An Early Passage Human Isolate of Kyasanur Forest Disease Virus Shows Acute Neuropathology in Experimentally Infected CD-1 Mice

BasuAtanu,; Yadav, Pragya D; PrasadSharda,; BadoleSachin,; PatilDilip,; Motilal, KohlapureRajendra; MouryaDevendra, T

doi:10.1089/vbz.2015.1917

Cited by 10 publications

(8 citation statements)

References 5 publications

(9 reference statements)

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“…Unlike 100% mortality observed in previous macaque studies 11 , 12 , we observed severe disease in 2/10 macaques. However, the similar low passage strain of KFDV used in an earlier study produced neuropathology in CD1 mice 21 . The dose of infection in the present study has also not shown any effect on mortality.…”

Section: Discussionmentioning

confidence: 89%

“…KFDV (NIV-12839) isolated from acute phase human serum sample from Thirthahalli, Karnataka propagated in Baby hamster kidney (BHK) -21 cells (Passage number 6) having a tissue culture infective dose 50 (TCID50) titer of 10 5.57 /ml was used for the study 21 . 6–8 weeks old, female, BALB/c mice procured from Animal House facility of ICMR-NIV, Pune was used to assess the virus lethal dose 50 (LD50).…”

Section: Methodsmentioning

confidence: 99%

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Study of Kyasanur forest disease viremia, antibody kinetics, and virus infection in target organs of Macaca radiata

Patil

Yadav

Shete

et al. 2020

Sci Rep

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The present manuscript deals with experimental infections of bonnet macaques ( Macaca radiata ) to study disease progression for better insights into the Kyasanur Forest Disease (KFD) pathogenesis and transmission. Experimentally, 10 monkeys were inoculated with KFD virus (KFDV) (high or low dose) and were regularly monitored and sampled for various body fluids and tissues at preset time points. We found that only 2 out of the 10 animals showed marked clinical signs becoming moribund, both in the low dose group, even though viremia, virus shedding in the secretions and excretions were evident in all inoculated monkeys. Anti-KFDV immunoglobulin (Ig)M antibody response was observed around a week after inoculation and anti-KFDV IgG antibody response after two weeks. Anaemia, leucopenia, thrombocytopenia, monocytosis, increase in average clotting time, and reduction in the serum protein levels were evident. The virus could be re-isolated from the skin during the viremic period. The persistence of viral RNA in the gastrointestinal tract and lymph nodes was seen up to 53 and 81 days respectively. Neuro-invasion was observed only in moribund macaques. Re-challenge with the virus after 21 days of initial inoculation in a monkey did not result in virus shedding or immune response boosting.

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Section: Discussionmentioning

confidence: 89%

Section: Methodsmentioning

confidence: 99%

Study of Kyasanur forest disease viremia, antibody kinetics, and virus infection in target organs of Macaca radiata

Patil

Yadav

Shete

et al. 2020

Sci Rep

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“…Epidemiological studies and case reports have not provided clear evidence to ascertain if neurological symptoms are a common or rare sequalae in recovered individuals [3][4][5][6]. Attempts to establish viral replication in a mouse model have shown the absence of fever and progression of neurologic disturbance with viral RNA [7], viral antigen [8] and infectious virus [9] being detected in the brain. The high prevalence of neurological infection in mice may contradict human symptoms of disease progression.…”

Section: Objectivementioning

confidence: 99%

Kyasanur Forest disease virus non-mouse animal models: a pilot study

et al. 2020

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Objectives: Mouse models have delivered variable recapitulation of Kyasanur Forest disease (KFD) pathology and consistently demonstrated neurological involvement which may be a limited feature of human disease. With the purpose of more accurately modelling human disease progression we infected several small-mammalian models: guinea pigs, hamsters and ferrets with a titered infectious dose of Kyasanur Forest disease virus (KFDV). Clinical indicators of disease severity were observed for seventeen days, on day eighteen a visual post-mortem analysis of visceral organs was conducted. Viral load in selected tissues was measured to infer disease signs and the establishment of viral replication. Data description: Daily monitoring did not reveal any observable signs of illness; weight loss was minimal across species and gross pathology did not indicate severe viral infection. Tissue specific tropism and establishment of viral infection was monitored by quantitative real-time polymerase chain reaction (qRT-PCR). No viral replication was detected in ferrets (n = 0/3), but was present in the spleen of guinea pigs (n = 3/3) and the brain of hamsters (n = 3/3). Low levels of viral RNA were detected in multiple hamster tissues (kidney, liver, lung and spleen) suggesting the possibility of viral tropism and possible adaptation to the host. No serological tests were performed.

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“…These vector-transmitted viruses include -Yellow Fever, Dengue virus (DENV), Japanese encephalitis virus, Chikungunya virus, West Nile virus and Zika virus (Brehin, et al, 2008;Chen LH & Wilson, 2016;Das, et al, 2010;Fernandez-Garcia, et al, 2009;Huang YJ, et al, 2014;Jhan, et al, 2017;Kimura T, et al, 2010;Lannes, et al, 2017;Lindenbach & Rice, 2003;Lum, et al, 2017). Disease from flaviviruses can range from asymptomatic to symptomatic manifestations, with high fever, chills, headache, back and muscle aches, dizziness, anorexia, nausea, and vomiting (Gould & Solomon, 2008;Murphy BR & Whitehead, 2011), and can sometimes result in fatal illness, such as encephalitis and hemorrhagic fever (Basu, et al, 2016;Imaizumi, et al, 2005). In addition, flavivirus infections can cause inflammation of the CNS (Furr & Marriott, 2012;Roach & Alcendor, 2017;Tsai, et al, 2016).…”

Section: Flaviviruses-the Flaviviridae Family Consists Of Positive Smentioning

confidence: 99%

Endothelins in inflammatory neurological diseases

D’Orléans-Juste

Ndunge

Desbiens

et al. 2019

Pharmacology & Therapeutics

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Endothelins were discovered more than thirty years ago as potent vasoactive compounds. Beyond their well-documented vasomodulatory properties, however, the contributions of the endothelin pathway have been demonstrated in several neuroinflammatory processes and the peptides have been reported as a clinically relevant biomarkers in neurodegenerative diseases. Several published works suggest that endothelin-1 greatly contributes to the progression of neuroinflammatory processes, particularly during infections in the central nervous system (CNS), and is associated with a loss of endothelial integrity at the blood brain barrier level. Because of the paucity of clinical trials with endothelin-1 antagonists in several infectious and non-infectious neuroinflammatory diseases, it remains an open question whether the 21 amino acid peptide is a mediator rather than a biomarker of the progression of neurodegeneration. The present review focuses on the potential roles of endothelins in the pathology of neuroinflammatory processes, including infectious diseases of viral, bacterial or parasitic origin in which the synthesis of endothelins or its pharmacology have been investigated from the cell to the bedside in several cases, and non-infectious inflammatory processes such as neurodegenerative disorders like Alzheimers Disease or central nervous system vasculitis. Keywords Endothelin-1 (ET-1); cytokines; central nervous system; blood-brain barrier (BBB); chymase; mast cells; endothelin subtype B receptor (ET B); endothelin subtype A receptor (ET A); cerebral blood flow (CBF)

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An Early Passage Human Isolate of Kyasanur Forest Disease Virus Shows Acute Neuropathology in Experimentally Infected CD-1 Mice

Cited by 10 publications

References 5 publications

Study of Kyasanur forest disease viremia, antibody kinetics, and virus infection in target organs of Macaca radiata

Study of Kyasanur forest disease viremia, antibody kinetics, and virus infection in target organs of Macaca radiata

Kyasanur Forest disease virus non-mouse animal models: a pilot study

Endothelins in inflammatory neurological diseases

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