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Measles is a virus, abbreviated to MeV, thought to have existed around 4000 years ago that has long been known to be causal in infant disease affecting mortality and remaining a public health issue. The causal virion is defined biologically within the Family _Paraxmyxoviridae_, Genus _Morbillivirus_ and Species _MeaslesMorbillivirus. _Similar to other infections, MeV is an airborne infection with the virion particle composed of a negative (-ve) sense single–stranded (ss) ribonucleic acid (RNA) genome code, around 15-16kb in size, encoding for eight predominant proteins. The first isolation of MeV occurred in 1954 of MeV known as the “Edmonston strain” from David Edmonston, a student at Fay School in Boston. The lack of antigenic variation by the MeV particle is suggestive that the third pathogen with the potential to be eradicated requires further research. In 1954 knowledge of the immune system had only just started emerging. Just prior, in 1948, a pioneer Mark Adams examined how 7 bacterial viruses could be inactivated through gas/liquid exchange through bubbling nitrogen over _Escherichia coli. _This occurs through barriers known as the glycocalyx and endothelial surface layer (GC-ESL) together with immunological cell phenotypes that can restrict viral replication through respiratory epithelial and endothelial cell layers affected by MeV. Other proteins like cytokines, chemokines as well as adhesion molecules and receptors direct immune cell systems. Therefore it was then observed that a preventative chemical could inactivate pathogenic infection. Here is a discussion of contextual MeV immunological characteristics during infection. Potential explanations to elucidate this further with regards to past, present, and future research are considered. This outline will provide key insights and be useful to researchers, clinicians and academics in the future.
Measles is a virus, abbreviated to MeV, thought to have existed around 4000 years ago that has long been known to be causal in infant disease affecting mortality and remaining a public health issue. The causal virion is defined biologically within the Family _Paraxmyxoviridae_, Genus _Morbillivirus_ and Species _MeaslesMorbillivirus. _Similar to other infections, MeV is an airborne infection with the virion particle composed of a negative (-ve) sense single–stranded (ss) ribonucleic acid (RNA) genome code, around 15-16kb in size, encoding for eight predominant proteins. The first isolation of MeV occurred in 1954 of MeV known as the “Edmonston strain” from David Edmonston, a student at Fay School in Boston. The lack of antigenic variation by the MeV particle is suggestive that the third pathogen with the potential to be eradicated requires further research. In 1954 knowledge of the immune system had only just started emerging. Just prior, in 1948, a pioneer Mark Adams examined how 7 bacterial viruses could be inactivated through gas/liquid exchange through bubbling nitrogen over _Escherichia coli. _This occurs through barriers known as the glycocalyx and endothelial surface layer (GC-ESL) together with immunological cell phenotypes that can restrict viral replication through respiratory epithelial and endothelial cell layers affected by MeV. Other proteins like cytokines, chemokines as well as adhesion molecules and receptors direct immune cell systems. Therefore it was then observed that a preventative chemical could inactivate pathogenic infection. Here is a discussion of contextual MeV immunological characteristics during infection. Potential explanations to elucidate this further with regards to past, present, and future research are considered. This outline will provide key insights and be useful to researchers, clinicians and academics in the future.
Measles is a virus, abbreviated to MeV, thought to have existed around 4000 years ago affecting predominantly infants but also immunocompromised individuals and others remaining a public health issue. The causal virion is defined biologically within the Family _Paramyxoviridae_, Genus _Morbillivirus_ and Species _MeaslesMorbillivirus. _Similar to other infections, MeV is an airborne infection with the virion composed of an RNA genome code encoding for eight predominant proteins. The first isolation of MeV occurred in 1954 known as the “Edmonston strain” from David Edmonston, a student at Fay School in Boston. The lack of antigenic variation by the MeV particle discovered since is suggestive that the third pathogen with the potential to be eradicated requires further research. In 1954 knowledge of the immune system had only just started emerging. Immune cells traverse barriers known as the glycocalyx and endothelial surface layer (GC-ESL) requiring stimulation to restrict viral replication through antigenic challenge in the respiratory epithelial and endothelial cell layers. Immune cells have different phenotypes and regulate infection through inhibitory and stimulatory proteins like cytokines, and chemokines as well as adhesion molecules and receptors transversing permeable organ tissues from the lymphoid system. Here is a discussion of contextual MeV innate and adaptive immune responses to infection or immunisation. Potential explanations to elucidate this further with regard to past, present, and future research are considered. This outline will provide key insights and be useful to researchers, clinicians and academics in the future.
Measles virus (_Morbillivirus_ abbreviated as MV, but more recently MeV) is the causal agent of Measles disease, thought to have existed at least 4000 years ago, affecting predominantly infants, but also immunocompromised individuals and others remaining a public health issue today globally. In this review, we are discussing the historical background about MeV infection to modern–day research, then delving into Measles disease and discussing what is known about immunisation against the disease. We elucidate what is known about the viral structure and the function of the viral proteins. The genomic stability of the MeV particle is suggestive that the third pathogen with the potential to be eradicated (after the Variola and Rinderpest viruses) requires further biological and immunological clarification. Here therefore covers a bow from structure and mechanism to clinical aspects of MeV infection touching topics like cellular receptor–associated factors to the immunology of MeV infection. We highlight the actual knowledge about innate immune response during MeV infection, including chemokine and cytokine expression finalised by the current understanding of adaptive immune responses to MeV.
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