Herpes Virus Evasion of Cell Detection

This literature review discusses how herpes viruses evade the detection of cytotoxic T lymphocytes and killer cells. It explores the different mechanisms used by herpes viruses to avoid immune recognition, such as suppressing recognition, reducing MHC-1 appearance, and interfering with NK cell signaling. The study also highlights the downregulation of MHC class 1 particles by KSHV to evade recognition by cytotoxic T lymphocytes.

Running Head: VIRUS EVADE OF CELL DETECTION
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Herpes virus
Student name

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Table of Contents
Introduction...........................................................................................................................................2
Literature review...............................................................................................................................2
Conclusion.............................................................................................................................................6
References.............................................................................................................................................7

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Introduction
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.
Literature review
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

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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 (Jonjić, Babić, Polić, &
Krmpotić, (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).
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

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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

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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.
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

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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 (Lisnić, Gašparović, Krmpotić, and Jonjić,
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.

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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.
Jonjić, S., Babić, M., Polić, B., & Krmpotić, 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.
Lisnić, V.J., Gašparović, I., Krmpotić, A. and Jonjić, 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.

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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.