Case Analysis : Entebbe Bat Virus

* Flaviviruses: share a common size (40-60nm), symmetry (enveloped, icosahedral nucleocapsid), nucleic acid (positive-sense, single stranded RNA approximately 10,000-11,000 bases), and appearance in the electron microscope. Therefore, images of West Nile virus are representative for this group of viruses.

Viruses are microscopic particles that invade and take over both eukaryotic and prokaryotic cells. They consist of two structures, which are the nucleic acid and capsid. The nucleic acid contains all genetic material in the form of DNA or RNA, and is enclosed in the capsid, which is the protein coating that helps the virus attach to and penetrate the host cell. In some cases, certain viruses have a membrane surrounding the capsid, called an envelope. This structure allows viruses to become more stealthy and protected. There are two cycles in which a virus can go into: lytic and lysogenic. The lytic cycle consists of the virus attaching to a cell, injecting its DNA, and creating more viruses, which proceed to destroy the host. On the other hand, the lysogenic cycle includes the virus attaching to the cell, injecting its DNA, which combines with the cell’s DNA in order for it to become provirus. Then, the provirus DNA may eventually switch to the lytic cycle and destroy the host.

The virus fuses with the cell’s plasma membrane. The capsid proteins are removed, releasing the viral proteins and RNA. Reverse transcriptase catalyzes the synthesis of a DNA strand complementary to the viral RNA. Reverse transcriptase catalyzes the synthesis of a second DNA strand complementary to the first. The double-stranded DNA is incorporated as a provirus into the cell’s DNA. Proviral genes are transcribed into RNA molecules, which serve as genomes for the next viral generation and as mRNAs for translation into viral proteins. The viral proteins include capsid proteins and reverse transcriptase (made in the cytosol) and envelope glycoproteins (made in the ER). Vesicles transport the glycoproteins from the ER to the cell’s plasma membrane. Capsids are assembled around viral genomes and reverse transcriptase molecules. New viruses bud off from the host cell.

There is still a great deal of information to learn from the study of viruses and the continued exploration of the viral genome is crucial in understanding how viruses communicate, transmit from host to host and evade immune responses. The ever-change nature of the viral genome has shown us that the most dangerous viral infections of today may be undermined by newer and more effective viruses, resulting in catastrophic outcomes. Through the study of viruses, it is the hope of the scientific community to be ahead of the viral curve, preventing infections before they even

    The viral capsid acts as the barrier between the world and the most important part of the virus, the nucleic acid. The viral capsid is composed of matrix protein M1 (Virus Structure, fsu.edu) that holds everything together and plays a role in virus assembly. The viral capsid is the backbone of the virus that holds everything together and has three main functions: to protect the nucleic acid from digestion by enzymes, to hold the attachment proteins needed to enter cells, and it provides special sites on the surface that allow the virus to attach to cells.

as BamHI, a fragment of the EBV genome [6]. It is thought that viral proteins may

This intricate virus contains many structures that allow it to survive and be pathogenic. Constructed by lipids, the cells

Blok and Air 1982b; Fields et al. 1981 is one of the two major glycoproteins on the virus surface.

Replication pattern of HEV is still largely unknown because effective cell-culture system for HEV has been developed recently (Tanaka et al., 2007). It is believed that HEV enters the cell by binding to cellular receptor, heparin sulfate proteoglycans (HSPGs), with its capsid protein and viral entry is carried out by the binding of C-terminal region of ORF2 to the cell surface protein, heat shock cognate protein 70 (HSC70) (Zhou and Emerson, 2006; Kalia et al., 2009). Also, p239, a truncated partial homodimer of the HEV capsid protein (HEV239) potentially binds to the HEV receptor(s) on cells (He et al., 2008) and a cellular chaperone, glucose regulated protein (Grp78) (Yu et al., 2011). However, more studies should be conducted to confirm the cellular receptors for HEV. The mechanism of uncoating of the HEV genome after its entry into the cells is also unknown. One of the study has suggested that heat shock protein (HSP90) might be playing role in intracellular transport of HEV since the inhibition of HSP90 blocked the intracellular transport of the HEV239 capsid protein but did not affect the binding and entry of the truncated capsid protein (Zheng et al., 2010).

Recent data has shown that since 1998, NiV has infected nearly 477 people, while killing almost 252. These reported outbreaks have a “strong seasonal pattern and a limited geographical range”, with a fatality rate ranging from “40-70%...although it has been as high as 100% in some outbreaks” (World Health, p.3). As NiV was first recognized in an outbreak of 276 cases in Malaysia and Singapore from September 1998 to May 1999, most of the patients documented were noted to have had some contact with infected pigs. Autopsy findings showed diffused vasculitis within the central nervous system, including immunostaining of endothelial cells with anti-Nipah virus hyper immune serum. Of the “patients primarily with encephalitis; 39% died” (Hughes & Wilson, 2009, p.1). NiV was initially isolated from urine specimens collected from P. hypomelanus roost, as well as fruit partially eaten by bats in Malaysia. Experimental injections of Pteropus bats were conducted in order to identify the existence of the NiV virus within the mammals; however, it does not cause illness in the bats. While over fifty species of Pteropus bats live in the South and South East Asia areas, “Pteropus giganteus, [is] the only…species found in Bangladesh [with an] antibody to NiV” (Hughes & Wilson, 2009). Following the outbreak of the Nipah virus in Malaysia, no human cases

The family of Arenaviruses is genomically a negative single strand RNA virus. It has an enveloped, icosahedral symmetry with a diameter of approximately 120nm. Its ambisense genome is segmented into two divisions. The derivation of its name is from the Latin word ‘arena’ which translates to sandy. Many sources indicate this is due to its appearance microscopically of a grainy or sandy particle.(2) This appearance is due to ribosomes being present throughout the virus. The entry of the virus into the host cell is via clathrin mediated endocytosis and reproduction is via budding from the host’s cell membrane. The initial Arenavirus was discovered in 1933-1934 by scientists who were studying encephalitis. It was called LCM (lymphocytic choriomeningitis virus).(4) Over the next decades, more

In the last two-decade, numbers of giant dsDNA, icosahedral viruses have been discovered and assigned to the NCLDV clade. The major capsid proteins of these viruses consist of two consecutive jelly-roll domains, assembled into trimers, with six fold symmetry. The capsomers are assembled into arrays that have either p6 as in Paramecium bursaria Chlorella virus 1 or p3 symmetry as in Mimivirus (Xiao & Rossmann 2011).

This little package of mayhem consists of relatively few parts. A virus is simply a protein capsule called a capsid, sometimes surrounded by an envelope, containing a genome. The genome consists of nucleic acids arranged as DNA or less commonly, RNA. Dozens of variants of this fundamental arrangement exist with differences in the structure of the capsule and the arrangement of the genome. Small differences or changes in these components allow some viruses to continue to outmaneuver researchers, while millions of dollars are spent trying to understand and eliminate them.

Geminiviruses are a large, unique family of plant viruses that have the ability to infect multiple different plants around the world. [1, 2] Geminiviruses consist of four genera, Mastrevirus, Curtovirus, Begomovirus, and Topocuvirus based on host ranges, vector specificities, and genome organizations. Characteristics of geminiviruses include their circular, single-stranded DNA genome and geminate-shaped virus particles. These viruses-- exhibit both prokaryotic and eukaryotic features-- replicate in the nuclei of the host cell and depend on host machineries for transcription [1]. The majority of the Old World begomoviruses have monopartite genomes while the New World begomoviruses are exclusively bipartite. [3] Whiteflies, often found on the underside of leaves are typically responsible for transmitting the monopartite begomovirus Ageratum yellow vein virus (AYVV) which has been previously characterized in Escherichia coli (E. coli) cells harboring single copies of the AYVV genome [1, 4].

Dengue virus(50nm) belongs to family Flaviviridae. The mature dengue virion consists of a positive (+)single-stranded RNA genome surrounded by an icosahedral or isometric nucleocapsid about 30 nm in diameter. This nucleocapsid is covered by a lipid envelope. The complete