Rabies virus molecular weight

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Select a section on the left to see content. Most abundant protein in the virion. By similarity. Alternative name s :. Name: M. ModBase i Search The term 'domain' is intended here in its wide acceptation, it may be a structural domain, a transmembrane region or a functional domain. Several domains are described in this subsection. Belongs to the lyssavirus matrix protein family. The information is filed in different subsections. Length: Mass Da : 23, It is useful for tracking sequence updates.

The acute neurologic period begins with objective signs of central nervous system dysfunction. The disease may be classified as furious rabies if hyperactivity i.

Fever, paresthesia, nuchal rigidity, muscle fasciculations, focal and generalized convulsions, hyperventilation, and hypersalivation may occur in both forms of the disease. At the end of the acute neurologic phase, periods of rapid, irregular breathing may begin; paralysis and coma soon follow. Respiratory arrest may occur thereafter, unless the patient is receiving ventilatory assistance, which may prolong survival for days, weeks, or longer, with death due to other complications.

Although life support measures can prolong the clinical course of rabies, rarely will they affect the outcome of disease.

The possibility of recovery, however, must be recognized, and when resources permit, every effort should be made to support the patient. It is composed of an internal protein core or nucleocapsid, containing the nucleic acid, and an outer envelope, a lipid-containing bilayer covered with transmembrane glycoprotein spikes Fig. The virus genome encodes five proteins associated with either the ribonucleoprotein RNP complex or the viral envelope Fig.

These aggregate in the cytoplasm of virus-infected neurons and compose Negri bodies, the characteristic histopathologic finding of rabies virus infection. The M matrix and G glycoprotein proteins are associated with the lipid envelope. The G protein forms the protrusions that cover the outer surface of the virion envelope and is the only rabies virus protein known to induce virus-neutralizing antibody.

Genome of rabies virus ERA strain. The genus Lyssavirus includes rabies virus and the antigenically- and genetically-related rabies- like viruses: Lagos bat, Mokola, and Duvenhage viruses, and two suggested subtypes of European bat lyssaviruses.

Cross-protection studies suggest that animals immunized with traditional rabies vaccines may not be fully protected if challenged with other lyssaviruses. Rabies viruses may be categorized as either fixed adapted by passage in animals or cell culture or street wild type.

The use of monoclonal antibodies and genetic sequencing to differentiate street rabies viruses has been helpful in identifying viral variants originating in major host reservoirs throughout the world and suggesting the likely sources of human exposure when a history of definitive animal bite was otherwise missing from a patient's case history. The replication of rabies virus is believed to be similar to that of other negative-stranded RNA viruses.

The virus attaches to the host cell membranes via the G protein, penetrates the cytoplasm by fusion or pinocytosis, and is uncoated to RNP. Each RNA is then translated into an individual viral protein.

After viral proteins have been synthesized, replication of the genomic RNA continues with the synthesis of full length, positive-stranded RNA, which acts as a template for the production of progeny negative-stranded RNA. Rabies virus is most commonly transmitted through the bite of an infected mammal, all of which may be susceptible, but to greatly varying degrees.

The virus may enter the peripheral nervous system directly, or may replicate in muscle tissue after entering the host, remaining at or near the site of introduction for most of the incubation period. However, the precise sites of viral sequestration remain unknown, since neither antigen nor virus can usually be found in any organ during this phase.

Virus may enter the peripheral nervous system via the neuromuscular junctions, and moves rapidly centripetally to the central nervous system for replication; symptoms may develop shortly thereafter. The virus then begins to pass centrifugally to many tissues and organs, such as the salivary glands.

In general, gross examination of the brain shows mild congestion of the meningeal vessels; microscopic examination usually demonstrates slight perivascular cuffing, limited tissue necrosis, acidophilic intracytoplasmic neuronal inclusions, and rarely, neuronophagia.

The host animal species, viral variant, inoculum concentration, body location and severity of exposure, and host immune status have been associated with overt susceptibility to infection and with different incubation periods. The association of virus-neutralizing antibody, principally IgG, and protective immunity is well known. Production of cytokine, such as interferon, induced during rabies virus infection or vaccination, has been reported to abort the disease if it occurs shortly after viral infection.

In one clinical trial, however, all subjects died despite experimental treatment with high doses of alpha interferon. Recently it has been demonstrated that animals immunized with purified RNP complexes or recombinant nucleoprotein vaccines resisted lethal challenge with rabies virus, although the role of N protein in protection, illness, or recovery is unclear.

Rabies has been recognized for over 4, years. Today it is found in most countries, with the exception of those regions from which it has not been naturally reported, including many Australian islands, or areas achieving secondary elimination, such as the United Kingdom.

Almost all human rabies is caused by the bite of a rabid animal Fig The risk of rabies is highest in countries with hyperendemic canine rabies, including most of Asia, Africa, and Latin America.

Wildlife rabies in the United States occurs primarily among wild terrestrial carnivores, such as raccoons, skunks, foxes, and coyotes, and in insectivorous bats. Human rabies is almost always attributable to a bite any penetration of the skin by the teeth. Nonbite exposures contamination of an open wound or a mucous membrane via scratches, licks, and inhalation of aerosol rarely cause rabies in humans.

Of these five human cases, four were apparently attributable via exposure to aerosols containing highly concentrated live rabies virus: two in spelunkers cave explorers and two in rabies research laboratory workers. The fifth case occurred in the recipient of a cornea transplanted from a patient dying of unsuspected rabies encephalitis. This may be attributable either to an inability of the patient to recognize actual rabies exposure at the time, or a failure to properly question the patient concerning potential animal contact.

Although it is now a rare human disease in the United States, its actual incidence may be higher than generally believed. The initial suspicion of rabies only occurred at postmortem examination in five reported human cases in the United States since The diagnosis of human rabies is usually suggested by epidemiologic and clinical findings and confirmed in the laboratory.

The diagnosis is not difficult if there is a history of animal bite exposure and if a full spectrum of symptoms and signs has appeared.

Otherwise, careful but rapid assessment of the epidemiologic and clinical features of less typical cases is essential before special laboratory tests are performed. Every patient with neurologic signs or symptoms or unexplained encephalitis should be questioned about the possibility of animal exposure in a rabies-endemic area inside or outside the country of residence.

The failure to suspect rabies in several of the recent human deaths in the United States may have occurred because no thorough exposure history had been sought. Early in the course of illness, rabies can mimic numerous infectious and noninfectious diseases. Many other encephalitides, such as those caused by herpesviruses and arboviruses, resemble rabies. Other infectious diseases also may resemble rabies, such as tetanus, cerebral malaria, rickettsial diseases, and typhoid. Paralytic infectious illnesses that may be confused with rabies include poliomyelitis, botulism, and simian herpes type B encephalitis.

Noninfectious diseases that may be confused with rabies encompass a number of neurologic syndromes, especially acute inflammatory polyneuropathy Guillain-Barre syndrome , as well as allergic postvaccinal encephalomyelitis secondary to vaccination with nervous-tissue rabies vaccines, intoxication with poisons or drugs, withdrawal from alcohol, acute porphyria, and rabies hysteria.

Guillain-Barre syndrome may be mistaken for the paralytic form of rabies, and vice versa. The detection of rabies antigen, antibody, viral RNA, or the isolation of virus establishes a diagnosis of rabies. Because any individual test may not be positive in a patient with rabies, serial serum specimens for detection of rabies antibodies, saliva specimens for culture of virus, and skin biopsies for direct immunofluorescence testing for virus antigen are sometimes necessary, especially when rabies is strongly suspected.

One of the most rapid methods to diagnose rabies antemortem in humans is to perform a direct immunofluorescence test on a skin biopsy from the nape of the neck for evidence of rabies antigen. The direct immunofluorescence test is the most sensitive and specific method of detecting rabies antigen in skin and other fresh tissue e. If fresh tissue is unavailable, enzyme digestion of fixed tissues may enhance the reactivity of the immunofluorescence test; however, sensitivity may be unacceptably low.

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The polypeptides of adenovirus. Evidence for multiple protein components in the virion and a comparison of types 2, 7A, and Protein synthesis in vesicular stomatitis virus-infected HeLa cells.

Biochem Biophys Res Commun. Purification of rabies virus grown in tissue culture. Biochemical and biophysical studies on the nucleocapsid and on the RNA of rabies virus. Proteins spcified by herpes simplex virus. Viral glycoprotins associated with cellular membranes. Studies on the nature of dengue viruses. The structural proteins of type 2 dengue virus. Carbohydrate content of the membrane protein of Sindbis virus. Structural proteins of vesicular stomatitis viruses.