves to reduce the inoculum, to select attenuated variants, or to provide a protective immune response, it is clear that the mucosal route attenuates the infection substantially in comparison to the intravenous route.…”
Section: Subclinical Transient Mucosal Infection Of Rhesus Macaques Bmentioning
Arenaviruses can cause hemorrhagic fever and death in primates and guinea pigs, but these viruses are not highly pathogenic for most rodent carriers. In the United States, arenaviruses precipitated outbreaks of hepatitis in captive monkeys, and they present an emerging health threat in the tropical areas of Africa and South America. We describe infection of rhesus macaques with the prototype arenavirus, lymphocytic choriome-ningitis virus (LCMV), using the WE strain that has been known to cause both encephalopathy and multifocal hemorrhage. Five macaques were inoculated: two by the intravenous (i.v.) and three by the intragastric (i.g.) route. Whereas the two i.v.-inoculated monkeys developed signs and lesions consistent with fatal hemorrhagic fever, the i.g.-inoculated monkeys had an attenuated infection with no disease. Pathological signs of the primate i.v. infection differ significantly from guinea pig arenavirus infections and make this a superior model for human viral hemorrhagic disease.
“…Lassa virus is carried primarily by the multimammate mouse Mastomys natalensis and causes up to 300,000 infections annually, of which approximately 30% result in disease varying from mild influenza-like illness to lethal hemorrhagic fever (HF) (23,38,40,41). It has been shown that hunting rodents and consuming their meat are major risk factors for rodent-to-human transmission (33,60). Our experimental studies with LCMV-infected mice (52,53) and monkeys (reference 35 and this study) indicate that oral inoculation leads to attenuated infections that occasionally cause disease.…”
mentioning
confidence: 99%
“…inoculation with high-dose LCMV-WE usually leads to subclinical infection, occasionally leads to disease, and rarely leads to death (I. S. Lukashevich et al, unpublished data). Taken together with the studies implicating consumption of rodents as a risk factor for infection, it is reasonable to propose that the mucosal route (via airways or the gastrointestinal tract) is a natural mode of virus transmission that could account for high levels of seropositive survivors in areas where Lassa virus is endemic (32,33,60).…”
Lymphocytic choriomeningitis virus (LCMV) and Lassa virus can cause hemorrhagic fever and liver disease in primates. The WE strain of LCMV (LCMV-WE) causes a fatal Lassa fever-like disease in rhesus macaques and provides a model for arenavirus pathogenesis in humans. LCMV-WE delivered intravenously or intragastrically to rhesus macaques targets hepatocytes and induces high levels of liver enzymes, interleukin-6 (IL-6), soluble IL-6 receptor (sIL-6R), and soluble tumor necrosis factor receptors (sTNFRI and -II) in plasma during acute infection. Proinflammatory cytokines TNF-␣ and IL-1 were not detected in plasma of infected animals, but increased plasma gamma interferon was noted in fatally infected animals. Immunohistochemistry of acute liver biopsies revealed that 25 to 40% of nuclei were positive for proliferation antigen Ki-67. The increases in IL-6, sIL-6R, sTNFR, and proliferation antigen that we observe are similar to the profile of incipient liver regeneration after surgical or toxic injury (N. Fausto, Am. J. Physiol. 277:G917-G921, 1999). Although IL-6 was not directly induced by virus infection in vitro, peripheral blood mononuclear cells from acutely infected monkeys produced higher levels of IL-6 upon lipopolysaccharide stimulation than did healthy controls. Our data confirm that acute infection is associated with weak inflammatory responses in tissues and initiates a program of liver regeneration in primates.
“…While the detection of a new positive IgG titer combined with an IgM response in the correct clinical setting may support a diagnosis of Lassa fever, the detection of a positive IgG response alone is insufficient to make a diagnosis. Lassa IgG titers may persist for decades (64), and seroprevalence studies in regions of endemicity have shown 4 to 55% of healthy individuals living in areas where the virus is endemic have detectable Lassa virus IgG titers (14,52,55,65,66).…”
Section: Antigen and Antibody Detection Assaysmentioning
Lassa virus remains an important cause of illness in West Africa and among the travelers returning from this region with an acute febrile illness. The symptoms of Lassa fever can be nonspecific and mimic those of other endemic infections, especially early in illness, making a clinical diagnosis difficult; therefore, laboratory testing is needed to confirm the diagnosis. An early identification of Lassa fever is crucial for maximizing the benefit of available antiviral therapy, as treatment efficacy rapidly decreases following the clinical onset of the disease. This minireview provides an overview of the currently available diagnostic tests for Lassa fever and their strengths and weaknesses.
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