Ecoclimber
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This maybe of interest to some on here:
Background information from Wikipedia on the JC Virus:
The JC virus or John Cunningham virus (JCV) is a type of human polyomavirus (formerly known as papovavirus) and is genetically similar to BK virus and SV40. It was identified by electron microscopy in 1965 by ZuRhein and Chou, and by Silverman and Rubinstein, and later isolated in culture and named using the two initials of a patient with progressive multifocal leukoencephalopathy (PML).The virus causes PML and other diseases only in cases of immunodeficiency...
...The virus is very common in the general population, infecting 70 to 90 percent of humans; most people acquire JCV in childhood or adolescence...
...The initial site of infection may be the tonsils, or possibly the gastrointestinal tract. The virus then remains latent in the gastrointestinal tract and can also infect the tubular epithelial cells in the kidneys, where it continues to reproduce, shedding virus particles in the urine...
...JCV can cross the blood–brain barrier into the central nervous system, where it infects oligodendrocytes and astrocytes, possibly through the 5-HT2A serotonin receptor. JC viral DNA can be detected in both non-PML affected and PML-affected (see below) brain tissue...
...JCV found in the central nervous system of PML patients almost invariably have differences in promoter sequence to the JCV found in healthy individuals. It is thought that these differences in promoter sequence contribute to the fitness of the virus in the CNS and thus to the development of PML...
...Immunodeficiency or immunosuppression allows JCV to reactivate. In the brain it causes the usually fatal progressive multifocal leukoencephalopathy, or PML, by destroying oligodendrocytes. Whether this represents the reactivation of JCV within the CNS or seeding of newly reactivated JCV via blood or lymphatics is unknown. Several studies since 2000 have suggested that the virus is also linked to colorectal cancer...
...Since immunodeficiency causes this virus to progress to PML, immunosuppressants are contraindicative to those infected...
...The boxed warning for the drug rituximab (Rituxan, co-marketed by Genentech BioOncology and Biogen Idec) includes a statement that JC virus infection resulting in progressive multifocal leukoencephalopathy, and death has been reported in patients treated with the drug..More
Premission to repost by Prof. Gavin Giovannoni
There are some in the ME/CFS medical field that believe ME/CFS is 'MS Light' or 'Atypical MS'. The reason I post these articles is the fact that research in one area may spill over into another area of research or the fact that researchers reviewing a site may look at the research in another disease category that could be related to theirs and it might raise their interest level.
Futhermore, research may be further ahead in another field that ME/CFS researchers wish to explore if they had the funding and the researchers to explore such as EBV, HERVs, Autoimmune diseases, Fibromyalgia, Lyme etc. Below is recent research concerning the JC Virus:
A step forwards to a drug to getting rid of JC Virus
Dang X, Chalkias S, Koralnik IJ. JC virus-iLOV fluorescent strains enable the detection of early and late viral protein expression. J Virol Methods. 2015 Jul 20. pii: S0166-0934(15)00239-6. doi: 10.1016/j.jviromet.2015.07.006. [Epub ahead of print]
JC virus (JCV) is highly prevalent in humans, and may cause progressive multifocal leukoencephalopathy (PML), JCV granule cell neuronopathy (JCV GCN), JCV encephalopathy (JCVE) and JCV meningitis (JCVM) in immunocompromised individuals.
There is no treatment for JCV, and a growing number of multiple sclerosis patients treated with immunomodulatory medications have developed PML.
Antiviral agents against JCV are therefore highly desirable but remain elusive, due to the difficulty of determining their effect in vitro. A JCV strain carrying a fluorescent protein gene would greatly simplify and accelerate the drug screening process.
To achieve this goal, we selected the 366bp improved Light, Oxygen or Voltage-sensing domain (iLOV) of plant phototropin gene and created two full-length JCV-iLOV constructs on the prototype JCV Mad1 backbone. The iLOV gene was inserted either before the early regulatory T gene (iLOV-T), or after the late Agno gene (iLOV-Agno).
Both JCV iLOV strains were replication-competent in vitro and emitted a fluorescent signal detectable by confocal microscope, but JCV iLOV-T exhibited higher cellular and supernatant viral loads compared to JCV iLOV-Agno. JCV iLOV-T could also produce infectious pseudovirions.
These data suggest that JCV iLOV constructs may become valuable tools for anti-JCV drug screening.
Comment and post by MouseDoctor:
High throughput screens to test the defects of a drug library with thousands/millions of chemicals depend on a simple screening assay. In this study they made JC virus glow in the dark...when a ultraviolet light is shone on them.
In addition to encoding the structural and regulatory proteins, many viruses encode auxiliary proteins, some of which have been shown to play important roles in lytic and latent states of the viruses.
The human neurotropic JC virus (JCV) genome encodes an auxiliary protein called Agno. The Agno protein of JCV, which is produced late during the late phase of the lytic cycle, can physically and functionally interact with the viral early protein, T antigen, and downregulate viral gene expression and DNA replication. The T-antigen mediates transcription of the viral late gene promoter and induces replication of viral DNA.
Now you can screen for a drug to kill them.
Background information from Wikipedia on the JC Virus:
The JC virus or John Cunningham virus (JCV) is a type of human polyomavirus (formerly known as papovavirus) and is genetically similar to BK virus and SV40. It was identified by electron microscopy in 1965 by ZuRhein and Chou, and by Silverman and Rubinstein, and later isolated in culture and named using the two initials of a patient with progressive multifocal leukoencephalopathy (PML).The virus causes PML and other diseases only in cases of immunodeficiency...
...The virus is very common in the general population, infecting 70 to 90 percent of humans; most people acquire JCV in childhood or adolescence...
...The initial site of infection may be the tonsils, or possibly the gastrointestinal tract. The virus then remains latent in the gastrointestinal tract and can also infect the tubular epithelial cells in the kidneys, where it continues to reproduce, shedding virus particles in the urine...
...JCV can cross the blood–brain barrier into the central nervous system, where it infects oligodendrocytes and astrocytes, possibly through the 5-HT2A serotonin receptor. JC viral DNA can be detected in both non-PML affected and PML-affected (see below) brain tissue...
...JCV found in the central nervous system of PML patients almost invariably have differences in promoter sequence to the JCV found in healthy individuals. It is thought that these differences in promoter sequence contribute to the fitness of the virus in the CNS and thus to the development of PML...
...Immunodeficiency or immunosuppression allows JCV to reactivate. In the brain it causes the usually fatal progressive multifocal leukoencephalopathy, or PML, by destroying oligodendrocytes. Whether this represents the reactivation of JCV within the CNS or seeding of newly reactivated JCV via blood or lymphatics is unknown. Several studies since 2000 have suggested that the virus is also linked to colorectal cancer...
...Since immunodeficiency causes this virus to progress to PML, immunosuppressants are contraindicative to those infected...
...The boxed warning for the drug rituximab (Rituxan, co-marketed by Genentech BioOncology and Biogen Idec) includes a statement that JC virus infection resulting in progressive multifocal leukoencephalopathy, and death has been reported in patients treated with the drug..More
Premission to repost by Prof. Gavin Giovannoni
There are some in the ME/CFS medical field that believe ME/CFS is 'MS Light' or 'Atypical MS'. The reason I post these articles is the fact that research in one area may spill over into another area of research or the fact that researchers reviewing a site may look at the research in another disease category that could be related to theirs and it might raise their interest level.
Futhermore, research may be further ahead in another field that ME/CFS researchers wish to explore if they had the funding and the researchers to explore such as EBV, HERVs, Autoimmune diseases, Fibromyalgia, Lyme etc. Below is recent research concerning the JC Virus:
A step forwards to a drug to getting rid of JC Virus
Dang X, Chalkias S, Koralnik IJ. JC virus-iLOV fluorescent strains enable the detection of early and late viral protein expression. J Virol Methods. 2015 Jul 20. pii: S0166-0934(15)00239-6. doi: 10.1016/j.jviromet.2015.07.006. [Epub ahead of print]
JC virus (JCV) is highly prevalent in humans, and may cause progressive multifocal leukoencephalopathy (PML), JCV granule cell neuronopathy (JCV GCN), JCV encephalopathy (JCVE) and JCV meningitis (JCVM) in immunocompromised individuals.
There is no treatment for JCV, and a growing number of multiple sclerosis patients treated with immunomodulatory medications have developed PML.
Antiviral agents against JCV are therefore highly desirable but remain elusive, due to the difficulty of determining their effect in vitro. A JCV strain carrying a fluorescent protein gene would greatly simplify and accelerate the drug screening process.
To achieve this goal, we selected the 366bp improved Light, Oxygen or Voltage-sensing domain (iLOV) of plant phototropin gene and created two full-length JCV-iLOV constructs on the prototype JCV Mad1 backbone. The iLOV gene was inserted either before the early regulatory T gene (iLOV-T), or after the late Agno gene (iLOV-Agno).
Both JCV iLOV strains were replication-competent in vitro and emitted a fluorescent signal detectable by confocal microscope, but JCV iLOV-T exhibited higher cellular and supernatant viral loads compared to JCV iLOV-Agno. JCV iLOV-T could also produce infectious pseudovirions.
These data suggest that JCV iLOV constructs may become valuable tools for anti-JCV drug screening.
Comment and post by MouseDoctor:
High throughput screens to test the defects of a drug library with thousands/millions of chemicals depend on a simple screening assay. In this study they made JC virus glow in the dark...when a ultraviolet light is shone on them.
In addition to encoding the structural and regulatory proteins, many viruses encode auxiliary proteins, some of which have been shown to play important roles in lytic and latent states of the viruses.
The human neurotropic JC virus (JCV) genome encodes an auxiliary protein called Agno. The Agno protein of JCV, which is produced late during the late phase of the lytic cycle, can physically and functionally interact with the viral early protein, T antigen, and downregulate viral gene expression and DNA replication. The T-antigen mediates transcription of the viral late gene promoter and induces replication of viral DNA.
Now you can screen for a drug to kill them.