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How do herpesviruses evade detection by natural killer cells and cytotoxic T-lymphocytes?

Literature review

Herpes viruses are defined as single species that have separate epidemiological or biological features and distinct genomes that signify independent duplicating ancestries. Natural killer are deliberated part of the body’s native protective system as they can quickly react to contaminations and due to their expression of germline-encoded immune identification receptors. Cytotoxic T-lymphocytes (CTLs) are principal effectors to remove malignant cells in the antigen and cell contact-dependent way and persuade long-lasting tumor deterioration. Cytotoxic T lymphocytes terminate virus-infected and cancerous cells by the stimulation of apoptosis. In this particular literature review, the process of herpes virus evades the cytotoxic t lymphocytes cells and Killer cells will be discusesed.

These lymphocytes and body’s T lymphocytes are the key important cells of the human protective system that prevent the invasion of microorganisms or pathogens. Herpes virus is the pathogen that can cause contagious sores most commonly around the mouth or on the genitals. This virus is able to invade the immune system even in the presence of both t lymphocytes and NTKs. According to De Pelsmaeker, Romero, Vitale, & Favoreel (2018), herpesviruses usually overpower identification and eradication of contaminants by killer cells, it has been identified that these types of cells cause a very imperative danger to the pathogen. They also reported that The NK cell avoidance methods are specific to every human herpes virus probable reflecting assortment forces encountered in the numerous contamination niches engaged by the microorganisms. Their study on the herpes virus also revealed that the shortage of processes of K cell immune-evasion by the herpes viruses such as VZV and HSV is confusing. A well-identified perseverance is there of the Virus in individuals with defective killer cell and the significance of its contribution in the monitor of illness. Ongoing investigation may probable to disclose as yet unidentified processes of immune-evasion by the α herpes viruses A range of herpes viruses also leads to cutaneous and ocular contaminations with the possibility for permanent illness (Jonji?, Babi?, Poli?, & Krmpoti?, (2008).

Nachmani, Stern-Ginossar, Sarid, & Mandelboim, (2009), revealed that herpes viruses use mutual approaches for immune avoidance; they stated that the approach of applying the miRNA to object a host resistant gene may also be preserved amongst diverse herpes viruses

Odom, Gaston, Markert, & Cassady, (2012) identified that several humanoid herpes viruses reduce MHC-I exhibition of its antigens to evade recognition by cytotoxic T-cells, these processes may counterbalance the cost of Natural killer cell reserve from the Missing Self. The authors also suggested that the HSV categories and 2 US12 genetic factor product like impaired cell protein, ICP47 down-moderates MHC-I superficial appearance by overpowering MHC-I transportation from the Endoplasmic reticulum. They also found thatICP47 attaches to the TAP or Transporter Associated with Antigen Presentation and also in doing so hinders MHC-I antigen packing and appearance of antigenic peptides produced by proteasomal deprivation that futher transfer to the ER lumen from the cytosol. Cells plotted to appearance ICP47 unsuccessful to prompt antigenic peptides. Fascinatingly, HSV-1 persuades appearance of various HLA-G isoforms though diminishing the outward appearance of others (Odom, Gaston, Markert, & Cassady, 2012).

Herpes Simplex Virus-1

According to Ma, & Kuang (2016), the dreadful conditions of NKG2D ligands are an additional effective approach to hinder NK cell activation. US20 and HCMV US18 affect MICA for the lysosomal deprivation, dropping NK appointment with virus impacted cells. This kind of avoidance is activated by humanoid herpesvirus-7 in which the U21 protein redirects ULBP one to the lysosomal section for deprivation and down-regulates the external appearance of MICB and MICA by weakening. Lee, Lee, Chaudhary, Gill, & Jung, (2010) reported that C-type lectin (AICL) activated by KSHV ubiquitin E3 ligase K5 ubiquitinates MICA, a MICB and the NKp80 type ligand stimulation-persuaded, which persuades their proteasomal deprivation and decreases their external appearance, ultimately allowing the pathogen to avoid the damage by killer cells

Pegram, Andrews, Smyth, Darcy, & Kershaw (2011), suggested that most of the viral strategies contain processes to suppress the identification of diseased cells by triggering receptors of NK cell or to prompt signaling of inhibitory NK cell. They also reported that most of the important herpes virus NK elusion strategies include meddling with triggering NK signaling or enlarged/reserved inhibitory signalling of NK cell.

Another study conducted by Gewurz, Vyas, & Ploegh, (2007), revealed that Discerning pressure applied by adaptive protection has led the viruses to convergent change an astonishing quantity of immuno-evasions that precisely deregulate T-cell reactions. They also concluded that numerous herpes virus-encoded micro-RNAs have been exposed, and might well assist as immune-evasions

According to Yuan, Weiming & Dasgupta, Anindya & Cresswell, Peter (2006), HSV-1 contamination activates speedy, considerable and particular down-regulation of CD1d superficial appearance in humanoid DCs. Their study further revealed that the consequence is functionally essential because inferior CD1d external expression leads to decreased stimulation of CD1d-limited T cells. Consequently, this approach permits HSV-one to efficiently avoid Killer cell investigation throughout contamination in vivo.

Griffin, Verweij, & Wiertz, (2010) also published an article on the similar topic and found that the prohibition of the MHC category one antigen handling and performance passageway, thus dropping the appearance of virus-resultant epitopes on the external part of the diseased cell. Herpes virus proteins are capable to preserve MHC catagory I particles in the ER or endoplasmic reticulum, or regulate their backward transportation from ER or endocytosis to the cell sheath, with the following deprivation. The subsequent down-instruction of cell exterior MHC category one peptide developments prevents the capability of cytotoxic T lymphocytes to identify and eradicate cells infected by the virus. 

According to Retamal-Díaz, Tognarelli, Kalergis, Bueno, & González, (2016), T cells are able to carry out various functions based upon their phenotype. Whereas T cells are dedicated to assassinating pathogen-contaminated cells, controlling T lymphocytes cells or Tregs are particular inside others in monitoring the level of the body’s protective reaction to antigens. In this admiration, HSV appears to endorse the propagation of controlling T cells by the attachment of gD to HVEM receptors of external part of cell to encourage the excretion of cytokines accredited to these body cells, like IL-10. The elevation of Tregs may modify the action of T cells planned to regulate the pathogen.

Human Cytomegalovirus

Horst, Verweij, Davison, Ressing, & Wiertz, (2011), Found that HSVs delay the appearance of virus-related antigens by obstructing the role of host’s TAP protein or carrier related to antigen handling, which transfers internal and external peptides of cytoplasm part into the cell’s rough ER for peptide filling onto MHC-I particles; TAP prohibition is facilitated by the HSV protein ICP47and the US3 kinase. Hansen, & Bouvier, (2009), decreased peptide MHC multiplexes on the external of contaminated cells intensely decreases the probabilities of T cells discovering HSV-contaminated cells, and also the capability of HSV-infested specialized antigen offering cells to stimulate immature T cells.

According to (Thomas et al., 2008), like other pathogenic herpes viruses, Kaposi's sarcoma-related herpesvirus down-modulate MHC category I particles to evade recognition by T lymphocytes, however, reduces cells vulnerable to cytotoxicity of killer cell. They also presented that the KSHV resilient avoidance gene, K5, decreases cell surface appearance of the NKG2D ligands MHC category one-associated sequence A (MICA), MICB, and the freshly distinct ligand specific to NKp80, stimulation-encouraged C-form lectin (AICL). Down-modulation of both AICL and MICA needs the ubiquitin E-three ligase action of K5 to react on substrate cytoplasmic end lysine particles (Lisni?, Gašparovi?, Krmpoti?, and Jonji?, 2010). 

Conclusion

Natural killer cells are helpful in keeping the body safe from the pathogens by quickly reacting on the infection. Herpes viruses are the single species that possess specific epidemiological and biological characteristics. These viruses use various mechanism or approaches to avoid the identification by the t lymphocytes and killer cells such as suppressing the recognition by using miRNA to target immune system, reducing the MHC-1 appearance, diminishing the surface recognition, lysosome deprivation, interfering with captivating NK cell signaling, and deregulation of T cells response. Another type of herpes virus called KSHV downregulates the particles of MHC class 1 that ultimately results in avoiding recognition by cytotoxic t lymphocytes.

References

De Pelsmaeker, S., Romero, N., Vitale, M., & Favoreel, H. W. (2018). Herpesvirus evasion of Natural Killer cells. Journal of Virology, JVI-02105.

Gewurz, B. E., Vyas, J. M., & Ploegh, H. L. (2007). Herpesvirus evasion of T-cell immunity.

Griffin, B. D., Verweij, M. C., & Wiertz, E. J. (2010). Herpesviruses and immunity: the art of evasion. Veterinary Microbiology, 143(1), 89-100.

Hansen, T. H., & Bouvier, M. (2009). MHC class I antigen presentation: learning from viral evasion strategies. Nature Reviews Immunology, 9(7), 503.

Horst, D., Verweij, M. C., Davison, A. J., Ressing, M. E., & Wiertz, E. J. (2011). Viral evasion of T cell immunity: ancient mechanisms offering new applications. Current opinion in immunology, 23(1), 96-103.

Jonji?, S., Babi?, M., Poli?, B., & Krmpoti?, A. (2008). Immune evasion of natural killer cells by viruses. Current opinion in immunology, 20(1), 30-38.

Lee, H. R., Lee, S., Chaudhary, P. M., Gill, P., & Jung, J. U. (2010). Immune evasion by Kaposi’s sarcoma-associated herpesvirus. Future Microbiology, 5(9), 1349-1365.

Lisni?, V.J., Gašparovi?, I., Krmpoti?, A. and Jonji?, S., 2010. Virus Interactions with NK Cell Receptors. In Natural Killer Cells (pp. 125-152). Springer, Berlin, Heidelberg.

Ma, Y., Li, X., & Kuang, E. (2016). Viral evasion of natural killer cell activation. Viruses, 8(4), 95.

Nachmani, D., Stern-Ginossar, N., Sarid, R., & Mandelboim, O. (2009). Diverse herpesvirus microRNAs target the stress-induced immune ligand MICB to escape recognition by natural killer cells. Cell host & microbe, 5(4), 376-385.

Odom, C. I., Gaston, D. C., Markert, J. M., & Cassady, K. A. (2012). Human herpesviridae methods of natural killer cell evasion. Advances in virology, 2012.

Pegram, H. J., Andrews, D. M., Smyth, M. J., Darcy, P. K., & Kershaw, M. H. (2011). Activating and inhibitory receptors of natural killer cells. Immunology and cell biology, 89(2), 216-224.

Retamal-Díaz, A. R., Tognarelli, E., Kalergis, A. M., Bueno, S. M., & González, P. A. (2016). Immune evasion by herpes simplex viruses. In Herpesviridae. InTech.

Thomas, M., Boname, J. M., Field, S., Nejentsev, S., Salio, M., Cerundolo, V., & Lehner, P. J. (2008). Down-regulation of NKG2D and NKp80 ligands by Kaposi's sarcoma-associated herpesvirus K5 protects against NK cell cytotoxicity. Proceedings of the National Academy of Sciences, 105(5), 1656-1661.

Yuan, Weiming & Dasgupta, Anindya & Cresswell, Peter. (2006). Herpes simplex virus evades natural killer T cell recognition by suppressing CD1d recycling. Nature immunology. 7. 835-42.

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