LaCrosse Encephalitis virus

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LaCrosse Encephalitis Virus (LACV or LAC virus), is just one of a group of viruses that can cause encephalitis. The LAC virus was discovered in LaCrosse, Wisconsin in 1963, and is responsible for the viral disease LaCrosse encephalitis (Elliot 19). The reservoirs for the LACV are squirrels and chipmunks. The vector is the mosquito, specifically the Aedes triseriatus. Although humans get infected with virus, they are dead end hosts. The topics covered in this paper about the LAC virus are the structure and classification, the life cycle, the disease, the treatment, and impact on public health.

The LAC virus is an arbovirus that belongs to the Bunyaviridae family. The Bunyaviridae are a family of RNA viruses that are unique when compared to other enveloped, arthropod-borne, viruses in that their virions contain a single-stranded, segmented RNA genome. Serological studies have indicated that some 90 bunyaviruses can be grouped into 11 serogroups with members of each group being serologically more closely related to other members of that group than to members of another group. The LACV belongs to a supergroup known as the Bunyamwera supergroup (Mahy, Berry 62). Arboviruses are transmitted to vertebrates by the bite of certain insects. These insects include the mosquito, tick, and sand fly. This virus is a Baltimore class 5 negative single-stranded RNA virus, and is also classified as a California serogroup virus. The high mutation rate characteristic of many RNA viruses can be expected to lead to some variation in virulence properties of California serogroup viruses. The LACV mutates by both antigenic shift and antigenic drift. This characteristic is achieved only by segmented viruses which LACV happens to be. Antigenic shifts can make hybrid viruses, but these shifts only occur between LACV and other viruses that are closely related to it.

The virions of Bunyaviridae are enveloped (from Golgi apparatus), and spherical in shape. These particular viruses also have no matrix proteins. A lipid membrane envelopes the virus that aids in structural support, and is crucial for their infectivity. This lipid bilayer is sensitive to lipid solvents such as soaps and detergents. Two glycoproteins (G1 and G2) located on the surface of the LACV. These are transmembrane proteins that are vital to this virus's infectivity, because these proteins bind to the host cell. They are the major determinant of virulence transmission in arthropod vectors. The three internal nucleocapsids are circular and somewhat helical in design. Each contains a unique negative-sense viral RNA species, many copies of nucleocapsid protein (N), and a few copies of large protein (L) that is the virus transcriptase and serves as the virus replicase during infection. Bunyaviridae have ambisense RNA that contain 3 segments which are the small (S), medium (M), and large (L) sections.

The first step in the life cycle of the LACV is attachment. This is mediated by interaction of the viral glycoproteins and cell receptors which are unknown at this time. Next, entry and uncoating occurs by endocytosis of virions and fusion of the viral membrane with the endosomal membrane to release the three nucleocapsids into the cell cytoplasm. It should be mentioned that in this virus fusion to the host cell is pH-dependent. Then primary transcription is performed. This is the synthesis of the three subgenomic, viral complementary mRNA species from the three genome templates. Primary transcription involves the host cell mRNA-derived primers and the virion associated polymerase, and occurs in the cytoplasm. Translation of primary L and S segment mRNAs by free ribosomes and translation of M segment RNAs by membrane-bound ribosomes produce the viral structural and nonstructural proteins which are required for the following replication steps. Primary glycosylation and cotranslational processing of nascent envelope proteins occur in the Golgi.

This is followed by mRNA synthesis (gene expression) and the encapsidation by N protein of full-length, exact copy viral complementary RNA to serve as templates for the next synthesis of genomic RNA. Since viral-complementary RNA lacks a 5' cap, it steals one from the host RNA. Genome RNA replication using the exact copy replicative intermediate before it, provides full length copies of each of the viral RNA species. These RNA species are also in the form of nucleocapsids. Secondary transcription involves the augmented synthesis of the three mRNA species when the newly synthesized viral RNA species are available. There is more S mRNA species than M mRNA species, which in turn is more abundant than the L mRNA. The reasons for these differences are unknown. Further translation, RNA replication and transcription occur in the final stages of infection and during the time when progeny viruses are released. Morphogenesis, including the increase of viral glycoproteins in the Golgi apparatus, terminal glycosylation, attainment of modified host membranes, and budding into the Golgi cisternae leads to the accumulation of virions in the cytoplasmic vesicles. Finally, fusion of cytoplasmic vesicles containing viruses with the surface membrane of the cell results in the release of mature virions by exocytosis.

An important part of the LACV life cycle is that overwinters (survives the winter) in the northern Midwest through its persistent infection of female mosquitoes, which may emerge infected following hibernation. Additionally, infected females will transmit virus transovarially to eggs which also overwinter in tree holes. Elliot states that, "Transmission between mosquitoes may provide an alternative cycle that does not require a vertebrate host, and venereal transmission from infected males to uninfected females has been documented" (Elliot 230).

The pathogenesis of the LACV is of the typical arbovirus. LACV gains entry through the skin by the bite of an infected arthropod (mainly the mosquito here in the southeast of the U.S.). The mosquito saliva enters the dermis and at times enters the small capillaries directly when the mosquito's proboscis passes into the vessel. The virus initially replicates in the dermal tissues, although it is possible that virus is transported directly in the blood to primary target organs. Replication also occurs in the regional lymph nodes and from there the blood is infected, inducing a secondary viremia, which in turn carries virus to infect muscle and connective tissue cells. This viremia is often of very high concentration and is accompanied by fever, leukopenia, and malaise. It is during this viremic phase that an arthropod may feed and become infected (Specter, Lancz 447). The period between infection and viremia (intrinsic incubation period) is usually short, from one to three days. Viremia may last two to five days.

The clinical disease caused by LACV is an acute encephalitis, preceded by a nonspecific febrile illness. The incubation period is around one week. Antibody is produced and it complexes with and neutralizes circulating virus. The process is followed by complete recovery and leads to the presence of life-long antibody. Occasionally, however, an infected person develops encephalitis. This is the case with some individuals who are infected with LACV. The mechanism entry of virus into the central nervous system (CNS) is not completely understood. It is also not understood why some individuals develop encephalitis and another apparently similar individual does not. Virus may reach the brain by passing through cerebral capillaries during viremia, then by direct invasion of the brain parenchyma through the capillary walls (Specter, Lancz 449). On the other hand, certain neural cells such as the olfactory neurons are directly exposed to circulating blood. Viremia may pass through these nerve endings and the virus may pass directly to the olfactory lobe of the brain. Regardless of the mechanism, it is important to note that the process of passing into the brain and infection of the brain cells takes time. By the time the patient presents with encephalitis, serum antibody is usually detectable as is antibody in the CSF. At this stage of infection, viremia has ceased and diagnosis is made by serologic assay. Fever, malaise, and often severe headache usually precede neurologic signs. LaCrosse encephalitis patients often present with seizures, which are sometimes uncontrollable with antiseizure medication. These symptoms can last up to ten days during which most infected children are hospitalized. The most severe cases of LaCrosse encephalitis can cause death. Some long term effects of this disease can include memory loss, fatigue, weakness, lack of muscle coordination, and hearing or vision problems.

The humoral immune response to LACV is to produce antibodies against the G1 protein. These antibodies are capable of neutralization, inhibition of hemagglutination, and can block cell to cell fusion. Some neutralizing anti-G1 antibodies will inhibit virus binding to susceptible cells. High titer neutralizing antibodies are probably sufficient to protect the organism against repeated challenges with the same virus strain. There is currently no treatment for La Crosse encephalitis only supportive therapy and prevention. Supportive therapy just treats the symptoms of this disease and not the disease itself. Mosquito control is essential in the prevention of this disease. Using insect repellent with DEET, mosquito netting, and reducing the amount of standing water in mosquito prone areas are just a few prevention methods to control mosquitoes.

The majority of cases of encephalitis caused by California serogroup viruses are associated with LACV infection. LACV is endemic in North America specifically in the upper Midwestern states, and more recently in the mid-Atlantic and southeastern states. Campers and hikers, children under sixteen, the elderly, the rural poor, and the immunocompromised are high risk groups for this disease/infection.

In conclusion, LaCrosse encephalitis is a disease caused by the LACV. This virus is an arbovirus and is transmitted by arthropods such as mosquitoes and ticks. An important part of the viruses its pathogenesis is its ability to overwinter in female mosquitoes. These females are able to transmit the virus to their eggs. LaCrosse encephalitis is not fatal in most cases, and most individuals make a complete recovery. Support therapy and prevention are the only methods to help LAC encephalitis. Those most likely to encounter this virus/disease are those who are outdoors a great deal, children under 16, the immunocompromised, and the elderly. This can be a serious disease so it is smart to take preventative measures to decrease the likely hood of contracting it.

References

  1. Elliot, Richard M.. The Bunyaviridae. New York: Plenum Press, 1996.
  2. Specter, Steven, and Gerald Lancz. Clinical Virology Manual, Second Edition. New York, Amsterdam, London, Tokyo: Elsevier Science Publishing Company, Inc., 1992.
  3. Mahy, B.W.J., and R.D. Barry. Negative Strand Viruses and the Host Cell. London, New York, San Francisco: American Press Inc., 1978.
  4. "La Crosse Encephalitis". CDC. March 23, 2010. http://www.cdc.gov/lac/tech/virus.html
  5. "Minnesota Department of Health Fact Sheet: LaCrosse Encephalitis". Minnesota Department of Health. March 23, 2010. http://www.echominnesota.org/pdf/resource/LaCrosse.pdf
  6. Parilla, Jessica, Dr. "Arboviruses" (Lecture). GSU, Atlanta. March 2, 2010.

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