Kinetic Study of Platelets and Fibrinogen in Lassa Virus-Infected Monkeys and Early Pathologic Events in Mopeia Virus-Infected Monkeys

Lange, James V.; Mitchell, Sheila; McCormick, Joseph B.; Walker, David H.; Evatt, Bruce L.; Ramsey, Rosemary B.

doi:10.4269/ajtmh.1985.34.999

Cited by 57 publications

(53 citation statements)

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“…Our clinical observations are consistent with those previously described in rhesus/cynomolgus monkeys and marmosets infected with the Josiah strain of LV (7,10,33): they include fever, anorexia, weight loss, and depression. In addition, acute respiratory syndrome and hypothermia were observed in the terminal stages in moribund monkeys.…”

Section: Discussionsupporting

confidence: 91%

“…Other mediators, such as anti-inflammatory cytokines or glucocorticoids, may counteract the effect of IL-6 and events downstream from IL-6 signaling, for example, decreased levels of prostaglandin E2, may inhibit fever (49). Transient thrombocytopenia was observed in all infected monkeys, whatever the outcome of the infection, as previously described (17,33). However, the number of circulating platelets remained low until death in fatalities but returned to baseline values in survivors.…”

supporting

confidence: 69%

“…Here, we report some virological, pathological, and immunological variables associated with fatal and nonfatal outcomes after LV infection of cynomolgus monkeys. Both rhesus monkeys (7,26,33,65) and cynomolgus monkeys have frequently been used as models for Lassa fever, and similar clinical signs and pathological events have been observed after LV infection in these closely related species (16,21,27,29,58). We used two different doses of virus to assess the influence of the viral inoculum on the disease course, and because the AV strain of LV has never been evaluated in primate models.…”

Section: Discussionmentioning

confidence: 99%

“…However, the number of circulating platelets remained low until death in fatalities but returned to baseline values in survivors. The thrombocytopenia could have been caused by either alterations of hematopoiesis or increased splenic pooling, as disseminated intravascular coagulation is not observed during LV infection in primates (33). Failure of the bone marrow to produce platelets is probably the main cause of thrombocytopenia, as suggested by Lange et al (33).…”

mentioning

confidence: 96%

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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

173

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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Section: Discussionsupporting

confidence: 91%

supporting

confidence: 69%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 96%

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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

173

213

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“…Mature DC are also susceptible to LV infection, although to a lesser extent than their immature counterparts. Thus, APC from the spleen and lymph nodes may also act as a reservoir for LV during the course of the disease, which is consistent with the presence of LV Ags in APC and the high viral load observed in the spleen and lymph nodes of LV-infected monkeys (26,27). Furthermore, other Arenaviruses, such as LCMV and Junin virus, are known to infect splenic DC and MP (17,20).…”

Section: Discussionsupporting

confidence: 53%

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

192

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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Pathogenesis of the Old World Arenaviruses in Humans

Lukashevich

2015

Human Emerging and Re‐emerging Infections

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Kinetic Study of Platelets and Fibrinogen in Lassa Virus-Infected Monkeys and Early Pathologic Events in Mopeia Virus-Infected Monkeys

Cited by 57 publications

References 0 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

Pathogenesis of the Old World Arenaviruses in Humans

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