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Junín Virus Pathogenesis and Virus Replication
Ashley Grant,Alexey Seregin,Cheng Huang,Olga Kolokoltsova,Allan Brasier,Clarence Peters,Slobodan Paessler
Viruses , 2012, DOI: 10.3390/v4102317
Abstract: 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.
Host immunity in the protective response to vaccination with heat-killed Burkholderia mallei
Gregory C Whitlock, Roman A Lukaszewski, Barbara M Judy, Slobodan Paessler, Alfredo G Torres, D Mark Estes
BMC Immunology , 2008, DOI: 10.1186/1471-2172-9-55
Abstract: While protection with heat-killed bacilli did not result in sterilizing immunity, limited protection was afforded against an otherwise lethal infection and provided insight into potential host protective mechanisms. Our results demonstrated that mice depleted of either B cells, TNF-α or IFN-γ exhibited decreased survival rates, indicating a role for these effectors in obtaining partial protection from a lethal challenge by the intraperitoneal route. Additionally, complement depletion had no effect on immunoglobulin production when compared to non-complement depleted controls infected intranasally.The data provide a basis for future studies of protection via vaccination using either subunit or whole-organism vaccine preparations from lethal infection in the experimental BALB/c mouse model. The results of this study demonstrate participation of B220+ cells and pro-inflammatory cytokines IFN-γ and TNF-α in protection following HK vaccination.Burkholderia mallei, the etiologic agent of glanders, is a gram-negative, capsulated, non-motile, facultative intracelluar bacterium. Most known members of the Burkholderiaceae are resident in the soil; however, B. mallei is thought to be an obligate mammalian pathogen. Horses are highly susceptible to infection and considered the natural reservoir for infection, although mules and donkeys are also susceptible [1]. Clinically, glanders in solipeds can present as either a chronic (horses) or acute (mules and donkeys) form. Naturally acquired human infection with B. mallei, although not seen in the United States since 1945, has occurred rarely and sporadically among laboratory workers and those in direct contact with infected animals [2]. However, glanders is endemic among domestic animals in Africa, Asia, the Middle East, and Central and South America. The course of infection is dependent on the route of exposure. Direct contact with the skin can lead to a systemic infection. Inhalation of aerosol or dust containing B. mallei can le
Potent Inhibition of Junín Virus Infection by Interferon in Murine Cells
Cheng Huang,Aida G. Walker,Ashley M. Grant,Olga A. Kolokoltsova,Nadezhda E. Yun,Alexey V. Seregin,Slobodan Paessler
PLOS Neglected Tropical Diseases , 2014, DOI: 10.1371/journal.pntd.0002933
Abstract: The new world arenavirus Junín virus (JUNV) is the causative agent of Argentine hemorrhagic fever, a lethal human infectious disease. Adult laboratory mice are generally resistant to peripheral infection by JUNV. The mechanism underlying the mouse resistance to JUNV infection is largely unknown. We have reported that interferon receptor knockout mice succumb to JUNV infection, indicating the critical role of interferon in restricting JUNV infection in mice. Here we report that the pathogenic and vaccine strains of JUNV were highly sensitive to interferon in murine primary cells. Treatment with low concentrations of interferon abrogated viral NP protein expression in murine cells. The replication of both JUNVs was enhanced in IRF3/IRF7 deficient cells. In addition, the vaccine strain of JUNV displayed impaired growth in primary murine cells. Our data suggested a direct and potent role of host interferon response in restricting JUNV replication in mice. The defect in viral growth for vaccine JUNV might also partially explain its attenuation in mice.
Junín Virus Infection Activates the Type I Interferon Pathway in a RIG-I-Dependent Manner
Cheng Huang equal contributor,Olga A. Kolokoltsova equal contributor,Nadezdha E. Yun,Alexey V. Seregin,Allison L. Poussard,Aida G. Walker,Allan R. Brasier,Yingxin Zhao,Bing Tian,Juan Carlos de la Torre,Slobodan Paessler
PLOS Neglected Tropical Diseases , 2012, DOI: 10.1371/journal.pntd.0001659
Abstract: Junín virus (JUNV), an arenavirus, is the causative agent of Argentine hemorrhagic fever, an infectious human disease with 15–30% case fatality. The pathogenesis of AHF is still not well understood. Elevated levels of interferon and cytokines are reported in AHF patients, which might be correlated to the severity of the disease. However the innate immune response to JUNV infection has not been well evaluated. Previous studies have suggested that the virulent strain of JUNV does not induce IFN in human macrophages and monocytes, whereas the attenuated strain of JUNV was found to induce IFN response in murine macrophages via the TLR-2 signaling pathway. In this study, we investigated the interaction between JUNV and IFN pathway in human epithelial cells highly permissive to JUNV infection. We have determined the expression pattern of interferon-stimulated genes (ISGs) and IFN-β at both mRNA and protein levels during JUNV infection. Our results clearly indicate that JUNV infection activates the type I IFN response. STAT1 phosphorylation, a downstream marker of activation of IFN signaling pathway, was readily detected in JUNV infected IFN-competent cells. Our studies also demonstrated for the first time that RIG-I was required for IFN production during JUNV infection. IFN activation was detected during infection by either the virulent or attenuated vaccine strain of JUNV. Curiously, both virus strains were relatively insensitive to human IFN treatment. Our studies collectively indicated that JUNV infection could induce host type I IFN response and provided new insights into the interaction between JUNV and host innate immune system, which might be important in future studies on vaccine development and antiviral treatment.
RIG-I Enhanced Interferon Independent Apoptosis upon Junin Virus Infection
Olga A. Kolokoltsova, Ashley M. Grant, Cheng Huang, Jennifer K. Smith, Allison L. Poussard, Bing Tian, Allan R. Brasier, Clarence J. Peters, Chien-Te Kent Tseng, Juan C. de la Torre, Slobodan Paessler
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0099610
Abstract: Junin virus (JUNV) is the etiological agent of Argentine hemorrhagic fever (AHF), a human disease with a high case-fatality rate. It is widely accepted that arenaviral infections, including JUNV infections, are generally non-cytopathic. In contrast, here we demonstrated apoptosis induction in human lung epithelial carcinoma (A549), human hepatocarcinoma and Vero cells upon infection with the attenuated Candid#1 strain of, JUNV as determined by phosphatidylserine (PS) translocation, Caspase 3 (CASP3) activation, Poly (ADP-ribose) polymerase (PARP) cleavage and/or chromosomal DNA fragmentation. Moreover, as determined by DNA fragmentation, we found that the pathogenic Romero strain of JUNV was less cytopathic than Candid#1 in human hepatocarcinoma and Vero, but more apoptotic in A549 and Vero E6 cells. Additionally, we found that JUNV-induced apoptosis was enhanced by RIG-I signaling. Consistent with the previously reported role of RIG-I like helicase (RLH) signaling in initiating programmed cell death, we showed that cell death or DNA fragmentation of Candid#1-infected A549 cells was decreased upon siRNA or shRNA silencing of components of RIG-I pathway in spite of increased virus production. Similarly, we observed decreased DNA fragmentation in JUNV-infected human hepatocarcinoma cells deficient for RIG-I when compared with that of RIG-I-competent cells. In addition, DNA fragmentation detected upon Candid#1 infection of type I interferon (IFN)-deficient Vero cells suggested a type I IFN-independent mechanism of apoptosis induction in response to JUNV. Our work demonstrated for the first time apoptosis induction in various cells of mammalian origin in response to JUNV infection and partial mechanism of this cell death.
Fractal Dimension in Animal Model of Alzheimer’s Dementia  [PDF]
Ljiljana Marta?, Slobodan Sekuli?
Journal of Behavioral and Brain Science (JBBS) , 2018, DOI: 10.4236/jbbs.2018.89031
Abstract: The aim of this study was to qualitatively described effect of the oxidative stress, neurotransmission change and the neurodegeneration in animal model of chronic intoxication by aluminum. Electrocortical brain activity of animal model of stress and neurodegeneration is comparable with Alzheimer’s Dementia (AD). We used adult animals, during 6 weeks intraperitoneally treated with aluminum. Both animals and patients with Alzheimer’s Dementia have increased relative spectral power in delta range. By fractal analysis we described changes in electrocortical activity of aluminum intoxication animals compare to physiological control. We used change in delta range to calculate fractal dimension for the pathophysiological state of disease. We evaluate effect of stress and neurodegeneration, oxidative stress and accumulation of beta amyloid and neurofibrillary tangles as change in fractal dimension (FD). We conclude that change in fractal dimension could be used for prognosis of AD. Results show that decrease in fractal dimension could be used for evaluation of changes in neural activity in occurrence of AD.
IL-10 is a critical negative regulator of macrophage activation syndrome
Canna Scott,Slade Katharine,Paessler Michele,Kreiger Portia
Pediatric Rheumatology , 2012, DOI: 10.1186/1546-0096-10-s1-a110
Could a simple surgical intervention eliminate HIV infection?
Slobodan Tepic
Theoretical Biology and Medical Modelling , 2004, DOI: 10.1186/1742-4682-1-7
Abstract: However, the models also predict the existence of a virus-free equilibrium. Which one of the equilibrium states the system selects depends on its parameters. One of these is the net extinction rate of the preferred HIV target, the CD4+ lymphocyte. The theory predicts, somewhat counterintuitively, that above a critical extinction rate, the host could eliminate the virus. The question then is how to increase the extinction rate of lymphocytes over a period of several weeks to several months without affecting other parameters of the system.Proposed here is the use of drainage, or filtration, of the thoracic duct lymph, a well-established surgical technique developed as an alternative for drug immunosuppression for organ transplantation. The performance of clinically tested thoracic duct lymphocyte depletion schemes matches theoretically predicted requirements for HIV elimination.Reports on the high turnover rates of HIV and its preferred target, CD4+ lymphocytes, during the latent phase of HIV infection [1-3] have established the virus as a prime suspect for direct demolition of the immune system. These clinical findings have also stimulated further efforts at modeling [4,5], and quantitative experimental observation [6]. Major journals have a preference for experimental or clinical data, and the results of mathematical modelling have not reached the broader AIDS research community. For example, the most interesting result of a simple dynamic model published several years ago [7], namely the existence of multiple equilibrium states, one of which is virus-free, has not been discussed in any of the recent publications on HIV response to anti-viral drugs.For a general medical audience it would be desirable to describe the basic features of the dynamics of HIV infection without recourse to any mathematical formulations. Dynamics implies change over time and the behavior of a dynamic system is defined by stating how the system variables affect each other during a unit of ti
Preference and performance of the gypsy moth cater-pillars on sweet chestnut and some oak species
Milanovi? Slobodan
Glasnik ?umarskog Fakulteta , 2010, DOI: 10.2298/gsf1001113m
Abstract: In the establishment of mixed plantations, it is necessary to examine previously the relations of the principal and the admixed species and the most significant pests. This paper presents the results of the study of the gypsy moth caterpillar preference and performance on sweet chestnut and four oak species. Preference index is the highest for Hungarian oak (0.83) and Turkey oak (0.77), for sessile oak it is significantly lower (0.33), and for common oak it is equal to 0. In combination with sweet chestnut, the gypsy moth second-instar caterpillars prefer Hungarian oak, i.e. Turkey oak leaves. In combination with sessile oak or common oak, the gypsy moth caterpillars prefer sweet chestnut leaves. The analyzed parameters which characterise the performance of the gypsy moth fourth-instar caterpillars are lower for all study oak species compared to sweet chestnut, except in the case of Turkey oak. Based on the study results and the adopted principle that the mixture should be composed of the most favourable species, which will serve as the 'trap plant' during the gypsy moth outbreak, it can be concluded that Turkey oak is more favourable for the mixture with sweet chestnut than the other analyzed oak species.
Development of gypsy moth (Lymantria dispar L) on the foliage of Quercus cerris L., Q. Petraea (matt) Liebl. and Q. Robur L. in the controlled conditions
Milanovi? Slobodan
Glasnik ?umarskog Fakulteta , 2007, DOI: 10.2298/gsf0796055m
Abstract: The development of Gypsy moth (Lymantria dispar L) was monitored in laboratory conditions, on the foliage of the species Quercus cerris L. Quercus petraea (Matt) Liebl. and Quercus robur L. The experiment was established in the controlled environmental conditions, at the temperature of 25°C, photoperiod 14:10 (day: night) and relative humidity 70%. The objective of the research was to determine the suitability of the study host plant species for gypsy moth development. The study results show that Gypsy moth caterpillars cultivated on Q. petraea foliage had a lower survival, higher number of moultings, longer preadult development and lower fecundity, which makes this species less suitable compared to the other two. Gypsy moth caterpillars cultivated on Q. cerris foliage had the highest survival degree the lowest number of moultings, the shortest preadult development and the highest fecundity, which makes this species the most favourable for gypsy moth development. Q. robur was between the former two species in this respect.
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