Retrovirus: Ebola Virus, Essay Example

Retroviruses are a family of small RNA viruses that are characterized by their similarities in structure, replication, and composition.  The viruses are composed of an outer lipid layer of viral glycoproteins with an inner protein core.  This family of viruses undergoes a unique replication strategy where their RNA forms a linear double stranded DNA through a process referred to as reverse transcription.  Retroviruses are segmented into two different categories: simple and complex, depending on genetic composition.  In addition, these viruses are further segmented into seven different groups in regards to evolutionary relationships.  The groups consist of oncogenic viruses, lentiviruses and spumaviruses. (Hughes and Varmus, 1997)

Retroviruses are important in scientific research for various science groups, such as microbiology, biology, genetics, cancer, medicine, and biotechnology.  Some current research in microbiology in regard to retroviruses is geared towards the study of diseases with unknown etiologies that can cause an epidemic, such as the Ebola virus.  The Ebola virus is known as a harsh and aggressive virus.  The virus was first observed in 1976 near the Ebola River in Zaire, Africa.  Since the initial observation, the Ebola virus has caused numerous outbreaks in central Africa resulting in many human fatalities, as well as mortalities of ape communities.  One of the most important reasons for additional research into this retrovirus is the lack of etiology of a host and the fast progression.  Without the knowledge of the etiology, a management system is impossible to create in order to eliminate and prevent disease occurrence and spread of an epidemic.  In addition, the virus replicates and causes problems very quickly in humans preventing the ability to establish immunity and fight the disease.  The virus has been shown to occur from 2-3 weeks after initial infection.  The resulting symptoms include fever, myalgia, and malaise, as well as severe bleeding, which is ultimately the cause of death.   Specifically, the virus releases cytokines which trigger a cellular inflammatory response, which further damages the liver and moves into the vascular system causing hemorrhagic bleeding, hence the term “Hemorrhagic fever” as the common name for Ebola virus.  The virus is fatal with no effective vaccination or antiviral drug to prevent disease progression. (Sullivan et al., 2003)

The Ebola virus can be detected through diagnostic examination in the acute stages of the disease.  Specimens containing potential Ebola virus are managed with caution and prepared in a biosafety procedure.  There are different methods for diagnosis using acute serum or post-mortem tissues from the infected individual or animal.  The developed tests are important as they can measure the degree of illness.  The microbiological tests used for detecting Ebola virus include: ELISA, Nucleic acid detection, Virus isolation, and immunohistochemical staining.  ELISA testing is able to detect the virus antigen in specimens such as blood, tissue or serum.  Nucleic acid techniques use the reverse transcriptase polymerase chain reaction (real-time PCR).  This technique is faster than ELISA and provides genetic data of the virus. Virus isolation is a simple test; however, it takes longer and a Biosaftey Level-4 laboratory setting is needed. Immunohistochemical staining can localize the virus in tissue samples and find the how the virus entered the host.  (CDC, 2013)

Although there are tests that can identify the disease after transmission, origin of the disease is still unknown. Scientists have introduced a few different hypotheses about the origin of the disease. For one, scientists suggest that the virus has been in the environment for a long period of time, but in a cryptic area with infrequent contact.  The second hypothesis suggests that the virus has recently been introduced to the environment and has spread via susceptible hosts.  (Groseth et al., 2007)  A third hypothesis suggests that bats are the reservoir host for the disease.  Scientists indicate that epizootic occurrences are happening and producing a high mortality rate in non-human primates, which has been known to precede human disease occurrences.  It is theorized that the infected bats will affect wild animals and human contact with the infected animal can result in disease transmission.  In addition, once transmitted in a human, human to human transmission occurs.  (CDC, 2014)

Since there is no known etiology of the Ebola virus, it is important that researchers study the components and mechanisms of how the virus enters the host’s cells.  This is specifically important due to the lack of vaccinations and medications, as well as the threat of use of the Ebola virus in biowarfare.  Recent research has focused on the cellular properties of the Ebola virus.  For instance, research has found that the viral glycoprotein plays an integral role in the disease transmission of the Ebola virus.  The surface glycoprotein is structured in a way that it empties its cellular contents into the host cell, in which it releases the cytokines causing symptoms to occur in the host.  Researchers suggest that it is the molecular expression of the glycoprotein and the gene products that cause this effect. (Simmons et al., 2002; Yang et al., 2000)  In addition, additional research has focused on peplomers on the glycoprotein surface of the virus. The peplomers are attached to the cellular membrane within the lipid bilayer.  It has been found that the peplomers are responsible for the facilitation of the virus into the host cell through the glycoprotein surface. It has also been found that the process of entry involves the binding to specific receptors. Researchers have then focused on mutating the genetic sequence in the virus, specifically at the peplomer process, in order to prevent the virus from entering the host cell, as well as preventing glycoprotein synthesis.  (Jeffers et al., 2002)

Jeffers et al. (2002) focused on preventing the synthesis of the Ebola virus glycoprotein. The glycoprotein genetic sequence was mutated and the effects of the mutation were observed for viral entry into host cells. The study focused primarily on the investigation of a genetic mutation on the plasmid DNA and the cysteine in the glycoprotein. It was suggested that interruption of the cysteine would result in formation of the viral glycoprotein.  Results found that with the mutation in the cysteine, the glycoprotein secretion occurred at a higher rate in comparison to glycoprotein secretion from a non-mutated cysteine.  In addition, it was found that the mutation in the cysteine protein ended the ability for the glycoprotein to form on the retrovirus, which prevents the virus from entering host cells.    From this research, scientists have been able to develop a greater understanding of the function of glycoproteins in Ebola virus.  (Jeffers et al., 2002)

The results of this study reported by Jeffers et al. (2002) illustrated the need for additional research into the mechanisms and role of glycoproteins in the transmission of the Ebola virus to host cells.  This information is extremely important to the medical field, in regard to disease transmission of the Ebola virus.  This information is also significant to the government as well since the Ebola virus is considered a biosafety threat. For instance, after the initial outbreak in Zaire, the Soviet Union began testing the virus in violation of the Biological Weapons Convention.  In fact, it was reported that the Soviet Union was developing the virus to be used as a biological weapon. (Alibek and Handelman, 1999)

In addition to the hypotheses mentioned previously, researchers have suggested the possibility that the Ebola virus has evolved from avian species.  The results in Jeffers (et al., 2002) illustrated a similarity between the glycoprotein and an oncogenic retrovirus observed in avian species; therefore, it can be suggested that there is an evolutionary basis for this virus. The suggested hypotheses indicated that more research should be conducted in regard to evolutionary retroviruses and viral glycoproteins in order to understand the transmission and etiology of the Ebola virus.

References

Alibek, K., Handelman, S. (1999). Biohazard. Random House, New York, NY, USA.

CDC. (2014).  Ebola virus.  Retrieved on 3/19/14 from: http://www.cdc.gov/vhf/ebola/resources/virus-ecology.html

CDC.  (2013). Ebola Hemorrhagic Fever.  Retrieved on 3/19/2014 from: http://www.cdc.gov/ncidod/dvrd/spb/outbreaks/qaEbolaRestonPhilippines.htm.

Groseth, A., Feldman, H., Strong, J. (2007).  The ecology of the Ebola virus. Microbiology. 15(9):408-416.

Hughes, C. and Varmus, H.  (1997).  . The Place of Retroviruses in Biology. Cold Spring Harbor (NY): Cold Spring Harbor Laboratory Press. Available from: http://www.ncbi.nlm.nih.gov/books/NBK19382/

Jeffers, S.A., Sanders, D.A., Sanchez, A.  (2002).  Covalent Modifications of the Ebola Virus Glycoprotein.  Journal of Virology.  76(24): p. 12463–12472

Simmons, G., R. J. Wool-Lewis, F. Baribaud, R. C. Netter, and P. Bates. (2002). Ebola virus glycoproteins induce global surface protein down-modulation and loss of cell adherence. J. Virol. 76:2518-2528.

Sullivan, N., Yang, Z., and Nabel, G.J.  (2003).  Ebola Virus Pathogenesis: Implications for Vaccines and Therapies.  J. Virol. 77(18): 9733-9737.

Yang, Z.-Y., H. J. Duckers, N. J. Sullivan, A. Sanchez, E. G. Nabel, and G. J. Nabel. (2000). Identification of the Ebola virus glycoprotein as the main viral determinant of vascular cell cytotoxicity and injury. Nat. Med. 6:886-889.