https://www.cnn.com/us/live-news/us-coronavirus-update-04-22-20/h_d7714f05dc8e434921f5b48ecce4484b
We still don't know if pigs in Wuhan and Hubei have been tested for COVID-19. If they are positive for that virus, is it possible that they also transmitted African Swine Fever to COVID-19 patients? Despite what the media has generally reported, people can become infected with African Swine Fever virus.
Is mysterious blood-clotting problem reported on by the Washington Post actually caused by
African Swine Fever virus? Is it a coinfection of COVID-19?
https://www.washingtonpost.com/health/2020/04/22/coronavirus-blood-clots/
Am J Vet Res. 1984 Nov;45(11):2414-20.
Coagulation changes in African swine fever virus infection.
Abstract
Pigs were infected with highly virulent (Tengani '62), with moderately virulent (DR '79) African swine fever (ASF) virus, or with virulent hog cholera (HC) virus. Changes in platelet counts, selected coagulation assays and concentrations of factor VIII-related antigen (VIIIR:Ag) were monitored. Permeability of aortic endothelium was studied after the injection of Evan's blue dye on various days after infection with DR '79 ASF virus. Virulent ASF virus caused prolongation of the activated partial thromboplastin time (APTT), 1-stage prothrombin time, and thrombin clotting time as early as postinoculation day (PID) 4. These changes became progressively more severe until death. Both virulent HC and DR'79 viruses induced an increase APPT and thrombin clotting time at PID 3 to 4, only occasionally did the prothrombin time increased significantly (P less than 0.01). The APPT began to decrease on PID 7 and 8, but only DR'79-infected pigs lived long enough to regain a normal APTT. Infection by ASF viruses caused acute thrombocytopenia after PID 6 and platelet counts of HC virus-infected pigs decreased progressively from the onset of fever to levels of 1 to 2 X 10(5)/mm3 at PID 6 to 7. All ASF virus-infected pigs had an increase in VIIIR:Ag beginning at PID 3, with maximum increases at PID 6 to 7. Hog cholera virus infection did not cause consistent changes in levels of VIIIR:Ag. Pigs infected with DR'79 virus did not have increased vascular permeability to Evan's blue dye during infection; however, there was markedly decreased staining of the aorta after pigs became thrombocytopenic.
African Swine Fever Virus Infection of Porcine Aortic Endothelial Cells Leads to Inhibition of Inflammatory Responses, Activation of the Thrombotic State, and Apoptosis
ABSTRACT
African swine fever (ASF) is an asymptomatic infection of warthogs and bushpigs, which has become an emergent disease of domestic pigs, characterized by hemorrhage, lymphopenia, and disseminated intravascular coagulation. It is caused by a large icosohedral double-stranded DNA virus, African swine fever virus (ASFV), with infection of macrophages well characterized in vitro and in vivo. This study shows that virulent isolates of ASFV also infect primary cultures of porcine aortic endothelial cells and bushpig endothelial cells (BPECs) in vitro. Kinetics of early and late gene expression, viral factory formation, replication, and secretion were similar in endothelial cells and macrophages. However, ASFV-infected endothelial cells died by apoptosis, detected morphologically by terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling and nuclear condensation and biochemically by poly(ADP-ribose) polymerase (PARP) cleavage at 4 h postinfection (hpi). Immediate-early proinflammatory responses were inhibited, characterized by a lack of E-selectin surface expression and interleukin 6 (IL-6) and IL-8 mRNA synthesis. Moreover, ASFV actively downregulated interferon-induced major histocompatibility complex class I surface expression, a strategy by which viruses evade the immune system. Significantly, Western blot analysis showed that the 65-kDa subunit of the transcription factor NF-κB, a central regulator of the early response to viral infection, decreased by 8 hpi and disappeared by 18 hpi. Both disappearance of NF-κB p65 and cleavage of PARP were reversed by the caspase inhibitor z-VAD-fmk. Interestingly, surface expression and mRNA transcription of tissue factor, an important initiator of the coagulation cascade, increased 4 h after ASFV infection. These data suggest a central role for vascular endothelial cells in the hemorrhagic pathogenesis of the disease. Since BPECs infected with ASFV also undergo apoptosis, resistance of the natural host must involve complex pathological factors other than viral tropism.
Haemostatic abnormalities in African swine fever/A comparison of two virus strains of different virulence (Dominican Republic '78 and Malta '78)
Summary
African swine fever (ASF) virus strains cause haemorrhage by producing a variety of defects, which vary in severity from strain to strain. To distinguish the main haemostatic defects leading to haemorrhage, two groups of pigs were infected with moderately virulent (Dominican Republic '78) and less virulent (Malta '78) ASF virus strains. Mortality rate and severity of clinical observations were greater in pigs infected with DR '78 virus compared with pigs infected with Malta '78 virus. The animals became febrile from day 3 to 4 onwards at a time when the viraemia was high (107 to 108 HAD50/ml). No difference was found during the period observed in their pattern of viraemia or pyrexia. Thrombocytopenia developed in both groups but with different kinetics, suggesting two different mechanisms of sequestration of platelets. When coagulation tests were performed, significant abnormalities were found, including evidence for disseminated intravascular coagulation. These abnormalities were much less pronounced in the group infected with Malta '78. Antithrombin III activity did not change significantly in either group. Decreased plasminogen activity was found in the early phase of disease in DR '78 infected pigs. These results indicate that when haemorrhage does occur in DR '78 infected pigs, it is a consequence of more pronounced degrees of haemostatic impairment probably due to a marked endothelial injury and/or generation of procoagulant activity.
African Swine Fever is a big story already because, when and if it spreads to all of Western Europe, all of Asia and the USA (where it may already be in pigs), it will cause the collapse of a major portion of the agricultural export economies of the affected countries. We're talking about many billions of dollars of losses. And the problem is not temporary because those countries will be suspected of harboring the disease in their wild boar and ticks for decades to come. The disease could easily become endemic.
But the issue is so much more important because of the disturbing body of evidence that shows that African Swine Fever Virus can infect humans (despite what authorities currently insist). Thus far, Europe and America's leading publications and journalists have failed to warn the public of the impending ASFV risk to their health. Here are the biggest African Swine Fever stories they have missed.
1. The African Swine Fever Vaccine for humans.
"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
2. Evidence of African Swine Fever found in people with fevers.
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.
"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/
4. 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."
http://www.ncbi.nlm.nih.gov/pubmed/19812170?dopt=Abstract
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."
http://www.ncbi.nlm.nih.gov/pubmed/19812170?dopt=Abstract
5. How the American science Robert Gallo may have stolen the African Swine Fever research of a Boston University scientist and may have given African swine Fever the fraudulent new name of "HHV-6."
"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
6. The epidemiology that suggests that African Swine Fever in people in Sardinia is misidentified as HHV-8.
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.
7. ASF virus, adapted to grow in VERO cells, produces a strong cytopathic effect in human macrophages leading to cell destruction.
8. A sick child tests positive for African Swine Fever virus.
9. Newspaper publisher writes The Chronic Fatigue Syndrome Epidemic Cover-up, a memoir about uncovering the African Swine Fever cover-up in America.
The Chronic Fatigue Syndrome Epidemic Cover-up details the investigative reporting of a New York Native that reveals the Centers for Disease Control and the United States Department of Agriculture lied about the presence of African Swine Fever in pigs and people.
10. Journalist pens The African Swine Fever Novel, an Orwellian novel warning about the consequences of an African Swine Fever Virus epidemic in humans.
The African Swine Fever Novel is available here
11. Prisoners fed meat infected with African Swine Fever
http://www.globalmeatnews.com/Industry-Markets/Russian-prisoners-fed-contaminated-pork
12. African Swine Fever seems to be in the USA already.
https://www.aphis.usda.gov/wildlife_damage/nwrc/publications/13pubs/cunningham131.pdfcanada!
12. African Swine Fever seems to be in the USA already.
https://www.aphis.usda.gov/wildlife_damage/nwrc/publications/13pubs/cunningham131.pdfcanada!
African Swine Fever University Report by rubiconmedia on Scribd
