Eastern equine encephalitis virus

From MicrobeWiki, the student-edited microbiology resource
This student page has not been curated.

1. Classification

Superkingdom: Viruses

Phylum: Kitrinoviricota

Class: Alsuviricetes

Order: Martellivirales

Family: Togaviridae

Genus: Alphavirus

Species: Eastern equine encephalitis virus (1)

2. Description and significance

Eastern equine encephalitis virus (EEEV) is an arbovirus (i.e. transmitted through arthropod vectors like mosquitos) that was discovered in 1933. EEEV has infected human and horse populations on the East Coast of the United States periodically through the years, resulting in death and extreme neurological impairments in those who survive (2). EEEV epidemics in humans are sporadic, but the number of cases has been rising in the last decade. The United States has an average of 11 human infections annually; however, in 2019, 38 cases were reported to the CDC (3). EEEV has a death rate estimated to be between 35 and 75%, the highest death rate of any mosquito-borne virus in North America (2).

While there is a correlation between changes in the weather and the seasons and increased EEE cases in the US, the exact cause is unknown (14). Current research focuses on the pathology of EEEV that is not fully understood and possible weaponization of the virus (17, 18).

3. Genome structure

EEEV belongs to the Alphavirus genus, which has a positive-sense single-stranded RNA genome that is approximately 12-kb and has a 5’ Cap and 3’ polyadenylated tail (4). The genome structure is highly conserved across strains of the virus (NA and SA EEEV). The genome encodes five structural proteins, which include the capsid and envelope proteins (E1, E2, E3, and 6K), and four non-structural proteins, nsP1-nsP4 (4, 5). The structural proteins are found near the 3’ polyadenylated tail and contain a subgenomic promoter (26S). The non-structural proteins are associated with viral genome replication and polypeptide processing and are found near the 5’ Cap (4,5). The positive-sense RNA can act as an mRNA because it is able to recruit eIF4E, which is a 5’ Cap binding protein that initiates translation by signaling the ribosomal subunits. This allows for the non-structural proteins to be translated (6).

4. Virion structure

The virus’s shell is icosahedral shaped and consists of two layers: outer transmembrane envelope and inner capsid layer. The outer layer contains E1 and E2 proteins. E1 protein’s function is associated with the fusion of the host cell and E2’s function is associated with receptor binding to the host cell (5). E2 has a binding site for heparan sulfate (HS), which allows the virus to avoid lymph node detection. The lymphatic system, which is a network of organs and tissues that filters out toxins, works in conjunction with the immune system by using lymphatic fluids to transport white blood cells and other antibodies. The lymph nodes, which contain immune cells, are able to signal an immune response in the presence of antigen such as a virus (7). E1 and E2 are unable to bind to DC-SIGN (dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin) and L-SIGN (liver/lymph node-specific intercellular adhesion molecule-3 grabbing non-integrin) (5). EEEV is internalized by the host through endocytosis, which allows the nucleocapsid to be released into the cytosol of the host. The capsid is able to bind to the host cell’s ribosomes (5).

5. Metabolic processes

Describe important sources of energy, electrons, and carbon (i.e. trophy) for the organism/organisms you are focusing on, as well as important molecules it/they synthesize(s).

6. Ecology and Pathology

EEEV is the only virus that is part of the Eastern equine encephalitis complex. EEEV is divided into four subtypes based on its antigenic properties. Subtype I/lineage I includes North American EEEV (NA EEEV) and most other strains from the Caribbean (9). Subtypes II to IV includes South and Central American (SA EEEV) strain. The division of NA EEEV and SA EEEV subtype is based on the substantial nucleotide divergence between the genomes of the two groups and their adaptation to different geographical areas and hosts. NA EEEV is highly conserved in its lineages; less than 2% nucleotide differences in the NA EEEV genome was observed between 1933 and 2007 (10, 11). While the transmission of NA EEEV is largely through an enzootic cycle between Culiseta melanura mosquitos and an avian host, the disease itself is spread by other mosquito species (i.e. Aedes), which are capable of building a bridge between the infected bird and uninfected mammals (12). The C. melanura preference to feed largely on birds may result in the genetic conservation and constraint observed in the NA EEEV strain (10).

The ecological understanding of SA EEEV is poor. Compared with NA EEEV, SA EEEV has a higher genetic diversity (9). This may be a result of their tropical forest habitat: SA EEEV vectors have a wide range of feeding behavior, which includes wild birds, ground-dwelling rodents, marsupials, and reptiles (9). This confers a broad range of vector diversity and could contribute to the diversity of SA EEEV genetic lineages. Most of the hosts are ground-dwelling mammals that limit the distribution of SA EEEV in comparison to the efficient geographical dispersion of NA EEEV by avian hosts (9). It may be possible that this limited mobility has allowed for higher diversity in SA EEEV lineages due to decreased competition amongst strains and increased independent evolution of certain SA EEEV strains (9).

7. Pathology

How does this organism cause disease? Human, animal, plant hosts? Virulence factors, as well as patient symptoms.

8. Current Research

Include information about how this microbe (or related microbes) are currently being studied and for what purpose

9. References

It is required that you add at least five primary research articles (in same format as the sample reference below) that corresponds to the info that you added to this page. [Sample reference] Faller, A., and Schleifer, K. "Modified Oxidase and Benzidine Tests for Separation of Staphylococci from Micrococci". Journal of Clinical Microbiology. 1981. Volume 13. p. 1031-1035.