- Dear Astraea...
-
- I've been trying to follow your terrible ordeal. This
is particularly bad news. Do you expect there could be MS in EVERY SARS-like
survivor? Or, is it just a result in some of those who became infected?
-
- There is good reason to suspect that MANY Americacs became
infected with SARS or SARS-like as early as last February and March.
-
- Will all good wishes,
- Jeff
-
-
- Dear Jeff,
-
- My visual observations in the outpatient clinic at Kaiser
Vallejo and the reports that I am getting from both physicians and scientists
on the West Coast would indicate a high and alarming number of new (within
the last year) of recently diagnosed M.S. patients.
-
- However, the amount of suspicious flu would be much larger,
so, without any hard data to evaluate with, I would say only some of the
possible SARS or SARS-LIKE patients appear to be getting M.S. Why this
is happening is a question of concern and interest probably to many of
us.
-
- Dr. Robert Lee has a long and technical explanation of
what was sequenced in samples of SARS or coronavirus and those indicated
in April 2003 that M.S. would be a highly probable outcome of SARS and
was not being reported. I personally suspect it has to do with an assault
on the thymus which would cause muscle degeneration in mass and tone.
-
- Dr. Lee is also explaining (below) the degeneration causes
here of the nerve sheath as in M.S. I would suspect minerals and nutrients
(or lack of them), would be a factor for why some people would become more
prone to M.S. and the B vitamins certainly do assist nerve functions.
Many studies show industrialized nations as deficient in B vitamins due
to our processed food and eating habits. Heavy metals in our systems could
be a contributing factor due to environmental pollution or water processing.
If we are having metals dropped in our strange chemtrail patterns and
we are inhaling or absorbing those metals, then that might be a factor
that would assist nerve demyelination also.
-
- I favor Dr. Lee's observations that T Cell destruction
and chemical breakdowns would contribute significantly to demyelination
of nerve sheaths. Again, this would happen from a retrovirus assault to
the Thymus, which appears likely in SARS research.
-
- Thank you for your good wishes, Jeff. I wish we could
get farther on improving health care worker safety by a stronger campaign
for front line workers to wear N95 masks when assessing flu or respiratory
infections. It is just too hard to sort symptoms and now SARS travel alert
advisories are lifted.
-
- However, people are still getting seriously ill with
similar symptoms of concern and those are still probably viruses and secretion
spread by cough or sneezing right at the face level of the health care
workers assessing the patients.
-
- Sincerely,
- Astraea
-
-
- From rense.com
-
- Posted by Dr. Robert E. Lee on April 7, 2003
- Hypotheses to test derived from below data:
-
- 1. SARS has persistent neurological effects which have,
to date, not been discussed in any literature.
- 2. SARS uses CCR5 and CD4+ cytokines to bind to glial
cells in infecting neurological circuits.
- 3. SARS will not readily infected individuals who do
not show CCR5 cell-surface receptors, i.e., Northern Europeans may be somewhat
less susceptible to SARS infection than Asians or Africans.
- 4. SARS may serve to trigger HERV-W retroposon activation
and cause an increase in schizophrenia and multiple sclerosis among SARS
infected individuals.
- 5. SARS cell-surface-binding may closely resemble that
which occurs in HIV cell-surface-binding. RANTES may be of interest in
study of SARS.
-
- The above hypotheses need be investigated.
-
- SARS may be neurotropic and cause persistent infection
- Bob Lee ® 04/07/2003, 01:19:23 Post Reply
Forum
- Closest relative to SARS appears to be Human Coronavirus
229E. If this is correct, SARS is likely to persistently infect glial cells
and cause neurological problems.See here:J Virol 1999 Apr;73(4):3326-37
-
- Persistent infection of human oligodendrocytic and neuroglial
cell lines by human coronavirus 229E.Arbour N, Ekande S, Cote G, Lachance
C, Chagnon F, Tardieu M, Cashman NR, Talbot PJ.Laboratory of Neuroimmunovirology,
Human Health Research Center, Armand-Frappier Institute, INRS, University
of Quebec, Laval, Quebec, Canada H7V 1B7.Human coronaviruses (HuCV) cause
common colds. Previous reports suggest that these infectious agents may
be neurotropic in humans, as they are for some mammals. With the long-term
aim of providing experimental evidence for the neurotropism of HuCV and
the establishment of persistent infections in the nervous system, we have
evaluated the susceptibility of various human neural cell lines to acute
and persistent infection by HuCV-229E. Viral antigen, infectious virus
progeny and viral RNA were monitored during both acute and persistent infections.
The astrocytoma cell lines U-87 MG, U-373 MG, and GL-15, as well as neuroblastoma
SK-N-SH, neuroglioma H4, and oligodendrocytic MO3.13 cell lines, were all
susceptible to an acute infection by HuCV-229E. The CHME-5 immortalized
fetal microglial cell line was not susceptible to infection by this virus.
The MO3.13 and H4 cell lines also sustained a persistent viral infection,
as monitored by detection of viral antigen and infectious virus progeny.
Sequencing of the S1 gene from viral RNA after approximately 130 days of
infection showed two point mutations, suggesting amino acid changes during
persistent infection of MO3.13 cells but none for H4 cells. Thus, persistent
in vitro infection did not generate important changes in the S1 portion
of the viral spike protein, which was shown for murine coronaviruses to
bear hypervariable domains and to interact with cellular receptor. These
results are consistent with the potential persistence of HuCV-229E in cells
of the human nervous system, such as oligodendrocytes and possibly neurons,
and the virus's apparent genomic stability.PMID: 10074187 Further, see
here:J Virol 2000 Oct;74(19):8913-21
-
- Neuroinvasion by human respiratory coronaviruses.Arbour
N, Day R, Newcombe J, Talbot PJ.Laboratory of Neuroimmunovirology, Human
Health Research Center, INRS-Armand-Frappier Institute, University of Quebec,
Laval, Quebec, Canada H7V 1B7.Human coronaviruses (HCoV) cause common colds
but can also infect neural cell cultures. To provide definitive experimental
evidence for the neurotropism and neuroinvasion of HCoV and its possible
association with multiple sclerosis (MS), we have performed an extensive
search and characterization of HCoV RNA in a large panel of human brain
autopsy samples. Very stringent reverse transcription-PCR with two primer
pairs for both viral strains (229E and OC43), combined with Southern hybridization,
was performed on samples from 90 coded donors with various neurological
diseases (39 with MS and 26 with other neurological diseases) or normal
controls (25 patients). We report that 44% (40 of 90) of donors were positive
for 229E and that 23% (21 of 90) were positive for OC43. A statistically
significant higher prevalence of OC43 in MS patients (35.9%; 14 of 39)
than in controls (13.7%; 7 of 51) was observed. Sequencing of nucleocapsid
protein (N) gene amplicons revealed point mutations in OC43, some consistently
found in three MS patient brains and one normal control but never observed
in laboratory viruses. In situ hybridization confirmed the presence of
viral RNA in brain parenchyma, outside blood vessels. The presence of HCoV
in human brains is consistent with neuroinvasion by these respiratory pathogens.
Further studies are needed to distinguish between opportunistic and disease-associated
viral presence in human brains.PMID: 10982334 New Microbiol 1997 Apr;20(2):105-14
-
- Human coronavirus polyadenylated RNA sequences in cerebrospinal
fluid from multiple sclerosis patients.Cristallo A, Gambaro F, Biamonti
G, Ferrante P, Battaglia M, Cereda PM.Institute of Biochemistry, University
of Pavia, Italy.Human coronaviruses, represented by the two prototype strains
HCV-OC43 and HCV-229E, are important human respiratory pathogens, also
associated with necrotizing enterocolitis. Two previous studies, one describing
the electron microscopic observation of doughnut-shaped particles, resembling
coronaviruses, in a perivascular inflammatory lesion of brain tissue taken
at autopsy from a multiple sclerosis patient, and the other one reporting
the isolation of coronaviruses from the brains of two multiple sclerosis
patients, suggested the possible association between coronaviruses and
human demyelinating diseases. We analysed polyadenylated RNAs extracted
from cerebrospinal fluid of twenty randomly selected multiple sclerosis
patients and ten patients with other neurological diseases (medullary atrophy,
Parkinson's disease, polyneuropathy, senile dementia, headache and toxic
polyneuropathy) by reverse transcription and polymerase chain reaction
searching for HCV-OC43 and HCV-229E sequences. By hybridization analysis
of amplification products, we detected HCV-OC43 polyadenylated RNAs in
ten specimens of patients with multiple sclerosis. Furthermore, we found
positive hybridization signals for HCV-OC43 in the other neurological diseases,
except for the toxic polyneuropathy specimen. Positivity for HCV-229E was
observed in seven specimens of multiple sclerosis cerebrospinal fluid;
one headache cerebrospinal fluid and the medullary atrophy specimen also
resulted positive for HCV-229E. Moreover, using a solid phase technique,
we report for the first time the sequence of a cDNA fragment derived from
RNA extracted from cerebrospinal fluid of multiple sclerosis patient, belonging
to the open reading frame which codes for the HCV-OC43 nucleoprotein N.
Furthermore, cDNA sequences revealed the presence of a mixed viral population.PMID:
9208420 It would appear that CCR5 and CD4+ cytokines are involved in SARS
infection. See here:J Virol 2003 Jan;77(1):191-8
-
- Functional expression of chemokine receptor CCR5 on CD4(+)
T cells during virus-induced central nervous system disease.Glass WG, Lane
TE.Department of Molecular Biology and Biochemistry, University of California,
Irvine 92697-3900, USA.Intracranial infection of C57BL/6 mice with mouse
hepatitis virus (MHV) results in an acute encephalomyelitis followed by
a demyelinating disease similar in pathology to the human disease multiple
sclerosis (MS). CD4(+) T cells are important in amplifying demyelination
by attracting macrophages into the central nervous system (CNS) following
viral infection; however, the mechanisms governing the entry of these cells
into the CNS are poorly understood. The role of chemokine receptor CCR5
in trafficking of virus-specific CD4(+) T cells into the CNS of MHV-infected
mice was investigated. CD4(+) T cells from immunized CCR5(+/+) and CCR5(-/-)
mice were expanded in the presence of the immunodominant epitope present
in the MHV transmembrane (M) protein encompassing amino acids 133 to 147
(M133-147). Adoptive transfer of CCR5(+/+)-derived CD4(+) T cells to MHV-infected
RAG1(-/-) mice resulted in CD4(+)-T-cell entry into the CNS and clearance
of virus from the brain. These mice also displayed robust demyelination
correlating with macrophage accumulation within the CNS. Conversely, CD4(+)
T cells from CCR5(-/-) mice displayed an impaired ability to traffic into
the CNS of MHV-infected RAG1(-/-) recipients, which correlated with increased
viral titers, diminished macrophage accumulation, and limited demyelination.
Analysis of chemokine receptor mRNA expression by M133-147-expanded CCR5(-/-)-derived
CD4(+) T cells revealed reduced expression of CCR1, CCR2, and CXCR3, indicating
that CCR5 signaling is important in increased expression of these receptors,
which aid in trafficking of CD4(+) T cells into the CNS. Collectively these
results demonstrate that CCR5 signaling is important to migration of CD4(+)
T cells to the CNS following MHV infection.PMID: 12477824 Relevance of
CCR5 and CD4+ cytokines relative to ethnicity:Nat Med 1997 Oct;3(10):1160-2
-
- The role of CCR5 and CCR2 polymorphisms in HIV-1 transmission
and disease progression.Michael NL, Louie LG, Rohrbaugh AL, Schultz KA,
Dayhoff DE, Wang CE, Sheppard HW.Division of Retrovirology, Walter Reed
Army Institute of Research, Rockville, Maryland 20850, USA.Entry of human
immunodeficiency virus type 1 (HIV-1) into target cells requires both CD4
(ref. 1, 2) and one of a growing number of G-protein-coupled seven-transmembrane
receptors. Viruses predominantly use one, or occasionally both, of the
major co-receptors CCR5 or CXCR4, although other receptors, including CCR2B
and CCR3, function as minor co-receptors. CCR3 appears critical in central
nervous system infection. A 32-base pair inactivating deletion in CCR5
(delta 32) common to Northern European populations has been associated
with reduced, but not absolute, HIV-1 transmission risk and delayed disease
progression. A more commonly distributed transition causing a valine to
isoleucine switch in transmembrane domain I of CCR2B (64I) with unknown
functional consequences was recently shown to delay disease progression
but not reduce infection risk. Although we confirm the lack of association
of CCR2B 64I with transmission, we cannot confirm the association with
delayed progression. Although subjects with CCR5 delta 32 defects had significantly
reduced median viral load at study entry, providing a plausible explanation
for the association with delayed progression, this association was not
seen with CCR2B 64I. Further studies are needed to define the role of CCR2B64I
in HIV pathogenesis.PMID: 9334732 Hypotheses to test derived from above
data:
-
- 1. SARS has persistent neurological effects which have,
to date, not been discussed in any literature.
- 2. SARS uses CCR5 and CD4+ cytokines to bind to glial
cells in infecting neurological circuits.
- 3. SARS will not readily infected individuals who do
not show CCR5 cell-surface receptors, i.e., Northern Europeans may be somewhat
less susceptible to SARS infection than Asians or Africans.
- 4. SARS may serve to trigger HERV-W retroposon activation
and cause an increase in schizophrenia and multiple sclerosis among SARS
infected individuals.
- 5. SARS cell-surface-binding may closely resemble that
which occurs in HIV cell-surface-binding. RANTES may be of interest in
study of SARS.The above hypotheses need be investigated.
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