Murine retroviruses and neurological disease

[Guest guest]

note this new xmrv is VERY closely related to murine leukemia viruses

Several murine leukemia viruses (MuLV) induce neurologic disease in

susceptible mice. To identify features of central nervous system (CNS)

infection that correlate with neurovirulence, we compared two

neurovirulent MuLV, Fr98 and Fr98/SE, with a nonneurovirulent MuLV,

Fr54. All three viruses utilize the polytropic receptor and are

coisogenic, each containing a different envelope gene within a common

genetic background. Both Fr98 and Fr98/SE induce a clinical neurologic

disease characterized by hyperexcitability and ataxia yet differ in

incubation period, 16 to 30 and 30 to 60 days, respectively. Fr54

infects the CNS but fails to induce clinical signs of neurologic

disease. In this study, we compared the histopathology, regional virus

distribution, and cell tropism in the brain, as well as the relative CNS

viral burdens. All three viruses induced similar histopathologic

effects, characterized by intense reactive astrogliosis and microglial

activation associated with minimal vacuolar degeneration. The infected

target cells for each virus consisted primarily of endothelial and

microglial cells, with rare oligodendrocytes. Infection localized

predominantly in white matter tracts of the cerebellum, internal

capsule, and corpus callosum. The only feature that correlated with

relative neurovirulence was viral burden as measured by both viral CA

protein expression in cerebellar homogenates and quantification of

infected cells. Interestingly, Fr54 (nonneurovirulent) and Fr98/SE (slow

disease) had similar viral burdens at 3 weeks postinoculation,

suggesting that they entered the brain with comparable efficiencies.

However, spread of Fr98/SE within the brain thereafter exceeded that of

Fr54, reaching levels of viral burden comparable to that seen for Fr98

(rapid disease) at 3 weeks. These results suggest that the determinants

of neurovirulence in the envelope gene may influence the efficiency of

virus spread within the brain and that a critical number of infected

cells may be required for induction of clinical neurologic disease.

full text via http://www.ncbi.nlm.nih.gov/pmc/articles/PMC191765/

[Guest guest]

natasa,

Would you mind giving a short explanation as I don't know what it means?

Margaret

>

> note this new xmrv is VERY closely related to murine leukemia viruses

>

> Several murine leukemia viruses (MuLV) induce neurologic disease in

> susceptible mice. To identify features of central nervous system (CNS)

> infection that correlate with neurovirulence, we compared two

> neurovirulent MuLV, Fr98 and Fr98/SE, with a nonneurovirulent MuLV,

> Fr54. All three viruses utilize the polytropic receptor and are

> coisogenic, each containing a different envelope gene within a common

> genetic background. Both Fr98 and Fr98/SE induce a clinical neurologic

> disease characterized by hyperexcitability and ataxia yet differ in

> incubation period, 16 to 30 and 30 to 60 days, respectively. Fr54

> infects the CNS but fails to induce clinical signs of neurologic

> disease. In this study, we compared the histopathology, regional virus

> distribution, and cell tropism in the brain, as well as the relative CNS

> viral burdens. All three viruses induced similar histopathologic

> effects, characterized by intense reactive astrogliosis and microglial

> activation associated with minimal vacuolar degeneration. The infected

> target cells for each virus consisted primarily of endothelial and

> microglial cells, with rare oligodendrocytes. Infection localized

> predominantly in white matter tracts of the cerebellum, internal

> capsule, and corpus callosum. The only feature that correlated with

> relative neurovirulence was viral burden as measured by both viral CA

> protein expression in cerebellar homogenates and quantification of

> infected cells. Interestingly, Fr54 (nonneurovirulent) and Fr98/SE (slow

> disease) had similar viral burdens at 3 weeks postinoculation,

> suggesting that they entered the brain with comparable efficiencies.

> However, spread of Fr98/SE within the brain thereafter exceeded that of

> Fr54, reaching levels of viral burden comparable to that seen for Fr98

> (rapid disease) at 3 weeks. These results suggest that the determinants

> of neurovirulence in the envelope gene may influence the efficiency of

> virus spread within the brain and that a critical number of infected

> cells may be required for induction of clinical neurologic disease.

>

> full text via http://www.ncbi.nlm.nih.gov/pmc/articles/PMC191765/

>

[Guest guest]

don't mind but not sure what you mean?

> >

> > note this new xmrv is VERY closely related to murine leukemia

viruses

> >

> > Several murine leukemia viruses (MuLV) induce neurologic disease in

> > susceptible mice. To identify features of central nervous system

(CNS)

> > infection that correlate with neurovirulence, we compared two

> > neurovirulent MuLV, Fr98 and Fr98/SE, with a nonneurovirulent MuLV,

> > Fr54. All three viruses utilize the polytropic receptor and are

> > coisogenic, each containing a different envelope gene within a

common

> > genetic background. Both Fr98 and Fr98/SE induce a clinical

neurologic

> > disease characterized by hyperexcitability and ataxia yet differ in

> > incubation period, 16 to 30 and 30 to 60 days, respectively. Fr54

> > infects the CNS but fails to induce clinical signs of neurologic

> > disease. In this study, we compared the histopathology, regional

virus

> > distribution, and cell tropism in the brain, as well as the relative

CNS

> > viral burdens. All three viruses induced similar histopathologic

> > effects, characterized by intense reactive astrogliosis and

microglial

> > activation associated with minimal vacuolar degeneration. The

infected

> > target cells for each virus consisted primarily of endothelial and

> > microglial cells, with rare oligodendrocytes. Infection localized

> > predominantly in white matter tracts of the cerebellum, internal

> > capsule, and corpus callosum. The only feature that correlated with

> > relative neurovirulence was viral burden as measured by both viral

CA

> > protein expression in cerebellar homogenates and quantification of

> > infected cells. Interestingly, Fr54 (nonneurovirulent) and Fr98/SE

(slow

> > disease) had similar viral burdens at 3 weeks postinoculation,

> > suggesting that they entered the brain with comparable efficiencies.

> > However, spread of Fr98/SE within the brain thereafter exceeded that

of

> > Fr54, reaching levels of viral burden comparable to that seen for

Fr98

> > (rapid disease) at 3 weeks. These results suggest that the

determinants

> > of neurovirulence in the envelope gene may influence the efficiency

of

> > virus spread within the brain and that a critical number of infected

> > cells may be required for induction of clinical neurologic disease.

> >

> > full text via http://www.ncbi.nlm.nih.gov/pmc/articles/PMC191765/

> >

>

[Guest guest]

I don't understand the significance of the study, that's all.

Margaret

> > >

> > > note this new xmrv is VERY closely related to murine leukemia

> viruses

> > >

> > > Several murine leukemia viruses (MuLV) induce neurologic disease in

> > > susceptible mice. To identify features of central nervous system

> (CNS)

> > > infection that correlate with neurovirulence, we compared two

> > > neurovirulent MuLV, Fr98 and Fr98/SE, with a nonneurovirulent MuLV,

> > > Fr54. All three viruses utilize the polytropic receptor and are

> > > coisogenic, each containing a different envelope gene within a

> common

> > > genetic background. Both Fr98 and Fr98/SE induce a clinical

> neurologic

> > > disease characterized by hyperexcitability and ataxia yet differ in

> > > incubation period, 16 to 30 and 30 to 60 days, respectively. Fr54

> > > infects the CNS but fails to induce clinical signs of neurologic

> > > disease. In this study, we compared the histopathology, regional

> virus

> > > distribution, and cell tropism in the brain, as well as the relative

> CNS

> > > viral burdens. All three viruses induced similar histopathologic

> > > effects, characterized by intense reactive astrogliosis and

> microglial

> > > activation associated with minimal vacuolar degeneration. The

> infected

> > > target cells for each virus consisted primarily of endothelial and

> > > microglial cells, with rare oligodendrocytes. Infection localized

> > > predominantly in white matter tracts of the cerebellum, internal

> > > capsule, and corpus callosum. The only feature that correlated with

> > > relative neurovirulence was viral burden as measured by both viral

> CA

> > > protein expression in cerebellar homogenates and quantification of

> > > infected cells. Interestingly, Fr54 (nonneurovirulent) and Fr98/SE

> (slow

> > > disease) had similar viral burdens at 3 weeks postinoculation,

> > > suggesting that they entered the brain with comparable efficiencies.

> > > However, spread of Fr98/SE within the brain thereafter exceeded that

> of

> > > Fr54, reaching levels of viral burden comparable to that seen for

> Fr98

> > > (rapid disease) at 3 weeks. These results suggest that the

> determinants

> > > of neurovirulence in the envelope gene may influence the efficiency

> of

> > > virus spread within the brain and that a critical number of infected

> > > cells may be required for induction of clinical neurologic disease.

> > >

> > > full text via http://www.ncbi.nlm.nih.gov/pmc/articles/PMC191765/

> > >

> >

>

[Guest guest]

brain pathology findings in these mice match closely those seen in autism (in johns hopkins autopsy study) - microglial/astocyte activation and neurotoxicity in absence of antibody infiltration to the brain...

the viruses in this study are very closely related to xmrv, the one making the news as found in most chronic fatigue patients, and lots of autism cases (althought very small sample tested 40-70% are testing postive so far)

natasa x

I don't understand the significance of the study, that's all.

Margaret

> > >

> > > note this new xmrv is VERY closely related to murine leukemia

> viruses

> > >

> > > Several murine leukemia viruses (MuLV) induce neurologic disease in

> > > susceptible mice. To identify features of central nervous system

> (CNS)

> > > infection that correlate with neurovirulence, we compared two

> > > neurovirulent MuLV, Fr98 and Fr98/SE, with a nonneurovirulent MuLV,

> > > Fr54. All three viruses utilize the polytropic receptor and are

> > > coisogenic, each containing a different envelope gene within a

> common

> > > genetic background. Both Fr98 and Fr98/SE induce a clinical

> neurologic

> > > disease characterized by hyperexcitability and ataxia yet differ in

> > > incubation period, 16 to 30 and 30 to 60 days, respectively. Fr54

> > > infects the CNS but fails to induce clinical signs of neurologic

> > > disease. In this study, we compared the histopathology, regional

> virus

> > > distribution, and cell tropism in the brain, as well as the relative

> CNS

> > > viral burdens. All three viruses induced similar histopathologic

> > > effects, characterized by intense reactive astrogliosis and

> microglial

> > > activation associated with minimal vacuolar degeneration. The

> infected

> > > target cells for each virus consisted primarily of endothelial and

> > > microglial cells, with rare oligodendrocytes. Infection localized

> > > predominantly in white matter tracts of the cerebellum, internal

> > > capsule, and corpus callosum. The only feature that correlated with

> > > relative neurovirulence was viral burden as measured by both viral

> CA

> > > protein expression in cerebellar homogenates and quantification of

> > > infected cells. Interestingly, Fr54 (nonneurovirulent) and Fr98/SE

> (slow

> > > disease) had similar viral burdens at 3 weeks postinoculation,

> > > suggesting that they entered the brain with comparable efficiencies.

> > > However, spread of Fr98/SE within the brain thereafter exceeded that

> of

> > > Fr54, reaching levels of viral burden comparable to that seen for

> Fr98

> > > (rapid disease) at 3 weeks. These results suggest that the

> determinants

> > > of neurovirulence in the envelope gene may influence the efficiency

> of

> > > virus spread within the brain and that a critical number of infected

> > > cells may be required for induction of clinical neurologic disease.

> > >

> > > full text via http://www.ncbi.nlm.nih.gov/pmc/articles/PMC191765/

> > >

> >

>