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According to the Center for Disease Control, Measles, caused by the Measles Virus, had acclaimed approximately 450 deaths each year in the United States alone, since 1953. However, since the introduction of the Measles vaccine in 1963, Measles is looked at as a farfetched disease of the past. However, this is not case in many third world developing countries, specifically Somalia (CDC 2010).
Today, Somalia still suffers from this seemingly viral infection of the past. "Measles is an important public health problem in Somalia. While there is scarcity of information on the overall burden of the disease, limited data indicates that it is a significant cause of childhood death." (UNICEF 2008). As recently as November 2010, approximately 19 children died from Measles virus. (AHN 2010). These deaths most likely have resulted from the low immunization rate against the Measles virus, which is said to be on only 19%, as of September 2008 according to UNICEF. (UNICEF 2008). However, in the United States, as of 2000, the illness was said to be eradicated, due to great amount of research done and communication to the general public about Measles, but more specifically, the infamous Measles virus (NEJM 1994).
The Measles virus can be classified via the Baltimore Classification system. This system was used to distinguish all viruses from one another solely based on the mechanisms of viral genome replication and transcription strategies. According to Dr. Baltimore's scheme, the Measles virus is classified under Group V, where all viruses under this group is said to be composed of single stranded, negative-sense RNA. More specifically, the Measles virus is further classified under the Virus Family: Paramyxoviridae which is known to affect animals and humans alike. Thus, this method of classification makes it simpler to organize viruses into groups. (Nath 2003)
The Measles virus is a genetically unique virus, simply because it uses its RNA as a template for mRNA synthesis. However, the virus's genome must be equipped with its own RNA-dependent RNA polymerase enzyme, which will act like a usual RNA polymerase, only viral, in order to produce a positive-sense RNA. The positive-sense RNA molecule intermediate, will then acts as viral mRNA, which is translated into viral structural proteins, such as capsid proteins, movement proteins, and helicase, by the host cell's ribosome. Thus, the production of more single stranded negative-sense RNA makes it more likely to for the host to continuously replicate the viral genome of the Measles virus (Stange 2006).
The Measles virus can also be identified through it physical structures. It is an enveloped virus. The envelope itself is made up of the host's cell lipid bilayer membrane and viral glycoproteins such as Haemagglutinin protein, which serves as a way of attachment to potential target cells and short protein projections. The singles stranded, negative-sense, non-segmented RNA genome is said to be stored in a helical linear nucleocapsid. (Morgan 1977). The virus is approximately 15,984 nucleotides long. It is made up of only six genes: N, P/V/C, M, F, H, and L. The transcription genes encode for about eight proteins, however only six are known to be part of the virion itself. They include the Nucleocapsid protein, Phosphoprotein, Matrix protein, Fusion glycoprotein, Haemmagglutinin, and Large protein (Griffin 2009).
The pathogenesis of the Measles virus can be seen as efficient and complex. Just as in all illnesses, the virus goes through several steps of development in order to cause Measles. Throughout the maturation of virus, in the target host, there are many conformational changes that is necessary for the development of the disease (Dorland's Medical Dictionary for Health Consumers 2007). The morphological changes that virus goes through usually goes hand in hand with changes in the host cell; these specific changes are known as Cytopathic Effects. The usual Cytopathic effects are "cell rounding, disorientation, swelling or shrinking, death, detachment from the surface, etc." (University of South Carolina School of Medicine 2008)
The Measles virus can be characterized as an air-borne virus, meaning it usually enters the host via the upper respiratory tract. From there, it manifests in the lymph nodes and destroys the lymphocytes causing the condition of leucopenia. The Measles virus is also known for its two sets of viremia. The spread throughout the respiratory system is known as the primary viremia while the spread of virus through the blood and into the internal organs and skin is known as the secondary viremia (Virology Online 2010). However, the chief location of replication of the Measles virus lies within the lymph nodes, and therefore the virus itself can be isolated from the resident monocytes. These infected cells are usually described as being large rounded multi-nucleated cells due to the viral invasion. The Measles virus infects the monocytes by binding to the host cell's CD46 receptor. This specific receptor serves as the specific binding site for the Measles virus, similar to a lock key system. This binding then initiates a down regulation of the host cell's IL-12. This cytokine, which is secreted by lymphocytes, is usually responsible for the regulation of differentiation of T cells and the enhanced functions of Natural killer cells T cytotoxic cells. Therefore, the down regulation of IL-12, done by the Measles virus, inhibits the host cell ultimately from building an adaptive immunity, due to the general shutdown of the cell-mediated immune system (Plotkin 1998).
The Measles virus causes a severe systemic illness in which the entire body is affected. (Griffin 1994). The classic contagious rash that appears on the host's entire body is known as the Hallmark symptom of Measles. This rash is usually associated with unaffected specific T-cells attacking inflicted endothelial cells found in the blood vessels. Thus, this classic symptom serves as evidence of an immune response, even though the immune system seems to be the primary target of the Measles virus. Another physical symptom, which is caused by the virus, is the production of Koplik's Spots. These pathogenic spots are actually lesions from necrosis that are usually found in the mouth. Other symptoms include fever, runny nose, and cough (University of South Carolina School of Medicine 2008).
Measles can be classified as an acute virus, meaning its symptoms occur quickly, its manifest rapidly and usually has a short duration. However, unlike most acute viruses, the virus is deemed as infectious, meaning shedding (replication) of the virus, before the onset of symptoms and even throughout the illness. But just as other viral infections, Measles can undergo severe complications. These complications usually occur in patients with impaired cell-mediated immune responses, rather than in patients with impaired immunoglobulin proteins. Patients with impaired cell-mediated immune responses are often targeted since the Measles virus itself targets the T cell development. One of the main complications includes syncytia, where there is a great amount of cell to cell fusion growth, leading to pneumonia and the host cells become no longer functional. This complication then leads to secondary infections by bacteria and encephalitis which then in turn can cause possible manifestations of "deafness, seizures, and mental disorders" (University of South Carolina School of Medicine 2008).
In order for an infection to take place however, the Measles virus must be able to replicate. There are seven steps in the RNA virus life cycle: Attachment, Entry, Uncoating, Gene Expression, Genome Replication, Assembly and Egress. In order for the Measles virus to first attach and enter the target immune host cell, it uses its envelope glycoproteins: Hemagglutinin (H) and Fusion glycoprotein (F). The virus first fuses its pH-independent membrane with the immune cell's surface. Then, its H protein attaches to the cell receptor CD150 and CD46 glycoproteins, creating a lock key. The receptor-mediated attachment consequently leads to a change in confirmation of the H glycoprotein itself, which then in turn, activates the nearby viral F glycoprotein and initiate entry via fusion between the Measles viral envelope and the immune cell membrane. Having the specific viral cell receptors, determines whether the cell will be infected by the virus, this is also known as tropism. The Measles virus is known for its lymphotropism, meaning that it usually targets lymphocytes (immune cells) for attachment and entry. Being lymphotropic, the Measles virus can then be assumed that it plays a major role in the pathogenesis of the ailment Measles, due to the overall immunosuppression (Griffin 2009).
Once the Measles virus enters the host cell, it uncoats by disassembling its capsid using viral proteases and releasing its negative sense single stranded RNA genome into the host immune cell's cytoplasm. The next step in the life cycle is genome replication, which is known to be conserved. It is important to note that genome replication occurs at specific sites between the inner and outer nuclear membranes within the cytoplasm of the target cell (Griffin 2009). It's important to reiterate that the Measles virus' RNA genome is negatively sensed, and thus is deemed as non-infectious, so the Measles virus must be equipped with a polymerase that is able to modify the incoming negative strand RNA into a positive strand messenger RNA (mRNA). This step is known as transcription (University of South Carolina School of Medicine 2008). The virus's RNA Dependent RNA Polymerase (RdRp) subunit protein P is believed to bridge with the N and L subunit proteins of the viral nucleocapsid (which holds the RNA genome) of the Measles virus. The RdRp transcription starts at the 3' end (or at the N gene), resulting six mRNAs that are capped (with the aid of the L protein) and are polyadenylated like cellular mRNAs (with the aid of signaling at the gene's end) (Griffin 2009). The combination of the newly synthesized positive sense mRNA and the original negative sense RNA create a double stranded RNA. However, the double strands move apart and the RdRp attaches again to the 3' end and starts to synthesize another mRNA, which now happens to be negative sense. All newly synthesized strands are then coated with nucleocapsid proteins (N, P, and L proteins) and then serve as template (for replication/transcription) or just packaged into new virions (University of South Carolina School of Medicine 2008).
It is important to note that all new negative sensed strands consist of a Methyl Cap and Poly A Tail, which happens to be crucial for the Measles virus, in order to proceed to the next step, which is translation. During translation, the mRNA must be converted into specific viral proteins with the use of the host's cells ribosomes. Next, the Measles virus must assemble its viral proteins, which still occurs in the cytoplasm. The transmembrane proteins: H and F are shuttled to the host immune cell membrane. The viral M protein, found in the virus's membrane, allows the nucleocapsid (filled with newly synthesized negative sensed single stranded RNA), to associate with a specific section of the host cell's plasma membrane that is coated already with the viral surface glycoproteins: H and F. Finally, the new Measles virus is able to egress via budding from the host cell's membrane as a new now-enveloped negative sense single stranded RNA Measles virus (University of South Carolina School of Medicine 2008).