Name of virus causing rabies

The RNP-M complex migrates to an area of the plasma membrane containing glycoprotein inserts, and the M-protein initiates coiling. The M-RNP complex binds with the glycoprotein, and the completed virus buds from the plasma membrane.

Within the central nervous system CNS , there is preferential viral budding from plasma membranes. Conversely, virus in the salivary glands buds primarily from the cell membrane into the acinar lumen. Viral budding into the salivary gland and virus-induced aggressive biting-behavior in the host animal maximize chances of viral infection of a new host.

Rabies virions are bullet-shaped with nm spike-like glycoprotein peplomers covering the surface. The ribonucleoprotein is composed of RNA encased in nucleoprotein - , phosphorylated or phosphoprotein -Illistration of virus, and polymerase -virus. The cross-sectional diagram demonstrates the concentric layers: envelope membrane bilayer, M protein, and tightly coiled encased genomic RNA.

The rabies virus genome is single-stranded, antisense, nonsegmented, RNA of approximately 12 kb. Transcription synthesis of mRNAs. Translation Synthesis of structural proteins. Processing G-protein gycosylation. Replication production of genomic RNA from intermediate strand. Skip directly to site content Skip directly to page options Skip directly to A-Z link.

Section Navigation. Facebook Twitter LinkedIn Syndicate. What is Rabies? The incubation period in rabies, usually 30 to 90 days but ranging from as few as 5 days to longer than 2 years after initial exposure, is more variable than in any other acute infection. Incubation periods may be somewhat shorter in children and in individuals bitten close to the central nervous system e. Clinical symptoms are first noted during the prodromal period, which usually lasts from 2 to 10 days.

These symptoms are often nonspecific general malaise, fever, and fatigue or suggest involvement of the respiratory system sore throat, cough, and dyspnea , gastrointestinal system anorexia, dysphagia, nausea, vomiting, abdominal pain, and diarrhea , or central nervous systems headache, vertigo, anxiety, apprehension, irritability, and nervousness. More remarkable abnormalities agitation, photophobia, priapism, increased libido, insomnia, nightmares, and depression may also occur, suggesting encephalitis, psychiatric disturbances, or brain conditions.

Pain or paresthesia at the site of virus inoculation, combined with a history of recent animal bite, should suggest a consideration of rabies.

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. Two cases of rabies have been attributed to probable aerosol exposures in laboratories, and two cases of rabies have been attributed to possible airborne exposures in caves containing millions of free-tailed bats Tadarida brasiliensis in the Southwest.

However, alternative infection routes cannot be discounted. Parenteral injection, droplet or aerosol exposure of mucous membranes or broken skin with infectious fluids or tissues. Consultation is available to determine if vaccination with the Rabies vaccine is appropriate for personnel using rabies. There is no established treatment for rabies once symptoms have begun, but supportive therapy may include intubation, sedation, mechanical ventilation, fluid and electrolyte management, nutrition, and management of intercurrent illnesses and complications.

Incubation period of months is typical, although incubation more than 1 year has been reported in humans. Administration of rabies POST-exposure prophylaxis is a medical urgency, not a medical emergency, but decisions must not be delayed.

Prophylaxis is occasionally complicated by adverse reactions, but these reactions are rarely severe. Therefore, when a documented or likely exposure has occurred, POST-exposure prophylaxis should be administered regardless of the length of the delay, provided that compatible clinical signs of rabies are not present in the exposed person.

Rabies virus is inactivated by desiccation, ultraviolet irradiation, and other factors and does not persist in the environment. In general, if the suspect material is dry, the virus can be considered noninfectious.

Non-bite exposures other than organ or tissue transplants have almost never been proven to cause rabies, and post-exposure prophylaxis is not indicated unless the non-bite exposure met the definition of saliva or other potentially infectious material being introduced into fresh, open cuts in skin or onto mucous membranes. Copyright Complaints.