African Swine Fever Virus
African Swine Fever
Classical swine fever virus
Classical Swine Fever
Viral Structural Proteins
Yellow fever virus
Rift Valley fever virus
Molecular Sequence Data
Open Reading Frames
Amino Acid Sequence
Hemorrhagic Fever Virus, Crimean-Congo
Cytopathogenic Effect, Viral
Rift Valley Fever
Sequence Homology, Amino Acid
A lipid modified ubiquitin is packaged into particles of several enveloped viruses. (1/269)An anti-ubiquitin cross-reactive protein which migrates more slowly (6.5 kDa) by SDS-PAGE than ubiquitin was identified in African swine fever virus particles. This protein was extracted into the detergent phase in Triton X-114 phase separations, showing that it is hydrophobic, and was radiolabelled with both [3H]palmitic acid and [32P]orthophosphate. This indicates that the protein has a similar structure to the membrane associated phosphatidyl ubiquitin described in baculovirus particles. A similar molecule was found in vaccinia virus and herpes simplex virus particles, suggesting that it may be a component of uninfected cell membranes, which is incorporated into membrane layers in virions during morphogenesis. (+info)
Nuclear and nucleolar localization of an African swine fever virus protein, I14L, that is similar to the herpes simplex virus-encoded virulence factor ICP34.5. (2/269)PCR analysis of the genomes of 18 different African swine fever virus (ASFV) isolates showed that the I14L open reading frame (ORF) was present as either a long form or short form in all of the isolates. Sequencing of the ORF from eight isolates confirmed that both forms of the ORF were well conserved. Antisera raised against the I14L protein identified the long form of the protein as a 21 kDa protein expressed late during ASFV infection. Immunofluorescent analysis of transiently expressed haemagglutinin-tagged forms of the I14L protein showed that the long form of the protein localized predominantly to the nucleus and within the nucleoli. In contrast, although the short form of the protein was also present predominantly in the nucleus, it did not localize to the nucleoli. Deletion of the N-terminal 14 amino acids from the long form of the I14L protein, which includes a high proportion of basic Arg/Lys residues, abolished the specific nucleolar localization of the protein, although the protein was still present in the nucleus. Addition of this 14 amino acid sequence to beta-galactosidase or replacement of the N-terminal 14 amino acids of the I14L short form with those from the long form directed both of these modified proteins to the nucleolus. This indicates that this 14 amino acid sequence contains all the signals required for nucleolar localization. (+info)
Modulation of monocytic cell activity and virus susceptibility during differentiation into macrophages. (3/269)A major component of innate immune responses relies on monocytes and macrophages, virus infection of which will pose a particular problem for immunological defense. Consequently, the monocytic cell differentiation pathway was analyzed in terms of cellular modulations therein and their relation to monocytotropic virus infection. Differentiation was characterized by down-regulation of CD14, MHC Ags, the monocytic SWC1 marker, and p53; concomitant up-regulation of the SWC9 macrophage marker, a putative porcine CD80 (detected with anti-human CD80 Ab), and acid phosphatase secretion were also characteristic. Elevated phagocytic and endocytic activities as well as endosomal/lysosomal acidification were identified as being important to the macrophage. In contrast, monocytes possessed high accessory activity. This was multifactorial, concomitantly requiring 1) high MHC Ag expression; 2) enzyme activity of esterase, peroxidase, myeloperoxidase, and 5' nucleotidase in preference to glucosidase, galactosidase, and glucuronidase; and 3) elevated capacity for spontaneous IL-1 production. Only with all parameters was efficient stimulation of Ag-specific lymphocytes possible. These results point to a continuous process during differentiation, involving inter-related characteristics linking the more accessory monocyte to the scavenger macrophage, both in vitro and in vivo. Of particular interest was how these characteristics related to monocytotropic virus infection, and how a particular virus could show a clear preference for the differentiating macrophages. Such results not only further our understanding of porcine immunology, but also provide evidence and a potential model for the determination and characterization of monocytotropic virus-host cell interactions. (+info)
The biological effects induced in mice by p36, a proteinaceous factor of virulence produced by African swine fever virus, are mediated by interleukin-4 and also to a lesser extent by interleukin-10. (4/269)We have previously presented indirect evidence that both specific immunosuppression and lymphocyte mitogenicity induced in mice by p36, a proteinaceous factor of virulence produced by porcine monocytes infected by African swine fever virus, were consistent with a Th2-driven response. Here we show: (1) Interleukin-4 (IL-4) and interleukin-10 (IL-10) mRNA expression in the spleen and thymus of C57BL/6 mice were displayed early after p36 inoculation. The expression of thymic IL-10 mRNA occurred, however, later than that of IL-4 mRNA. (2) Increased serum levels of these two cytokines were also soon detected after the protein inoculation. (3) Both immunosuppressive and mitogenic effects of p36 were absent in IL-4 gene-targeted mice and partially abrogated in mice depleted of IL-4 by neutralizing monoclonal antibodies. (4) IL-10 depletion abrogated the immunosuppressive but not the p36 lymphocyte mitogenic biological effects. (5) The increase in the serum concentrations of both IL-4 and IL-10 were lower in thymectomized than in non-thymectomized mice. (6) The expression of interferon-gamma (IFN-gamma) mRNA was weakly or not at all induced in p36-treated mice. Taken together, these results are in agreement with the promotion of a Th2 immune response induced by p36. (+info)
Replication of African swine fever virus DNA in infected cells. (5/269)We have examined the ultrastructural localization of African swine fever virus DNA in thin-sections of infected cells by in situ hybridization and autoradiography. Virus-specific DNA sequences were found in the nucleus of infected Vero cells at early times in the synthesis of the viral DNA, forming dense foci localized in proximity to the nuclear membrane. At later times, the viral DNA was found exclusively in the cytoplasm. Electron microscopic autoradiography of African swine fever virus-infected macrophages showed that the nucleus is also a site of viral DNA replication at early times. These results provide further evidence of the existence of nuclear and cytoplasmic stages in the synthesis of African swine fever virus DNA. On the other hand, alkaline sucrose sedimentation analysis of the replicative intermediates synthesized in the nucleus and cytoplasm of infected macrophages showed that small DNA fragments ( approximately 6-12S) were synthesized in the nucleus at an early time, whereas at later times, larger fragments of approximately 37-49S were labeled in the cytoplasm. Pulse-chase experiments demonstrated that these fragments are precursors of the mature cross-linked viral DNA. The formation of dimeric concatemers, which are predominantly head-to-head linked, was observed by pulsed-field electrophoresis and restriction enzyme analysis at intermediate and late times in the replication of African swine fever virus DNA. Our findings suggest that the replication of African swine fever virus DNA proceeds by a de novo start mechanism with the synthesis of small DNA fragments, which are then converted into larger size molecules. Ligation or further elongation of these molecules would originate a two-unit concatemer with dimeric ends that could be resolved to generate the genomic DNA by site-specific nicking, rearrangement, and ligation as has been proposed in the de novo start model of Baroudy et al. (B. M. Baroudy, S. Venkatesam, and B. Moss, 1982, Cold Spring Harbor Symp. Quant. Biol. 47, 723-729) for the replication of vaccinia virus DNA. (+info)
The African swine fever virus prenyltransferase is an integral membrane trans-geranylgeranyl-diphosphate synthase. (6/269)In a previous study, it was shown that the protein encoded by the gene B318L of African swine fever virus (ASFV) is a trans-prenyltransferase that catalyzes in vitro the condensation of farnesyl diphosphate and isopentenyl diphosphate to synthesize geranylgeranyl diphosphate and longer chain prenyl diphosphates (Alejo, A., Yanez, R. J., Rodriguez, J. M., Vinuela, E., and Salas, M. L. (1997) J. Biol. Chem. 272, 9417-9423). To investigate the in vivo function of the viral enzyme, we have determined, in this work, its subcellular localization and activity in cell extracts. Two systems were used in these studies: cells infected with ASFV and cells infected with a recombinant pseudo-Sindbis virus carrying the complete B318L gene. In this latter system, the trans-prenyltransferase was found to colocalize with the endoplasmic reticulum marker protein-disulfide isomerase, whereas in cells infected with ASFV, the viral enzyme was present in cytoplasmic viral assembly sites, associated with precursor viral membranes derived from the endoplasmic reticulum. In addition, after subcellular fractionation, the viral enzyme partitioned into the membrane fraction. Extraction of membrane proteins with alkaline carbonate and Triton X-114 indicated that the ASFV enzyme behaved as an integral membrane protein. The membrane enzyme synthesized predominantly all-trans-geranylgeranyl diphosphate from farnesyl diphosphate and isopentenyl diphosphate. These results indicate that the viral B318L protein is a trans-geranylgeranyl-diphosphate synthase, being the only enzyme of this type that is known to have a membrane localization. (+info)
African swine fever virus: a B cell-mitogenic virus in vivo and in vitro. (7/269)The two major characteristics of pathogenesis in African swine fever virus (ASFV) infections of domestic pigs are massive B-cell apoptosis and haemorrhage. The effects of ASFV on porcine B cells have therefore been systematically examined in vivo, by using virus-infected pigs and SCID-Beige mice reconstituted with porcine bone marrow, and in vitro, by using porcine B-cell lines and B cells from normal and ASFV-infected pigs. Secretion of porcine Ig was stimulated by ASFV both in vivo and in bone marrow cultures in vitro, with the virulent Malawi isolate of ASFV being the most effective. Stimulation of Ig secretion in vitro depended on the presence of ASFV-infected macrophages and did not occur with supernatants from ASFV-infected macrophages. Although the virus alone did not stimulate proliferation of purified B cells in vitro, it was co-stimulatory with CD154 (CD40 ligand). The B cells recovered from ASFV-infected porcine lymphoid tissue were of activated surface marker phenotypes and, interestingly, expressed diminished levels of the B-cell co-stimulatory surface molecule CD21. In addition, they were highly sensitive to IL-4 and CD154. These results may be integrated into a model of pathogenesis in which those B cells activated indirectly as a result of virulent ASFV infection of macrophages are not rescued from apoptosis through interaction with CD154, due to the drastic depletion of T cells that occurs early in infection. The consequently diminished specific anti-ASFV antibody response would favour survival of the virus, with the non-specific hypergammaglobulinaemia being perhaps another example of pathogen-mediated immune deviation. (+info)
African swine fever virus replication in the midgut epithelium is required for infection of Ornithodoros ticks. (8/269)Although the Malawi Lil20/1 (MAL) strain of African swine fever virus (ASFV) was isolated from Ornithodoros sp. ticks, our attempts to experimentally infect ticks by feeding them this strain failed. Ten different collections of Ornithodorus porcinus porcinus ticks and one collection of O. porcinus domesticus ticks were orally exposed to a high titer of MAL. At 3 weeks postinoculation (p.i.), <25% of the ticks contained detectable virus, with viral titers of <4 log(10) 50% hemadsorbing doses/ml. Viral titers declined to undetectability in >90% of the ticks by 5 weeks p.i. To further study the growth defect, O. porcinus porcinus ticks were orally exposed to MAL and assayed at regular intervals p.i. Whole-tick viral titers dramatically declined (>1,000-fold) between 2 and 6 days p.i., and by 18 days p.i., viral titers were below the detection limit. In contrast, viral titers of ticks orally exposed to a tick-competent ASFV isolate, Pretoriuskop/96/4/1 (Pr4), increased 10-fold by 10 days p.i. and 50-fold by 14 days p.i. Early viral gene expression, but not extensive late gene expression or viral DNA synthesis, was detected in the midguts of ticks orally exposed to MAL. Ultrastructural analysis demonstrated that progeny virus was rarely present in ticks orally exposed to MAL and, when present, was associated with extensive cytopathology of phagocytic midgut epithelial cells. To determine if viral replication was restricted only in the midgut epithelium, parenteral inoculations into the hemocoel were performed. With inoculation by this route, a persistent infection was established although a delay in generalization of MAL was detected and viral titers in most tissues were typically 10- to 1,000-fold lower than those of ticks injected with Pr4. MAL was detected in both the salivary secretion and coxal fluid following feeding but less frequently and at a lower titer compared to Pr4. Transovarial transmission of MAL was not detected after two gonotrophic cycles. Ultrastructural analysis demonstrated that, when injected, MAL replicated in a number of cell types but failed to replicate in midgut epithelial cells. In contrast, ticks injected with Pr4 had replicating virus in midgut epithelial cells. Together, these results indicate that MAL replication is restricted in midgut epithelial cells. This finding demonstrates the importance of viral replication in the midgut for successful ASFV infection of the arthropod host. (+info)
The symptoms of ASF are varied and can include:
* High fever
* Loss of appetite
* Weakness and lethargy
* Reduced productivity and milk production in breeding pigs
* Hemorrhages and skin lesions, which can be severe and fatal.
ASF is transmitted through direct contact with infected animals or contaminated objects, such as meat products, animal feed, or farming equipment. The virus can also be spread by flies, ticks, and other insects that have fed on infected pigs.
There is no specific treatment for ASF, and control measures are largely focused on preventing the spread of the disease. These include:
* Implementing strict biosecurity measures, such as isolating infected animals, disinfecting equipment and facilities, and using protective clothing and gear.
* Vaccination of pigs, which can help reduce the severity of symptoms and prevent the spread of the disease.
* Culling of infected animals to prevent the spread of the disease and minimize economic losses.
* Implementing trade restrictions and surveillance programs to prevent the spread of ASF to other countries.
ASF has significant economic and social impacts on affected communities, particularly in Africa where it is a major threat to food security and livelihoods. The disease has also had significant impacts on global pork supplies, leading to increased prices and trade restrictions.
The virus is transmitted through contact with infected animals, contaminated objects or people, or through the consumption of contaminated food or water. The disease can be spread quickly in populations of pigs, especially in areas where there are high densities of animals.
Classical Swine Fever is characterized by a sudden onset of fever, loss of appetite, and vomiting, followed by hemorrhagic diarrhea, lethargy, and difficulty breathing. The disease can be fatal in up to 90% of cases, especially in young pigs.
Diagnosis is typically made through a combination of clinical signs, laboratory tests, and serology. There is no specific treatment for Classical Swine Fever, and control measures focus on preventing the spread of the disease. Vaccination is an important tool in controlling outbreaks, and strict biosecurity measures can help to reduce the risk of transmission.
In addition to its impact on animal health, Classical Swine Fever can also have significant economic and social implications for the swine industry. Outbreaks can lead to significant losses, and the disease can be difficult to control, especially in areas with limited resources and infrastructure.
A disease that affects pigs, including viral, bacterial, and parasitic infections, as well as genetic disorders and nutritional deficiencies. Some common swine diseases include:
1. Porcine Reproductive and Respiratory Syndrome (PRRS): A highly contagious viral disease that can cause reproductive failure, respiratory problems, and death.
2. Swine Influenza: A viral infection similar to human influenza, which can cause fever, coughing, and pneumonia in pigs.
3. Erysipelas: A bacterial infection that causes high fever, loss of appetite, and skin lesions in pigs.
4. Actinobacillosis: A bacterial infection that can cause pneumonia, arthritis, and abscesses in pigs.
5. Parasitic infections: Such as gastrointestinal parasites like roundworms and tapeworms, which can cause diarrhea, anemia, and weight loss in pigs.
6. Scrapie: A degenerative neurological disorder that affects pigs and other animals, causing confusion, aggression, and eventually death.
7. Nutritional deficiencies: Such as a lack of vitamin E or selenium, which can cause a range of health problems in pigs, including muscular dystrophy and anemia.
8. Genetic disorders: Such as achondroplasia, a condition that causes dwarfism and deformities in pigs.
9. Environmental diseases: Such as heat stress, which can cause a range of health problems in pigs, including respiratory distress and death.
It's important to note that many swine diseases have similar symptoms, making accurate diagnosis by a veterinarian essential for effective treatment and control.
There are different types of fever, including:
1. Pyrexia: This is the medical term for fever. It is used to describe a body temperature that is above normal, usually above 38°C (100.4°F).
2. Hyperthermia: This is a more severe form of fever, where the body temperature rises significantly above normal levels.
3. Febrile seizure: This is a seizure that occurs in children who have a high fever.
4. Remittent fever: This is a type of fever that comes and goes over a period of time.
5. Intermittent fever: This is a type of fever that recurs at regular intervals.
6. Chronic fever: This is a type of fever that persists for an extended period of time, often more than 3 weeks.
The symptoms of fever can vary depending on the underlying cause, but common symptoms include:
* Elevated body temperature
* Muscle aches
* Loss of appetite
In some cases, fever can be a sign of a serious underlying condition, such as pneumonia, meningitis, or sepsis. It is important to seek medical attention if you or someone in your care has a fever, especially if it is accompanied by other symptoms such as difficulty breathing, confusion, or chest pain.
Treatment for fever depends on the underlying cause and the severity of the symptoms. In some cases, medication such as acetaminophen (paracetamol) or ibuprofen may be prescribed to help reduce the fever. It is important to follow the recommended dosage instructions carefully and to consult with a healthcare professional before giving medication to children.
In addition to medication, there are other ways to help manage fever symptoms at home. These include:
* Drinking plenty of fluids to stay hydrated
* Taking cool baths or using a cool compress to reduce body temperature
* Resting and avoiding strenuous activities
* Using over-the-counter pain relievers, such as acetaminophen (paracetamol) or ibuprofen, to help manage headache and muscle aches.
Preventive measures for fever include:
* Practicing good hygiene, such as washing your hands frequently and avoiding close contact with people who are sick
* Staying up to date on vaccinations, which can help prevent certain infections that can cause fever.
Yellow fever is a serious and sometimes fatal disease, with a high mortality rate in unvaccinated individuals. However, it can be prevented through vaccination, which is recommended for all travelers to areas where the virus is present. The Centers for Disease Control and Prevention (CDC) and the World Health Organization (WHO) both recommend that travelers to these areas receive a yellow fever vaccine at least 10 days before travel to ensure adequate protection.
Yellow fever is not contagious, meaning it cannot be spread from person to person through casual contact. However, infected mosquitoes can transmit the virus to other animals and humans. The virus is most commonly found in monkeys and other primates, which can become carriers of the disease without showing any symptoms.
There are several strains of the yellow fever virus, with some being more virulent than others. The most common strain is the Asibi strain, which is found in West Africa and is responsible for most outbreaks of the disease. Other strains include the Central African, East African, and South American strains.
Yellow fever was first identified in the 17th century in West Africa, where it was known as "yellow jack" due to the yellowish tint of the skin of infected individuals. The disease spread throughout the Americas during the colonial period, where it caused devastating outbreaks and killed millions of people. In the United States, yellow fever was eradicated in the early 20th century through vaccination and mosquito control measures. However, it still remains a significant public health threat in many parts of the world today.
Prevention of yellow fever is primarily achieved through vaccination, which is recommended for travelers to areas where the disease is common. Vaccines are available in different forms, including injectable and oral versions, and they provide long-lasting protection against the virus. In addition to vaccination, other measures can be taken to prevent the spread of yellow fever, such as using insect repellents and wearing protective clothing to prevent mosquito bites.
There is no specific treatment for yellow fever, and treatment is primarily focused on managing symptoms and supporting the body's immune response. In severe cases, hospitalization may be necessary to provide intravenous fluids and other supportive care. Antiviral medications may also be used in some cases to help reduce the severity of the disease.
Prevention is key to avoiding yellow fever, and vaccination is the most effective way to protect against this deadly disease. By understanding the causes, symptoms, and prevention methods for yellow fever, individuals can take steps to protect themselves and their loved ones from this potentially deadly illness.
The symptoms of RVF in humans can range from mild to severe and include fever, headache, muscle pain, joint pain, and bleeding disorders. In severe cases, RVF can cause hemorrhagic fever, which can lead to death. Pregnant women, the elderly, and young children are at higher risk for developing severe forms of the disease.
RVF is typically diagnosed through a combination of physical examination, laboratory tests such as PCR or ELISA, and serology. Treatment is primarily focused on relieving symptoms and supporting vital organ function, and may include antiviral medications, antibiotics, and blood transfusions.
Prevention of RVF relies on controlling the transmission of the virus by reducing the population of infected mosquitoes through insecticides, eliminating standing water where mosquitoes can breed, and protecting against mosquito bites using personal protective measures such as long sleeves, pants, and insect repellents. Vaccines are also being developed to prevent RVF.
Rift Valley fever is a significant public health concern in Africa and the Arabian Peninsula, where it can have a significant impact on human health, animal production, and economic development. Outbreaks of RVF can lead to significant morbidity and mortality, as well as disruption of social and economic activities.
African swine fever virus
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Craig Mosman of Idaho Comments on African Swine Fever Crisis - Career Ramblings
- African swine fever (ASF) is a highly contagious and deadly hemorrhagic disease of domestic pigs caused by African swine fever virus (ASFV), a double-strand DNA virus of the family Asfarviridae and genus Asfivirus ( 1 ). (cdc.gov)
- Historically, all ASFV p72 genotypes have been circulating in eastern and southern Africa, and genotype I has been circulating in Europe, South America, the Caribbean, and western Africa ( 2 , 3 ). (cdc.gov)
- Spread of ASFV beyond traditional geographic boundaries occurred with incursion of p72 genotype II into the Republic of Georgia and its subsequent spread into Armenia, Azerbaijan, and Russia ( 4 , 5 ) and incursion of genotype IX into western Africa ( 6 ). (cdc.gov)
- A) Ticks fed on African swine fever virus (ASFV) strain OUR T88/1 at 4 log 10 50% hemadsorbing doses (HAD 50 )/mL. (cdc.gov)
- Ticks that fed on blood containing 6 log 10 HAD 50 ASFV on average had virus titers 2.15 log 10 HAD 50 higher than those for ticks that fed on blood containing 4 log 10 HAD 50 /mL. (cdc.gov)
- African swine fever virus (ASFV) causes a devastating hemorrhagic disease with worldwide circulation and no widely available therapeutic prevention. (bvsalud.org)
- African swine fever (ASF) is an acute, highly contagious, and highly contagious disease caused by ASFV, which is infected by pigs and wild boars. (yeasenbiotech.com)
- African swine fever virus (ASFV) causes a devastating disease in swine, called African swine fever (ASF), that is currently spreading across Europe and Asia. (usda.gov)
- In this study we were able to delete a structural protein in ASFV, however deletion of this structural protein did not have any effect on virus replication or virulence. (usda.gov)
- African swine fever virus (ASFV) causes a devastating disease of swine currently spread from Central Europe to Asia. (usda.gov)
- ASFV is a large, structurally complex virus with a large dsDNA genome encoding for more than 160 genes, most of them still uncharacterized. (usda.gov)
- p22, encoded by ASFV gene KP177R, is a structural virus protein located in the inner envelope of the ASFV particle. (usda.gov)
- Here we describe the development of a recombinant ASFV (ASFV-G-'KP177R) lacking the KP177R gene as a tool to evaluate p22 role in virus replication and virulence in swine. (usda.gov)
- African swine fever virus (ASFV) encodes more than 150 proteins, most of them of unknown function. (bvsalud.org)
- African swine fever virus (ASFV) infectious cycle starts with the viral adsorption and entry into the host cell. (bvsalud.org)
- African Swine Fever (ASF) caused by the African Swine Fever Virus (ASFV) is a highly contagious and fatal disease of feral and domestic swine that has recently caused worldwide economic and food security concerns. (careerramblings.com)
- Since the identification of ASFV more than 100 years ago, Craig Mosman of Idaho acknowledges that there has not been a recorded case where this complex virus mutated and infected humans. (careerramblings.com)
- Given the fact that ASFV is in this hemisphere, the hardiness of the virus, and the many methods…intentional and unintentional…that ASFV could travel to the US, it is likely that the US will experience an outbreak of ASFV in the next 12-18 months. (careerramblings.com)
- Previous studies suggest that it takes 3-4 weeks for ticks to completely digest and clear ingested blood and that virus isolated after this period is due to viral replication ( 5 , 6 ). (cdc.gov)
- By using magnetic beads with a unique separation function and carefully optimized buffer system to efficiently capture the released nucleic acid, it can be used to isolate and purify high-quality viral DNA / RNA from various swabs and virus culture supernatants. (yeasenbiotech.com)
- African swine fever is a viral disease that causes high fevers and haemorrhaging in pigs and wild boars. (thepigsite.com)
- Since that time, researchers around the world have identified thousands of different viruses, many of which still cause massive morbidity and mortality, despite intense global efforts to create anti-viral therapies. (nih.gov)
- African swine fever virus CD2v protein ELISA antibody detection kit can be used for the differential diagnosis of pigs infected with African swine fever virus wild strains and CD2v gene deletion strains by detecting African swine fever virus CD2v protein specific antibodies in pig serum. (hwtai.com)
- African swine fever is a highly contagious virus that causes high death rates in pigs. (wa.gov.au)
- Recently, the USDA put out warnings and resources for protecting pigs from African Swine Fever - a deadly virus affecting pigs. (sanctuaryfederation.org)
- Cebu Provincial Veterinarian Dr. Rose Vincoy on Monday (March 6, 2023) said Governor Gwendolyn Garcia has issued an executive order implementing a temporary ban on the entry of live hogs, sows, piglets, boar semen, pork, and pork-related products from Negros Island, after the detection of African swine fever virus from pigs that co-comingled with other pigs from the neighboring island. (gov.ph)
- There is no effective treatment or cure, and so the protocol used to stop the spread of the virus is to cull the pigs within a 2 mile radius of any outbreak. (careerramblings.com)
- It survives in soil and water, and studies have noted the spread of the virus in trucks used to transport pigs, and in clothes, equipment, or footwear that has come in contact with the virus. (careerramblings.com)
- Among laboratory detection technologies, qPCR is an important tool for routine diagnosis of African swine fever recommended by OIE, and it is also the preferred detection technology in China at the current stage of the African swine fever epidemic. (yeasenbiotech.com)
- TWiV provides updates on the new coronavirus causing respiratory disease in China, the current influenza season, and the epidemic of African swine fever, including determination of the three-dimensional structure of the virus particle. (virology.ws)
- As African swine fever has been spreading rapidly through Eastern Europe and now threatens to make inroads to the west, a cohort of Ukrainian lab technicians is now trained in the latest and most effective methods for diagnosing the disease and containing the epidemic, reports FAO. (thepigsite.com)
- The recombinant African swine fever virus CD2v protein was pre-coated on the wells of the microplate strip. (hwtai.com)
- Currently, there is no vaccine or effective treatment for African swine fever. (yeasenbiotech.com)
- Largely because there is no treatment or vaccine, the US remains defenseless to the virus. (careerramblings.com)
- IRP researchers have developed an Ebola vaccine, which is under clinical trials in Africa. (nih.gov)
- CEBU CITY - The provincial government of Cebu has banned the entry of live hogs, sows, piglets, boar semen, pork, and pork-related products from Negros Island after the detection of the African swine fever (ASF) virus in Carcar City. (gov.ph)
- The spectacular recent spread of African swine fever (ASF) in Eastern Europe and Asia has been strongly associated, as it is in the endemic areas in Africa, with free-ranging pig populations and low-biosecurity backyard pig farming. (mdpi.com)
- Disease is endemic in domestic swine in many African countries and Sardinia. (nih.gov)
Foreign Animal Diseases1
- Evaluating the sensitivity of US surveillance system for tier-1 foreign animal diseases of swine. (umn.edu)
- ORF-Interrupting Mutations in Monkeypox Virus Genomes from Washington and Ohio, 2022. (cdc.gov)
- On October 11th, GFAS will once again host Giving Day for Apes, a 24-hour event in which ape sanctuaries and rescue centers throughout North America, Africa and Asia will raise funds, raise awareness about their work, and compete for prizes throughout the day. (sanctuaryfederation.org)
- The Foundation for Food & Agriculture Research recently awarded a $150,000 Rapid Outcomes from Agriculture Research grant to Kansas State University to help with the development of vaccines for African swine fever virus. (k-state.edu)
- A plaque assay for ASF virus adapted to grow in VERO cells gives a titre similar to that obtained using the haemadsorption microtest, and in both the micromethod and the plaque assay infection may be produced by a single infective particle. (semanticscholar.org)
- 17. Inhibition of BET Family Proteins Suppresses African Swine Fever Virus Infection. (nih.gov)
- While the disease poses no danger to human health or to other animals, it threatens the entire European swine industry, jeopardising livelihoods, food security and nutrition. (thepigsite.com)
- The concept of a virus, an infectious particle that is generally much smaller than most bacteria, would not be published until 1892, five years after the NIH was established. (nih.gov)
- We need to have a new strategy of therapeutics and prophylactics that will stop the replication and spread of this deadly virus. (careerramblings.com)
- Ebola virus, affecting animal e.g. (dsv.com)
- Viruses have surface proteins which bind to host cells. (careerramblings.com)
- According to her, authorities detected the presence of the ASF virus in blood samples of hogs in the southern city of Carcar on March 1. (gov.ph)
- A Custom Hepatitis A Virus Assay for Whole-Genome Sequencing. (cdc.gov)
- Andriy Rozstalnyy, an animal health expert based at FAO's regional office in Budapest, explained: "The key to curbing the outbreak is identifying the virus and isolating all infected livestock quickly. (thepigsite.com)
- The technicians, coming from veterinary medicine laboratories across Ukraine, were trained to accurately and efficiently diagnose African swine fever using molecular genetics and serological research methods. (thepigsite.com)
- Virus titers were estimated on porcine bone marrow cells ( 7 ) and expressed as log 10 HAD 50 per tick. (cdc.gov)
- On a positive note, this virus is NOT yet in the United States, but is spreading in Europe, Haiti, Dominican Republic and Africa. (sanctuaryfederation.org)
- In the past few years this virus has already traveled quickly from Europe, across Russia, into China, throughout Southeast Asia, to India, and jumped the Atlantic to arrive in the Dominican Republic and Haiti. (careerramblings.com)
- UKRAINE - FAO reports that training sessions in Kiev in October have helped the country to improve control of African swine fever. (thepigsite.com)
- Did researchers actually discover the virus? (nomorefakenews.com)
- She said so far, the other tests have returned negative for the ASF virus. (gov.ph)
- Similar to other viruses, ASF virion is then internalized and incorporated into the endocytic pathway. (bvsalud.org)
- Click on the PDF icon to the left to view a copy of this virus entry in PDF format. (cdc.gov)
- Why do bat viruses keep infecting people? (cdc.gov)