Slow Virus Diseases
Pulmonary Adenomatosis, Ovine
Marburg Virus Disease
Ross River virus
Hemorrhagic Fevers, Viral
Alphavirus Infections
Creutzfeldt--Jakob disease. (1/23)
The laboratory transmission to animals of an apparently degenerative disease of the nervous system, Creutzfeldt-Jakob disease (CJD), is now well established. Important questions arising from this observation are the possibility of natural transmission or infectivity and the existence of other similarly transmissible diseases. Epidemiological studies have revealed some possible clusters of CJD and also an association with previous craniotomy, but there is no definite evidence of natural infection. A few instances have been reported of experimental CJD in animals following inoculation with material from Alzheimer's disease, but apart from this there is so far no evidence of transmission of any other form of degenerative nervous disease. (+info)Effects of 5-bromodeoxyuridine and 5-iododeoxyuridine on a latent herpes simplex virus infection. (2/23)
A latent herpes simplex virus infection was established in rabbit kidney cells. Treatment of the cells with 5-bromo-2-deoxyuridine after the latent infection was established had no effect on the rate of virus recovery but did extend the latent period before active virus growth resumed. In contrast to this, treatment of cells with 5-bromo-2-deoxyuridine or 5-iodo-2-deoxyuridine prior to infection with virus increased the subsequent rate of virus recovery. (+info)Fatal familial insomnia, a prion disease with a mutation at codon 178 of the prion protein gene. (3/23)
BACKGROUND: We previously described two members of a family affected by an apparently genetically determined fatal disease characterized clinically by progressive insomnia, dysautonomia, and motor signs and characterized pathologically by severe atrophy of the anterior ventral and mediodorsal thalamic nuclei. Five other family members who died of this disease, which we termed "fatal familial insomnia," had broader neuropathologic changes suggesting that fatal familial insomnia could be a prion disease. METHODS: We used antibodies to prion protein (PrP) to perform dot and Western blot analyses, with and without proteinase K, on brain tissue obtained at autopsy from two patients with fatal familial insomnia, three patients with sporadic Creutzfeldt-Jakob disease, and six control subjects. The coding region of the PrP gene was amplified and sequenced in the samples from the two patients with fatal familial insomnia. Restriction-enzyme analysis was carried out with amplified PrP DNA from 33 members of the kindred. RESULTS: Protease-resistant PrP was found in both patients with fatal familial insomnia, but the size and number of protease-resistant fragments differed from those in Creutzfeldt-Jakob disease. In the family with fatal familial insomnia, all 4 affected members and 11 of the 29 unaffected members had a point mutation in PrP codon 178 that results in the substitution of asparagine for aspartic acid and elimination of the Tth111 I restriction site. Linkage analysis showed a close relation between the point mutation and the disease (maximal lod score, 3.4 when theta was zero). CONCLUSIONS: Fatal familial insomnia is a prion disease with a mutation in codon 178 of the PrP gene, but the disease phenotype seems to differ from that of previously described kindreds with the same point mutation. (+info)Persistent or slow viral infections and related diseases. (4/23)
The discovery of persistent transmissible agents by veterinarians has led to striking advances in the infectious cause of neuropathies of human beings. There is evidence for persisting infection in congenital rubella and the herpes group of viruses including cytomegalovirus infections. Hepatitis types A and B are candidates for inclusion in the category of persisting viral infections. The rubeola or measles virus is established as a persistent virus which causes elevated antibodies in the serum and cerebrospinal fluid of many patients with severe demyelinating disease such as subacute sclerosing panencephalitis and multiple sclerosis. Elevated antibodies against vaccinia virus have been found in the cerebrospinal fluid of some patients with multiple sclerosis and neuromyelitis optica, a rare form of multiple sclerosis. (+info)Morphological and virological investigations of cell strains cultured from the brain in Jakob-Creutzfeldt disease and subacute sclerosing panencephalitis. (5/23)
Cell strains were established in culture from fragments of the brain from 2 cases each of Jakob-Creutzfeldt (JC) disease and subacute sclerosing panencephalitis (SSPE). After about 12 weeks strains from the former spontaneously formed persistent heaped up nodules of cells which appeared to produce reticulin-like fibrils as well as confluent sheets of rounded and spindle, fibroblast-like cells. Similar sheets of cells were obtained from the cases of SSPE but the only nodules formed were smaller and ephemeral. Attempts to detect virus in all 4 strains were made by inoculation of supernatant fluids into cultures of other laboratory cells, haemadsorption, co-cultivation, electron microscopy and immunofluorescence, and testing for interferon production. No evidence was found by any of these methods of the persistent presence of virus in the strains. Immunofluorescence revealed a probable anti-glial cell IgM autoantibody in one case of JC disease. Morphologically some cells resembled astrocytes and others fibroblasts. Those from JC disease contained more vacuoles and redundant membranes than did those from the cases of SSPE, features that are particularly striking in brain cells in human and animal cases of the spongiform encephalopathies. (+info)Epidemiological and experimental studies on a new incident of transmissible mink encephalopathy. (6/23)
Epidemiological investigation of a new incident of transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin, U.S.A. in 1985 revealed that the mink rancher had never fed sheep products to his mink but did feed them large amounts of products from fallen or sick dairy cattle. To investigate the possibility that this occurrence of TME may have resulted from exposure to infected cattle, two Holstein bull calves were injected intracerebrally with mink brain from the Stetsonville ranch. Each bull developed a fatal spongiform encephalopathy 18 and 19 months after inoculation, respectively, and both bovine brains passaged back into mink were highly pathogenic by either intracerebral or oral inoculation. These results suggest the presence of a previously unrecognized scrapie-like infection in cattle in the United States. (+info)Pathogenesis of the slow disease of the central nervous system associated with WM 1504 E virus. I. Relationship of strain susceptibility and replication to disease. (7/23)
Inbred mouse strains vary considerably in their susceptibility to the chronic neurologic disease caused by WM 1504 E virus. Although all strains inoculated with the virus showed evidence of viral replication, those strains destined to develop chronic disease showed consistently higher titers of viral antigen in their sera and also in their tissues, particularly in the central nervous system, than did resistant strains. Studies of hybrids made by mating susceptible C57BR/cdJ and resistant C57BL/6J strains indicated that resistance is dominant and not sex linked. The major areas of injury included neurons in the anterior horn of the spinal cord, the dentate nucleus of the cerebellum, and other nuclei in the brain stem. Involvement of oligodendrocytes with associated primary demyelination was also noted. Tissue damage accompanied intense gliosis but was without leukocyte infiltration. Immunopathologic studies and parabiotic experiments suggested that tissue injury was likely due to primary direct viral effects. Further, thymus-insufficient nude mice developed this chronic neurologic disease. (+info)Virus mutation during 'slow infection': temporal development and characterization of mutants of visna virus recovered from sheep. (8/23)
Visna virus could be recovered from peripheral blood leukocytes of sheep for years after intracerebral inoculation. Viruses recovered from sheep prior to and several months after development of antibody were antigenically identical to the parental strain used for inoculation. Subsequently, mutant viruses which were not neutralized by the animals' sera were obtained. Longitudinal studies of leukocyte viruses collected from two infected sheep showed that more than one strain of virus could co-exist in the animal. Virus neutralization tests using sequentially collected sera and the viruses recovered from leukocytes revealed a sequential development of antibody to parental and then to each strain of mutant virus. Characterization of two of the mutant viruses showed that they were antigenically stable, virulent in cell culture and when inoculated into new sheep, elicited antibodies which cross reacted with the parental virus from which they were derived. This continuous mutation of Visna virus in persistently infected sheep may be a mechanism for the production of chronic disease. (+info)Slow virus diseases, also known as persistent viral infections or chronic viral infections, are characterized by a lengthy incubation period and a slow progression of symptoms. These viruses can remain dormant in the body for extended periods, sometimes even years, before they start causing damage to cells and tissues.
The term "slow virus" is somewhat misleading because it does not necessarily mean that the virus itself is slow-replicating. Instead, it refers to the fact that the disease progression is slow and can take a long time to manifest symptoms. The immune system may have difficulty recognizing and eliminating these viruses, allowing them to persist in the body and cause ongoing damage over time.
Examples of slow virus diseases include:
1. Progressive multifocal leukoencephalopathy (PML): A rare and serious brain infection caused by the JC virus that primarily affects people with weakened immune systems, such as those with HIV/AIDS or those taking immunosuppressive drugs.
2. Subacute sclerosing panencephalitis (SSPE): A progressive neurological disorder caused by a measles virus infection that has become persistent in the brain. It primarily affects children and young adults who had measles during their early childhood.
3. Kuru: A rare, fatal degenerative neurological disorder that was once prevalent among the Fore people of Papua New Guinea. It is caused by an infectious protein called a prion, which can be transmitted through cannibalistic practices.
4. Creutzfeldt-Jakob disease (CJD): A rare and fatal brain disorder caused by prions. There are several types of CJD, including sporadic, hereditary, and acquired forms. The acquired form is a slow virus disease that can be transmitted through contaminated surgical instruments or dura mater grafts.
5. Human T-lymphotropic virus type 1 (HTLV-1) infection: A retrovirus that can cause adult T-cell leukemia/lymphoma and a progressive neurological disorder called HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP).
6. Progressive multifocal leukoencephalopathy (PML): A rare, often fatal demyelinating disease of the central nervous system caused by the JC polyomavirus. It primarily affects individuals with weakened immune systems, such as those with HIV/AIDS or those receiving immunosuppressive therapy for organ transplantation.
I'm sorry for any confusion, but "Viruses, Unclassified" is not a recognized medical or scientific category. Generally, viruses are classified based on various characteristics such as genome structure, mode of replication, host range, and symptoms they cause. The International Committee on Taxonomy of Viruses (ICTV) is the organization responsible for the formal classification of viruses.
If you have any specific questions about certain unclassified viral entities or phenomena, I'd be happy to help if I can! Please provide more context so I can give a more accurate and helpful response.
Pulmonary Adenomatosis, Ovine, also known as Jaagsiekte or ovine pulmonary carcinoma, is a contagious and fatal disease that affects the lungs of sheep. It is caused by a retrovirus called jaagsiekte sheep retrovirus (JSRV). The virus infects the cells in the lung tissue leading to the formation of tumors known as adenomatosis.
The disease is characterized by progressive respiratory distress, weight loss, and eventual death. It is transmitted through the respiratory route, and infected animals can shed the virus in their saliva, nasal secretions, and feces. The disease has a long incubation period, which can range from several months to years, making it difficult to control.
There is no effective treatment for pulmonary adenomatosis, ovine, and infected animals are usually euthanized to prevent the spread of the virus. Prevention measures include quarantine and testing of new sheep before introducing them into a flock, as well as reducing stress and maintaining good nutrition and overall health in the flock.
Marburg Virus Disease (MVD) is an acute and often fatal viral hemorrhagic fever illness caused by the Marburg virus, a member of the filovirus family. It's a highly infectious disease that can be transmitted from human to human through direct contact with infected bodily fluids, tissues, or indirectly through contaminated surfaces and materials.
The incubation period for MVD ranges from 2 to 21 days, after which symptoms such as fever, chills, headache, muscle aches, severe malaise, and progressive weakness appear. Around the fifth day of illness, a maculopapular rash may occur, followed by diarrhea, nausea, vomiting, abdominal pain, and non-bloody stools. In some cases, patients may develop severe bleeding disorders, shock, liver failure, and multi-organ dysfunction, which can lead to death in 24-48 hours.
Currently, there are no approved vaccines or antiviral treatments for MVD, but supportive care is crucial for managing the symptoms of the disease. Preventive measures such as avoiding contact with infected individuals and their bodily fluids, wearing protective clothing, and practicing good hygiene can help prevent the spread of the virus.
Viral diseases are illnesses caused by the infection and replication of viruses in host organisms. These infectious agents are obligate parasites, meaning they rely on the cells of other living organisms to survive and reproduce. Viruses can infect various types of hosts, including animals, plants, and microorganisms, causing a wide range of diseases with varying symptoms and severity.
Once a virus enters a host cell, it takes over the cell's machinery to produce new viral particles, often leading to cell damage or death. The immune system recognizes the viral components as foreign and mounts an immune response to eliminate the infection. This response can result in inflammation, fever, and other symptoms associated with viral diseases.
Examples of well-known viral diseases include:
1. Influenza (flu) - caused by influenza A, B, or C viruses
2. Common cold - usually caused by rhinoviruses or coronaviruses
3. HIV/AIDS - caused by human immunodeficiency virus (HIV)
4. Measles - caused by measles morbillivirus
5. Hepatitis B and C - caused by hepatitis B virus (HBV) and hepatitis C virus (HCV), respectively
6. Herpes simplex - caused by herpes simplex virus type 1 (HSV-1) or type 2 (HSV-2)
7. Chickenpox and shingles - both caused by varicella-zoster virus (VZV)
8. Rabies - caused by rabies lyssavirus
9. Ebola - caused by ebolaviruses
10. COVID-19 - caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
Prevention and treatment strategies for viral diseases may include vaccination, antiviral medications, and supportive care to manage symptoms while the immune system fights off the infection.
Ross River virus (RRV) is an infectious disease caused by the Ross River virus, which is a type of alphavirus. It is transmitted to humans through the bite of infected mosquitoes, primarily Aedes vigilax, Culex annulirostris, and Culex australicus in Australia.
RRV is endemic to Australia, Papua New Guinea, and some islands in the Pacific Ocean. The symptoms of RRV include fever, rash, joint pain and swelling, muscle aches, fatigue, and headache, which can last for several weeks to months. In severe cases, it can lead to chronic arthritis and other long-term complications.
There is no specific treatment for RRV, and management typically involves relieving symptoms with rest, fluids, and pain relief medications. Preventive measures include avoiding mosquito bites by using insect repellent, wearing protective clothing, and staying indoors during peak mosquito activity hours.
**Hemorrhagic fevers, viral** are a group of severe, potentially fatal illnesses caused by viruses that affect the body's ability to regulate its blood vessels and clotting abilities. These viruses belong to several different families including *Filoviridae* (e.g., Ebola, Marburg), *Arenaviridae* (e.g., Lassa, Machupo), *Bunyaviridae* (e.g., Hantavirus, Crimean-Congo hemorrhagic fever virus) and *Flaviviridae* (e.g., Dengue, Yellow Fever).
The initial symptoms are non-specific and include sudden onset of fever, fatigue, muscle aches, joint pains, headache, and vomiting. As the disease progresses, it may lead to capillary leakage, internal and external bleeding, and multi-organ failure resulting in shock and death in severe cases.
The transmission of these viruses can occur through various means depending on the specific virus. For example, some are transmitted via contact with infected animals or their urine/feces (e.g., Hantavirus), others through insect vectors like ticks (Crimean-Congo hemorrhagic fever) or mosquitoes (Dengue, Yellow Fever), and yet others through direct contact with infected body fluids (Ebola, Marburg).
There are no specific treatments for most viral hemorrhagic fevers. However, some experimental antiviral drugs have shown promise in treating certain types of the disease. Supportive care, such as maintaining blood pressure, replacing lost fluids and electrolytes, and managing pain, is critical to improving outcomes. Prevention measures include avoiding areas where the viruses are common, using personal protective equipment when caring for infected individuals or handling potentially contaminated materials, and controlling insect vectors.
Sources: Centers for Disease Control and Prevention (CDC), World Health Organization (WHO).
Alphavirus infections refer to a group of diseases caused by viruses belonging to the Alphavirus genus of the Togaviridae family. These viruses are transmitted to humans through the bite of infected mosquitoes, and can cause a range of symptoms depending on the specific virus and the individual's immune response.
Some of the more common alphaviruses that cause human disease include:
* Chikungunya virus (CHIKV): This virus is transmitted by Aedes mosquitoes and can cause a fever, rash, and severe joint pain. While most people recover from CHIKV infection within a few weeks, some may experience long-term joint pain and inflammation.
* Eastern equine encephalitis virus (EEEV): This virus is transmitted by mosquitoes that feed on both birds and mammals, including humans. EEEV can cause severe neurological symptoms such as fever, headache, seizures, and coma. It has a high mortality rate of up to 30-50% in infected individuals.
* Western equine encephalitis virus (WEEV): This virus is also transmitted by mosquitoes that feed on both birds and mammals. WEEV can cause mild flu-like symptoms or more severe neurological symptoms such as fever, headache, and seizures. It has a lower mortality rate than EEEV but can still cause significant illness.
* Venezuelan equine encephalitis virus (VEEV): This virus is transmitted by mosquitoes that feed on horses and other mammals, including humans. VEEV can cause mild flu-like symptoms or more severe neurological symptoms such as fever, headache, and seizures. It is considered a potential bioterrorism agent due to its ability to cause severe illness and death in large populations.
There are no specific treatments for alphavirus infections other than supportive care to manage symptoms. Prevention measures include avoiding mosquito bites through the use of insect repellent, wearing long sleeves and pants, and staying indoors during peak mosquito hours. Public health efforts also focus on reducing mosquito populations through environmental controls such as eliminating standing water and using insecticides.
Respiratory Syncytial Virus (RSV) infections refer to the clinical illnesses caused by the Respiratory Syncytial Virus. RSV is a highly contagious virus that spreads through respiratory droplets, contact with infected surfaces, or direct contact with infected people. It primarily infects the respiratory tract, causing inflammation and damage to the cells lining the airways.
RSV infections can lead to a range of respiratory illnesses, from mild, cold-like symptoms to more severe conditions such as bronchiolitis (inflammation of the small airways in the lungs) and pneumonia (infection of the lung tissue). The severity of the infection tends to depend on factors like age, overall health status, and presence of underlying medical conditions.
In infants and young children, RSV is a leading cause of bronchiolitis and pneumonia, often resulting in hospitalization. In older adults, people with weakened immune systems, and those with chronic heart or lung conditions, RSV infections can also be severe and potentially life-threatening.
Symptoms of RSV infection may include runny nose, cough, sneezing, fever, wheezing, and difficulty breathing. Treatment typically focuses on managing symptoms and providing supportive care, although hospitalization and more aggressive interventions may be necessary in severe cases or for high-risk individuals. Preventive measures such as hand hygiene, wearing masks, and avoiding close contact with infected individuals can help reduce the spread of RSV.
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