The Role of Mononuclear Blood Cells in Experimental Junin Virus Spread to the Central Nervous System

Medeot, Silvia; Contigiani, Marta Silvia; Sabattini, Marta S.; Cámara, Alicia

doi:10.1089/vim.1995.8.101

Cited by 4 publications

(5 citation statements)

References 6 publications

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“…The macrophage might also act as vehicle to transmit the virus to its target organs, the liver and the CNS. There is clearly precedence in the literature for viruses using the monocyte/macrophage to gain entry to the CNS in the case of Hepatitis C virus, Junin virus, Dengue virus, and HIV (Gras and Kaul, 2010;Koenig et al, 1986;Medeot et al, 1995;Miagostovich et al, 1997;Wilkinson et al, 2009). Further studies will need to be done to fully define the role of the macrophage in RVFV in vivo pathogenesis.…”

Section: Discussionmentioning

confidence: 99%

Rift Valley fever virus inhibits a pro-inflammatory response in experimentally infected human monocyte derived macrophages and a pro-inflammatory cytokine response may be associated with patient survival during natural infection

McElroy

Nichol

2012

Virology

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Rift Valley fever virus (RVFV) causes significant morbidity and mortality in humans and livestock throughout Africa and the Middle East. The clinical disease ranges from mild febrile illness, to hepatitis, retinitis, encephalitis and fatal hemorrhagic fever. RVFV NSs protein has previously been shown to interfere in vitro with the interferon response, and RVFV lacking the NSs protein is attenuated in several animal models. Monocytes and macrophages are key players in the innate immune response via expression of various cytokines and chemokines. Here we demonstrate that wild-type RVFV infection of human monocyte-derived macrophages leads to a productive infection and inhibition of the innate immune response via decreased expression of IFN-α2, IFN-β and TNF-α. Using a recombinant virus lacking the NSs protein, we show that this effect is mediated by the viral NSs protein. Finally, analysis of RVF patient samples demonstrated an association between a pro-inflammatory cytokine response and patient survival.

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Section: Discussionmentioning

confidence: 99%

Rift Valley fever virus inhibits a pro-inflammatory response in experimentally infected human monocyte derived macrophages and a pro-inflammatory cytokine response may be associated with patient survival during natural infection

McElroy

Nichol

2012

Virology

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“…A significant role for macrophages in the pathophysiology of JUNV infection has been indicated by studies in animal models, where they have been shown to produce high titres of infectious virus [31], [32]. Further, macrophage maturity has been shown to be important for age-related resistance to JUNV infection in the rat model [33].…”

Section: Discussionmentioning

confidence: 99%

Tacaribe Virus but Not Junin Virus Infection Induces Cytokine Release from Primary Human Monocytes and Macrophages

et al. 2011

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The mechanisms underlying the development of disease during arenavirus infection are poorly understood. However, common to all hemorrhagic fever diseases is the involvement of macrophages as primary target cells, suggesting that the immune response in these cells may be of paramount importance during infection. Thus, in order to identify features of the immune response that contribute to arenavirus pathogenesis, we have examined the growth kinetics and cytokine profiles of two closely related New World arenaviruses, the apathogenic Tacaribe virus (TCRV) and the hemorrhagic fever-causing Junin virus (JUNV), in primary human monocytes and macrophages. Both viruses grew robustly in VeroE6 cells; however, TCRV titres were decreased by approximately 10 fold compared to JUNV in both monocytes and macrophages. Infection of both monocytes and macrophages with TCRV also resulted in the release of high levels of IL-6, IL-10 and TNF-α, while levels of IFN-α, IFN-β and IL-12 were not affected. However, we could show that the presence of these cytokines had no direct effect on growth of either TCRV of JUNV in macrophages. Further analysis also showed that while the production of IL-6 and IL-10 are dependent on viral replication, production of TNF-α also occurs after exposure to UV-inactivated TCRV particles and is thus independent of productive virus infection. Surprisingly, JUNV infection did not have an effect on any of the cytokines examined indicating that, in contrast to other viral hemorrhagic fever viruses, macrophage-derived cytokine production is unlikely to play an active role in contributing to the cytokine dysregulation observed in JUNV infected patients. Rather, these results suggest that an early, controlled immune response by infected macrophages may be critical for the successful control of infection of apathogenic viruses and prevention of subsequent disease, including systemic cytokine dysregulation.

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“…In one another study, XJCl3 or Candid#1 production was detected in both adherent and non-adherent populations of PBMCs purified from guinea pig or C.musculinus 2–26 or 5–15 days p.i. respectively [ 80 , 81 ]. In addition, replication of JUNV has been observed in human monocytes and macrophages [ 82 ], as well as rat [ 83 ] and C. musculinus [ 84 ] macrophages cultures ex vivo .…”

Section: Target Cells and Cell Entrymentioning

confidence: 99%

“…Additionally, XJ infection became lethal (36% mortality rate) in normally virus-resistant adult rats upon pretreatment with silica [ 85 ]. Moreover, depletion of mononuclear phagocytes with silica treatment drastically reduced the Candid#1 neuroinvasion in C. musculinus [ 80 ].…”

Section: Target Cells and Cell Entrymentioning

confidence: 99%

Junín Virus Pathogenesis and Virus Replication

Grant

Seregin

Huang

et al. 2012

Viruses

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Junín virus, the etiological agent of Argentine hemorrhagic fever, causes significant morbidity and mortality. The virus is spread through the aerosolization of host rodent excreta and endemic to the humid pampas of Argentina. Recently, significant progress has been achieved with the development of new technologies (e.g. reverse genetics) that have expanded knowledge about the pathogenesis and viral replication of Junín virus. We will review the pathogenesis of Junín virus in various animal models and the role of innate and adaptive immunity during infection. We will highlight current research regarding the role of molecular biology of Junín virus in elucidating virus attenuation. We will also summarize current knowledge on Junín virus pathogenesis focusing on the recent development of vaccines and potential therapeutics.

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The Role of Mononuclear Blood Cells in Experimental Junin Virus Spread to the Central Nervous System

Cited by 4 publications

References 6 publications

Rift Valley fever virus inhibits a pro-inflammatory response in experimentally infected human monocyte derived macrophages and a pro-inflammatory cytokine response may be associated with patient survival during natural infection

Rift Valley fever virus inhibits a pro-inflammatory response in experimentally infected human monocyte derived macrophages and a pro-inflammatory cytokine response may be associated with patient survival during natural infection

Tacaribe Virus but Not Junin Virus Infection Induces Cytokine Release from Primary Human Monocytes and Macrophages

Junín Virus Pathogenesis and Virus Replication

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