Venezuelan equine encephalitis virus

Venezuelan equine encephalitis virus (VEEV)

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A Viral Biorealm page on the family Venezuelan equine encephalitis virus

Apis mellifera, a common host of Kashmir bee virus. [1].

Baltimore Classification

Group IV: (+) sense single-stranded RNA viruses

Higher Order Categories

Order: Togovirales
Family: Togaviridae
Genus: Alphavirus

Description and Significance

Venezuelan equine encephalitis virus (VEEV) is an important animal and human pathogen and potential bioweapon. It is part of a group of viruses called alphaviruses that include djl;j;lj;ljl;. besides Alphaviruses' importance as human and animal pathogens they have also been used as a model system for the study of enveloped virus structure.[1] (sounds weird)

infects many types of bees including Apis mellifera, the European honey bee [6]. The virus effects both brood and adult bees. Infected adults die within a few days of exposure to the virus but infected larvae may survive and develop into seemingly unaffected adults [2]. While Kashmir bee virus infection alone may not be of much significance, it has been implicated as part of a much larger agricultural issue.

A. mellifera is the species of bee used in the US for crop pollination and commercial honey production. In 2000, an estimated $14.6 billion of US crops were pollinated by A. mellifera [8]. However, recently, many A. mellifera colonies have been disappearing due to a phenomenon known as Colony Collapse Disorder (CCD) [1]. In the spring of 2007, many beekeepers across the US reported loss of 80-100% of their bee colonies. Although it is unclear exactly what causes CCD, a group of related bee viruses including KBV have been implicated [8]. It seems as if these viruses interact with parasitic mite infestations and other environmental factors to cause CCD. A better understanding of KBV and other bee viruses could aid in the control and prevention of CCD, rescuing the US from a potential agricultural crisis.

Genome Structure

VEEV has an 11.5 kb (+) sense ssRNA genome. The genome contains two reading frames that produce two different polyproteins. The structural polyprotein contains 5 proteins related to capsid formation and envelope proteins. The other polyprotein encodes four proteins responsible for genome replication including a viral RNA-dependent RNA polymerase. (MORE HERE!)more about the genome and the stuff it codes for.

The genome contains two open reading frames each coding for a polyprotein. These ORFs are separated by and intergenic region and flanked with short non-coding regions. [6] 

The 5’ ORF codes the non-structural polyprotein which includes three helicase domains, a 3C-protease domain, and 8 RNA polymerase domains (including an RNA-dependent RNA polymerase). The 3’ ORF codes for the structural polyprotein which contains two picornavirus-like capsid protein domains and other capsid proteins. [6]

Virion Structure of Venezuelan equine encephalitis virus

Venezuelan equine encephalitis virus is an enveloped isohedral virion. (sounds bad) consists of a non-enveloped, icosohedral capsid. The capsid is constructed from 3 structural proteins [5]. The capsid appears round and is approximately 30 nm in width [8].

Reproductive Cycle of Venezuelan equine encephalitis virus in a Host Cell

Little is specifically known about the KBV reproductive cycle. Some insight into the process can be gained by examining related viruses and examining the patterns of viral RNA and protein expression in infected bees.

The infective ability and life cycle of Rhopalosiphum padi virus (RhPV), also of the Cripavirus genus, has been studied to some extent. In cell culture, viral protein is localized to the cytoplasm, as visualized by immunogold labeling. This study also observed clusters of single membrane vesicles associated with virions in the early stages of infection. Crytalline arrays of virus particles and dense amorphous cytoplasmic structures were also observed.[3] Similar observations have been made for related viruses so it is reasonable to think that KBV infection may follow a similar scheme.

Another clue can be taken from the apparent ability of KBV to maintain a latent infection. Since KBV does not have a DNA intermediate, it cannot enter true lysogeny and splice into the host genome but it can remain in the cell without any observable pathology. Molecular evidence for latent infection was found when ELISA (immuno assay)results for viral-capsid proteins and RT-PCR amplification of viral RNA where compared as diagnostic techniques. In a majority of cases, viral RNA was present with little or no viral-capsid proteins.[9] This suggests that the viral RNA can persist in infected cells with limited replication and formation of new virus particles.

Viral Ecology & Pathology

animal hosts skeeters are vectors-what species specifically what it does-mostly flu-like illness, no biggie BUT can cause encephalitis and death KBV is known to infect many species of bees across a large geographic distribution. Cases of A. melifera infection have been reported worldwide, although cases involved in CCD have only been reported in the US. KBV is also known to infect A. cerana (Asiatic honey bee) in parts of Southeast Asia and India, where the virus is believed to have originated. KBV has also been reported in populations of Bombus spp. (bumble bees) in New Zealand and Vespula germanica (European wasp) in Australia. [6] Some evidence shows that mites such as Varroa destructor not only act as vectors for viral sread, but also as hosts in which viral replication occurs [9].

KBV is spread between bees in a colony and between colonies through many methods of transmission. KBV can be introduced to hives by mites such as Varroa destructor [4] and can also be spread between worker bees and from the queen bee to her offspring. Viral RNA has been amplified from queens and their eggs suggesting that the virus can be transferred via a transovarial route. Viral RNA has also been amplified from food sources such as honey, brood food, and royal jelly. Since these food sources are partially composed of secretions from worker bees, this is a likely method of bee-to-bee transmission. [9]

As mentioned previously, KBV infection of shows no visually detectable signs of pathology [9]. KBV is commonly found in bees co-infected with other related viruses.

References

[1] Jose, J., J.E. Snyder, R.J. Kuhn. “A structural and functional perspective of alphavirus replication and assembly.” Future Microbiology 4 (2009): 837-856

[2] Berenyi, O., T. Bakonyi, I. Derakhshifar, H. Koglberger, N. Nowotny. “Occurrence of Six Honeybee Viruses in Diseased Australian Apiaries.” Applied and Environmental Microbiology 72.4 (2006): 2412-2420.

[3] Boyapalle, S., N. Pal, W.A. Miller, B.C. Bonning. “A glassy-winged sharpshooter cell line supports replication of Rhopalosiphum padi virus (Dicistroviridae). Journal of Invertebrate Pathology 94 (2007): 130-139.

[4] Chen, Y.P., J.S. Pettis, A. Collins, M.F. Feldaufer. “Prevalence and Transmission of Honeybee Viruses.” Applied and Environmental Microbiology 72.1 (2006): 606-611.

[5] “Cripavirus.” ICTVdB Descriptions <www.ncbi.nlm.nih.gov/ICTVdb/ICTVdB/00.101.0.01.htm>

[6] de Miranda, J.R., M. Drebot, S. Tyler, M. Shen, C.E. Cameron, D.B. Stoltz, S.M. Camazine. “Complete nucleotide sequence of Kashmir bee virus and comparison with acute bee paralysis.” Journal of General Virology 85 (2004): 2263-2270.

[7] “Kashmir bee virus.” NCBI Taxonomy browser <www.ncbi.nlm.nih.gov/Taxonomy/Browser>

[8] Oldroyd, Benjamin P. “Unsolved Mystery: What’s Killing American Honey Bees?” PLoS Biology 5.6 (2007).

[9] Shen, M., L. Cui, N. Ostiguy, D. Cox-Foster. “Intricate transmission routes and interactions between picorna-like viruses (Kashmir bee virus and sacbrood virus) with the honeybee host and the parasitic varroa mite.” Journal of General Virology 86 (2005): 2281-2289.

[10] Slonczewski, J.L., J.W. Foster. “Chapter 6: Virus Structure and Function.” Microbiology: An Evolving Science (2009): 181-217.

Page authored for BIOL 375 Virology, September 2008