The pathology of lassa fever

Edington, G. M.; White, Helena

doi:10.1016/0035-9203(72)90268-4

Cited by 80 publications

(38 citation statements)

References 8 publications

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“…Cellular depletion of lymphoid tissues, necrosis of the splenic marginal zone, and transitory lymphopenia have been described in patients (15,17). Dendritic cells massively release LV particles but are not activated and do not produce cytokines, probably leading to defective T-cell responses (2,41).…”

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confidence: 99%

Early and Strong Immune Responses Are Associated with Control of Viral Replication and Recovery in Lassa Virus-Infected Cynomolgus Monkeys

Baize

Marianneau

Loth

et al. 2009

J Virol

168

213

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Lassa virus causes a hemorrhagic fever endemic in West Africa. The pathogenesis and the immune responses associated with the disease are poorly understood, and no vaccine is available. We followed virological, pathological, and immunological markers associated with fatal and nonfatal Lassa virus infection of cynomolgus monkeys. The clinical picture was characterized by fever, weight loss, depression, and acute respiratory syndrome. Transient thrombocytopenia and lymphopenia, lymphadenopathy, splenomegaly, infiltration of mononuclear cells, and alterations of the liver, lungs, and endothelia were observed. Survivors exhibited fewer lesions and a lower viral load than nonsurvivors. Although all animals developed strong humoral responses, antibodies appeared more rapidly in survivors and were directed against GP 1 , GP 2 , and NP. Type I interferons were detected early after infection in survivors but only during the terminal stages in fatalities. The mRNAs for CXCL10 (IP-10) and CXCL11 (I-TAC) were abundant in peripheral blood mononuclear cells and lymph nodes from infected animals, but plasma interleukin-6 was detected only in fatalities. In survivors, high activated-monocyte counts were followed by a rise in the total number of circulating monocytes. Activated T lymphocytes circulated in survivors, whereas T-cell activation was low and delayed in fatalities. In vitro stimulation with inactivated Lassa virus induced activation of T lymphocytes from all infected monkeys, but only lymphocytes from survivors proliferated. Thus, early and strong immune responses and control of viral replication were associated with recovery, whereas fatal infection was characterized by major alterations of the blood formula and, in organs, weak immune responses and uncontrolled viral replication.

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confidence: 99%

Early and Strong Immune Responses Are Associated with Control of Viral Replication and Recovery in Lassa Virus-Infected Cynomolgus Monkeys

Baize

Marianneau

Loth

et al. 2009

J Virol

168

213

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“…In contrast, severe LV infections seem to be associated with high levels of viremia and immunosuppression. Structural changes, the cellular depletion of secondary lymphoid tissues, necrosis of the splenic marginal zone, transitory lymphopenia, and the abolition of mitogenic T cell proliferation have been described in patients and nonhuman primates (7,14,15). The infection of MP in vitro leads to the release of viral particles, but not to an increase in the synthesis of TNF-␣ and IL-8 (9).…”

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“…Death may occur in the context of hypotensive, hypovolemic, and hypoxic shock. In surviving patients, symptoms disappear 10 -15 days after onset (7). However, deafness is a common complication of Lassa fever, affecting about one-third of survivors (8).…”

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Lassa Virus Infection of Human Dendritic Cells and Macrophages Is Productive but Fails to Activate Cells

Baize

Kaplon

Faure

et al. 2004

The Journal of Immunology

191

208

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Lassa fever is a hemorrhagic fever caused by Lassa virus (LV), an old-world Arenavirus. Little is known about the immune responses that occur during the disease, but protection seems to be linked to the induction of cellular responses specific for viral glycoproteins. Conversely, severe Lassa fever may be associated with immunosuppression. We studied the infection of human dendritic cells (DC) and macrophages (MP) by LV. Both these cell types are susceptible to LV infection. Viral nucleoprotein was detected in DC and MP, and high and moderate viral titers were obtained with culture supernatants of DC and MP, respectively. LV did not induce apoptosis in DC and MP. These cells were not activated by LV infection. No change was observed in the expression of surface molecules involved in activation, costimulation, adhesion, and Ag presentation following LV infection, or in the functional properties of DC. Inflammatory cytokine production was not detected at the mRNA or protein level after LV infection of DC and MP. Thus, MP, and particularly DC, are crucial targets for LV and are probably involved in the early replication of LV from the initial site of infection. The lack of activation and maturation of cells following infection may be associated with the immunosuppression observed in severe LV infection.

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“…Nonspecific signs appear in patients after a 6-to 12-day incubation period. In the most severe cases, leading to death, more-specific symptoms of hypotensive, hypovolemic, and hypoxic shock are then observed, but the pathogenesis of LF remains unclear (25). The damage to the endothelium and other organs is not severe enough to account for terminal shock and death, which seem rather to depend on the host response (13).…”

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confidence: 99%

“…Elevated viremia and immunosuppression seem to characterize severe LV infections. Other features observed in patients and nonhuman primates (NHP) include structural changes, cellular depletion of secondary lymphoid tissues, necrosis of the splenic marginal zone, transitory lymphopenia, and abolition of mitogenic T-cell proliferation (7,25,27,28).…”

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confidence: 99%

Human Dendritic Cells Infected with the Nonpathogenic Mopeia Virus Induce Stronger T-Cell Responses than Those Infected with Lassa Virus

Pannetier¹,

Reynard²,

Russier³

et al. 2011

J Virol

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The events leading to death in severe cases of Lassa fever (LF) are unknown. Fatality seems to be linked to high viremia and immunosuppression, and cellular immunity, rather than neutralizing antibodies, appears to be essential for survival. We previously compared Lassa virus (LV) with its genetically close but nonpathogenic homolog Mopeia virus (MV), which was used to model nonfatal LF. We showed that strong and early activation of antigen-presenting cells (

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The pathology of lassa fever

Cited by 80 publications

References 8 publications

Early and Strong Immune Responses Are Associated with Control of Viral Replication and Recovery in Lassa Virus-Infected Cynomolgus Monkeys

Early and Strong Immune Responses Are Associated with Control of Viral Replication and Recovery in Lassa Virus-Infected Cynomolgus Monkeys

Lassa Virus Infection of Human Dendritic Cells and Macrophages Is Productive but Fails to Activate Cells

Human Dendritic Cells Infected with the Nonpathogenic Mopeia Virus Induce Stronger T-Cell Responses than Those Infected with Lassa Virus

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