EU Cases of African Swine Fever Triple Those in Russia
http://farmgatetofork.com/2016/03/29/eu-cases-of-african-swine-fever-triple-those-in-russia/
Is this an indication that HHV-8 is really African Swine Fever Virus?
"Primary HHV-8 infection may be associated with fever and a maculopapular rash in immunocompetent children."
http://www.uptodate.com/contents/disease-associations-of-human-herpesvirus-8-infection
http://www.ncbi.nlm.nih.gov/pubmed/9607855
Did Gallo and Ablashi get this right?
HBLV[HHV-6] is not ASFV.
http://www.researchgate.net/publication/19958785_HBLV_is_not_ASFV
The African Swine Fever Virus Rights of Man
1. The right not to be lied to about whether African Swine Fever Virus is infecting human beings.
2. The right not to be lied to about how many different strains of African Swine Fever are capable of infecting humans.
3.
The right to know if African Swine Fever is being disguised in pigs by
giving it euphemisms of other diseases like PRRS and PEDV.
4. The right not to be lied to about the role of ASFV in AIDS.
5. The right not to be lied to about the role of ASFV in Chronic Fatigue Syndrome.
6. The right not to be lied to about the role of ASFV in Autism.
7.The right not to be lied to about the role of ASFV in Multiple Sclerosis.
8. The right not to be lied to about the role of ASFV in Brain Cancer.
9. The right not to be lied to about the role of ASFV in Heart Disease.
10. The right not to be lied to about the role of ASFV in Encephalitis.
11. The right not to be lied to about the role of ASFV in Cognitive Dysfunction.
12. The right not to be lied to about the role of ASFV in Drug Hypersensitivity Syndrome.
13. The right not to be lied to about the role of ASFV in Bone Marrow Suppression.
14. The right not to be lied to about the role of ASFV in Lymphadenopathy.
15. The right not to be lied to about the role of ASFV in Colitis.
16. The right not to be lied to about the role of ASFV in Endocrine Disorders.
17. The right not to be lied to about the role of ASFV in Liver Disease.
18. The right not to be lied to about the role of ASFV in Hodgkin's Lymphoma.
19. The right not to be lied to about the role of ASFV in Glioma.
20. The right not to be lied to about the role of ASFV in Cervical Cancer.
21. The right not to be lied to about the role of ASFV in Hypogammaglobulinemia.
22. The right not to be lied to about the role of ASFV in Optic Neuritis.
23. The right not to be lied to about the role of ASFV in Microangiopathy.
24. The right not to be lied to about the role of ASFV in Mononucleosis.
25. The right not to be lied to about the role of ASFV in Uveitis.
26. The right not to be lied to about the role of ASFV in Stevens-Johnson Syndrome.
27. The right not to be lied to about the role of ASFV in Rhomboencephalitis.
28. The right not to be lied to about the role of ASFV in Limbic Encephalitis.
29. The right not to be lied to about the role of ASFV in Encephalomyelitis
30. The right not to be lied to about the role of ASFV in Pneumonitis.
31. The right not to be lied to about the role of ASFV in GVHD.
32. The right not to be lied to about the role of ASFV in Ideopathic Pneumonia.
33. The right not to be lied to about the role of ASFV in Pediatric Adrenocortical Tumors
34. The right not to be lied to about the role of ASFV in the reactivation of endogenous retroviruses.
35. The right not to be lied to about the impact of ASFV on T-Cells.
36. The right not to be lied to about the impact of ASFV on B-Cells
37. The right not to be lied to about the impact of ASFV on Epithelial Cells.
38. The right not to be lied to about the the impact of ASFV on Natural Killer Cells.
39. The right not to be lied to about the the impact of HHV-6 on Dendritic Cells.
40. The right not to be lied to about the the impact of ASFV infection of the brain.
41. The right not to be lied to about the the impact of ASFV infection of the liver.
42. The right not to lied to about the ability of ASFV to affect cytokine production.
43. The right not to be lied to about the ability of ASFV to affect Aortic and Heart Microvascular Endothelial cells.
44. The right not be lied to about the relationship of ASFV to HHV-6, HHV-7 and HHV-8.
Background:
John Beldekas on HHV-6 and
African Swine Fever Virus
http://www.keephopealive.org/report10.html
Detection of Novel Sequences Related to African Swine Fever Virus in Human Serum and Sewage.
Loh J, Zhao G, Presti RM, Holtz LR, Finkbeiner SR, Droit L, Villasana Z, Todd C, Pipas JM, Calgua B, Girones R, Wang D, Virgin HW.
http://www.ncbi.nlm.nih.gov/pubmed/19812170?dopt=Abstract
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3274504/
http://link.springer.com/article/10.1007%2Fs11262-013-0878-2
African Swine Fever Primarily
Transmitted by Humans
http://www.aasp.org/news/story.php?id=4824
.44. The right not be lied to about the relationship of ASFV to HHV-6, HHV-7 and HHV-8.
Background:
John Beldekas on HHV-6 and
African Swine Fever Virus
In August, 1986, John Beldekas was invited to go to the NCI and
present his findings on the link between ASFV [African Swine Fever
virus] and AIDS, which he did. Beldekas gave samples of all his lab work
to Gallo. Later, the government asked Beldekas to turn over all his
reagents and lab work to the government, which he did. Beldekas had
found ASFV presence in nine of 21 AIDS patients using two standard
procedures. At the meeting, Gallo was reported saying: “we know it is
not ASFV.” How could Gallo know this as he hadn’t done any of his own
tests to look for ASFV?
Two months later, Gallo published an article in Science (Oct 31, 1986) that he discovered a new possible co-factor in AIDS, a virus he called Human B Cell Lymphotropic Virus which he named HBLV. Like ASFV, HBLV infected B cells and also lived in macrophages. Did Gallo steal Beldekas’s ASF virus he found in AIDS patients and rename it HBLV? Later on, when Gallo found that HBLV could also infect other immune cells, he changed the name of HBLV to HHV-6. Eventually, Gallo identified his HBLV as the variant A strain of HHV-6 and called it a human herpesvirus.
--Mark Konlee
Two months later, Gallo published an article in Science (Oct 31, 1986) that he discovered a new possible co-factor in AIDS, a virus he called Human B Cell Lymphotropic Virus which he named HBLV. Like ASFV, HBLV infected B cells and also lived in macrophages. Did Gallo steal Beldekas’s ASF virus he found in AIDS patients and rename it HBLV? Later on, when Gallo found that HBLV could also infect other immune cells, he changed the name of HBLV to HHV-6. Eventually, Gallo identified his HBLV as the variant A strain of HHV-6 and called it a human herpesvirus.
--Mark Konlee
http://www.keephopealive.org/report10.html
Russian Scientist: ASF could become a human health risk
"The African swine fever (ASF) virus, may in the future become
dangerous for humans, according to the head of the Russian Epidemiology
Service, Chief State Sanitary Doctor Gennady Onishchenko, at the
press-conference in St. Petersburg. According to him almost all viruses
from time to time go through mutation processes which can give them some
additional functions."
http://www.pigprogress.net/Health-Diseases/Outbreaks/2013/7/ASF-could-become-a-human-health-risk-1308047W/
Background on African Swine Fever Virus as a human pathogen:
"African Swine fever is an endemic disease in sub-Saharan Africa and
many other parts of the developing world. It is caused by the African
Swine virus that primarily replicates in macrophages and monocytes
leading to the impairment of the structure and function of the immune
system of the infected organisms. Until now the African Swine epidemic
continues to spread despite all efforts to contain it. Thus, there is
an objective need for effective, safe and affordable preventive and
therapeutic approaches, in particular for effective vaccines, to
control and eventually eradicate this disease. Since the characteristic
feature of the African Swine virus is to impair the immune system and
to cause immune deficiencies in its hosts the development of vaccines
and other therapeutic approaches against the African Swine virus has
implications for other immune deficiencies or diseases. Several other
viruses are also known to cause immunodeficiency-like syndromes in
humans, including cytomegalovirus, Epstein Barr Virus
and others. Moreover, a series of cases of so-called "idiopathic"
immunodeficiencies have been documented that display
CD4+T-lymphocytopenia with opportunistic infections, but show no
evidence of HIV infection. Since antibodies for the African Swine virus
have been detected in humans, the possibility of human infection with
the African Swine virus exists and may thus far have escaped any systematic screening. Thus, any preventive and therapeutic approach to African Swine fever can have far-reaching implications to control immune deficiency conditions in humans."http://www.faqs.org/patents/app/20080207875
Detection of Novel Sequences Related to African Swine Fever Virus in Human Serum and Sewage.
Loh J, Zhao G, Presti RM, Holtz LR, Finkbeiner SR, Droit L, Villasana Z, Todd C, Pipas JM, Calgua B, Girones R, Wang D, Virgin HW.
Departments of Pathology & Immunology and Molecular Microbiology,
Department of Medicine and Department of Pediatrics, Washington
University School of Medicine, St. Louis, Missouri; Department of
Biological Sciences, University of Pittsburgh, Pittsburgh,
Pennsylvania; Department of Microbiology, Faculty of Biology,
University of Barcelona, Barcelona, Spain.
"The family Asfarviridae contains only a single virus species, African
swine fever virus (ASFV). ASFV is a viral agent with significant
economic impact due to its devastating effects on populations of
domesticated pigs during outbreaks, but has not been reported to infect
humans. We report here the discovery of novel viral sequences in human
serum and sewage which are clearly related to the Asfarvirus family,
but highly divergent from ASFV. Detection of these sequences suggests
that greater genetic diversity may exist among Asfarviruses than
previously thought, and raises the possibility that human infection by
Asfarviruses may occur."
African Swine Fever Virus (Asfarviridae) sequences found in people with febrile illnesses
Abstract
Virus Identification in Unknown Tropical Febrile Illness Cases Using Deep Sequencing
Dengue virus is an emerging infectious agent that infects an estimated
50–100 million people annually worldwide, yet current diagnostic
practices cannot detect an etiologic pathogen in ∼40% of dengue-like
illnesses. Metagenomic approaches to pathogen detection, such as viral
microarrays and deep sequencing, are promising tools to address
emerging and non-diagnosable disease challenges. In this study, we
used the Virochip microarray and deep sequencing to characterize the
spectrum of viruses present in human sera from 123 Nicaraguan patients
presenting with dengue-like symptoms but testing negative for dengue
virus. We utilized a barcoding strategy to simultaneously deep
sequence multiple serum specimens, generating on average over 1
million reads per sample. We then implemented a stepwise bioinformatic
filtering pipeline to remove the majority of human and low-quality
sequences to improve the speed and accuracy of subsequent unbiased
database searches. By deep sequencing, we were able to detect virus
sequence in 37% (45/123) of previously negative cases. These included
13 cases with Human Herpesvirus 6 sequences. Other samples contained
sequences with similarity to sequences from viruses in the Herpesviridae, Flaviviridae, Circoviridae, Anelloviridae, Asfarviridae, and Parvoviridae
families. In some cases, the putative viral sequences were virtually
identical to known viruses, and in others they diverged, suggesting
that they may derive from novel viruses. These results demonstrate the
utility of unbiased metagenomic approaches in the detection of known
and divergent viruses in the study of tropical febrile illness.
Detection of African swine fever virus-like sequences in ponds in the Mississippi Delta through metagenomic sequencing
" . .. further study is needed to characterize their potential risks to both public health and agricultural development."http://link.springer.com/article/10.1007%2Fs11262-013-0878-2
ASF virus, adapted to grow in VERO cells, produces a strong cytopathic effect in human macrophages leading to cell destruction.
http://vir.sgmjournals.org/content/34/3/455.shortTransmitted by Humans
http://www.aasp.org/news/story.php?id=4824
Is this an indication that HHV-8 is really African Swine Fever Virus?
"Primary HHV-8 infection may be associated with fever and a maculopapular rash in immunocompetent children."
High prevalence of antibodies to human herpesvirus 8 in relatives of patients with classic Kaposi's sarcoma from Sardinia.
http://www.ncbi.nlm.nih.gov/pubmed/9607855
Infection with human herpesvirus type 8 and Kaposi's sarcoma in Sardinia.
http://www.ncbi.nlm.nih.gov/pubmed/16501902
Epidemiology of HHV8 in Sardinian emigrants
http://www.dsnm.univr.it/?ent=progetto&id=565
Both ASFV and HHV-8 Interfere with apoptosis.
Are ASFV-infected Pigs the viral source of HHV-8 related Kaposi's Sarcoma in Sardinia? Is a ASFV-related Kaposi's Sarcoma epidemic possible in Russia where ASFV is spreading?
https://hhv6.jottit.com/35._pigs_and_kaposi%27s_sarcoma_in_sardinia
The world's highest incidence of Kaposi's sarcoma occurs in Sardinia (Reference) Is it possible that it is due to the fact that African Swine Fever Virus is endemic on the island? (Reference) One study suggests that the incidence of K.S. in northern Sardinia is highest in a countryside area where people have contact with animals. (Reference) Given the high prevalence of HHV-8,--the so-called K.S. herpes virus--in Sardinia (Reference) is it at all possible that HHV-8 may have been misclassified and actually is a human-adapted form of African Swine Fever Virus? (ASFV has been at least visually mistaken for another herpes virus, CMV, in the past.)
A number of experiments could be conducted to explore this hypothesis. In addition to a direct comparison of ASFV and HHV-8, pigs with African Swine Fever Virus could be tested for sequences of HHV-8. People with Kaposi's sarcoma could be tested for sequences of African Swine Fever, including new Asfaviridae sequences recently discovered. (Reference)
A comparison of the K.S. lesions in humans and ASFV lesions in pigs might be in order.Given that African Swine Fever is currently spreading in Russia and is now threatening Europe and China, (Reference) it would be useful to know whether people who are exposed to pigs with ASFV are at increased risk for HHV-8, Kaposi's sarcoma and the other pathologies associated with HHV-8. A study in sub-Saharan Africa where ASFV is endemic and HHV-8 is also endemic (Reference) might be useful. And areas of Russia where ASFV is spreading could be monitored closely for any signs of an increase of K.S. or HHV-8 infection and HHV-8 related pathologies.HHV-8 is an emerging health problem. HHV-8-associated K.S. is a significant problem in AIDS patients. It may also be the key to Chronic Fatigue Syndrome. HHV-8 has been found in the cerebrospinal fluid of 50% of Chronic Fatigue Syndrome patients. (Reference) HHV-8 has been linked to type 2 diabetes. (Reference) HHV-8 has been detected in B-cells in Castleman's disease and primary effusion lymphoma. (Reference).
If HHV-8 is a form of ASFV, it is possible that pigs might constitute a useful animal model for the study of possible treatments for K.S. and other pathologies associated with HHV-8. And if there is any relationship between ASFV and HHV-8, people may have to be warned to take special precautions around pigs in areas where there are ASFV outbreaks. And countries where undercooked pork is consumed (like Ukraine where salo is a staple) may need to alert the public to cook all pork products thoroughly during ASFV epidemics.
A number of years ago, Neenyah Ostrom reported in the New
York Native on the lesions in CFS patients which seem
to resemble Kaposi's Sarcoma (KS). The current
thinking is that a virus called HHV-8 is the cause of
KS. (Although HHV-6 has recently also been implicated
once again.) If KS is a problem in CFS (and we
suspect it is) then one should be able to find HHV-8 and
HHV-6 in CFS patients. Apparently, in this small
study, one can. Below is a rather explosive abstract:
York Native on the lesions in CFS patients which seem
to resemble Kaposi's Sarcoma (KS). The current
thinking is that a virus called HHV-8 is the cause of
KS. (Although HHV-6 has recently also been implicated
once again.) If KS is a problem in CFS (and we
suspect it is) then one should be able to find HHV-8 and
HHV-6 in CFS patients. Apparently, in this small
study, one can. Below is a rather explosive abstract:
Prevalence in the cerebrospinal fluid of the following
infectious agents in a cohort of 12 CFS subjects:
human herpes virus-6 and 8; chlamydia species;
mycoplasma species; EBV; CMV; and Coxsackievirus.
Levine, S.
Journal of Chronic Fatigue Syndrome, 2001, 9, 1/2,
41-51.
infectious agents in a cohort of 12 CFS subjects:
human herpes virus-6 and 8; chlamydia species;
mycoplasma species; EBV; CMV; and Coxsackievirus.
Levine, S.
Journal of Chronic Fatigue Syndrome, 2001, 9, 1/2,
41-51.
Abstract:
Over the last decade a wide variety of infectious
agents have been associated with the CFS as potential
etiologies for this disorder. Many of these agents are
neurotrophic and have been linked previously to other
diseases involving the central nervous system (CNS).
Human herpes virus-6 (HHV-6), especially the B
variant, has been found in autopsy specimens of
patients who suffered from MS. Because patients with
CFS manifest a wide range of symptoms involving the
CNS as shown by abnormalities on brain MRIs, SPECT
scans of the brain and results of tilt table testing
we sought to determine the prevalence of HHV-6, HHV-8,
Epstein-Barr Virus (EBV), cytomegalovirus (CMV),
mycoplasma species, chlamydia species, and Coxsackie
virus in the spinal fluid of a group of 12 patients
with CFS (CDC criteria '94).
Over the last decade a wide variety of infectious
agents have been associated with the CFS as potential
etiologies for this disorder. Many of these agents are
neurotrophic and have been linked previously to other
diseases involving the central nervous system (CNS).
Human herpes virus-6 (HHV-6), especially the B
variant, has been found in autopsy specimens of
patients who suffered from MS. Because patients with
CFS manifest a wide range of symptoms involving the
CNS as shown by abnormalities on brain MRIs, SPECT
scans of the brain and results of tilt table testing
we sought to determine the prevalence of HHV-6, HHV-8,
Epstein-Barr Virus (EBV), cytomegalovirus (CMV),
mycoplasma species, chlamydia species, and Coxsackie
virus in the spinal fluid of a group of 12 patients
with CFS (CDC criteria '94).
We found evidence of HHV-6, HHV-8, chlamydia species,
CMV and Coxsackie virus in 6/12 samples. Plasma tests
were negative. It was surprising to obtain such a
relatively high yield of infectious agents in cell
free specimens of spinal fluid that had not been
centrifuged. Future research in spinal fluid analysis,
in addition to testing tissue samples by polymerase
chain reaction (PCR) and other direct viral isolation
techniques will be important in characterizing
subpopulations of CFS patients, especially those with
involvement of the CNS.
CMV and Coxsackie virus in 6/12 samples. Plasma tests
were negative. It was surprising to obtain such a
relatively high yield of infectious agents in cell
free specimens of spinal fluid that had not been
centrifuged. Future research in spinal fluid analysis,
in addition to testing tissue samples by polymerase
chain reaction (PCR) and other direct viral isolation
techniques will be important in characterizing
subpopulations of CFS patients, especially those with
involvement of the CNS.
The low rate of isolation of HHV-6 may be related to
the lack of gross neurological findings in the
patients at the time of testing.
the lack of gross neurological findings in the
patients at the time of testing.
An overview of KS:http://www.thebody.com/nmai/ks.html
Except for those who have made a lifelong commitment
to denial, finding the so-called "KS virus" (HHV-8)
and the "supporting KS virus" (HHV-6) in CFIDS patients
should help settle the question of the overlapping
nature of the AIDS and CFIDS epidemics.
to denial, finding the so-called "KS virus" (HHV-8)
and the "supporting KS virus" (HHV-6) in CFIDS patients
should help settle the question of the overlapping
nature of the AIDS and CFIDS epidemics.
More info on KS here.
Given that HHV-8 is part of the HHV-6 and HHV-7 family, this may be very important:
Journal of General virology (1995), 76, 147-152
Click here for more information on this issue.
Given that HHV-8 is part of the HHV-6 and HHV-7 family, this may be very important:
"The 19R Protein of HHV-6 has significant amino acid sequence homology . . . to a protein encoded by African Swine Fever Virus."
--Glenda L. Lawrence, John Nicholas and Bart G. BarrellJournal of General virology (1995), 76, 147-152
Click here for more information on this issue.
