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KLRD1, also known as Killer Cell Lectin Like Receptor D1, is expressed on the surface of natural killer cells in the innate immune system. KLRD1 functions as a receptor for the recognition of MHC class I HLA-E molecules by NK cells and some cytotoxic T-cells. KLRD1 can create disulfide-bonded heterodimer with NKG2 family members. CD94 & NKG2 complex interacts with (HLA)-E, Human Leukocyte Antigen on target cells on the surface of natural killer cells.

NS5A is a component of the replication complex which takes part in RNA-binding. NS5A protein’s hyperphosphorylated form is an inhibitor of viral replication. NS5A interacts with Human VAPB and through it targets the viral replication complex to vesicles. NS5A down-regulates viral IRES translation initiation and mediates interferon resistance by interacting and inhibiting human EIF2AK2/PKR. NS5a is also inhibits apoptosis by interacting with BIN1 and FKBP8.

KLRB1 has an inhibitory role on natural killer (NK) cells cytotoxicity which are lymphocytes who facilitate cytotoxicity and secrete cytokines subsequent to immune stimulation. Some genes of the C-type lectin superfamily, like the rodent NKRP1 family of glycoproteins, are expressed by NK cells and take part in NK cell function regulation. KLRB1 holds an extracellular domain with a few characteristic motifs of C-type lectins, a transmembrane domain, and a cytoplasmic domain. Due to its external C terminus KLRB1 is considered to be a type II membrane protein.

GARS is an (alpha)2 dimer which is a member of the class II family of tRNA synthetases. GARS is a glycyl-tRNA synthetase, one of the aminoacyl-tRNA synthetases which charge tRNAs with their cognate amino acids. GARS catalyzes the attachment of glycine to tRNA(Gly). In addition, GARS is able to produce diadenosine tetraphosphate (Ap4A), which is a universal pleiotropic signaling molecule required for cell regulation pathways, by direct condensation of two ATPs. GARS has been demonstrated to be a target of autoantibodies in the human autoimmune diseases, polymyositis or dermatomyositis.

Human T-lymphotropic virus (HTLV) is a human, single-stranded RNA retrovirus that causes T-cell leukemia and T-cell lymphoma. The virus activates a subset of T-helper cellscalled Th1cells. The result is a proliferation of Th1 cells and overproduction of Th1 related cytokines (mainly IFN-gamma and TNF-alpha). Feedback mechanisms of these cytokines cause a suppression of the Th2 lymphocytes and a reduction of Th2 cytokine production (mainly IL-4, IL-5, IL-10 and IL-13). The end result is a reduction in the ability of the infected host to mount an adequate immune response to invading organisms that require a predominantly Th2 dependant response (these include parasitic infections and production of mucosal and humoral antibodies).

TBE is caused by tick-borne encephalitis virus (TBEV), a member of the family Flaviviridae.
A closely related virus in Far Eastern Eurasia, Russian spring-summer encephalitis virus (RSSEV).
The family Flaviviridae includes other tick-borne viruses are closely related to TBEV and RSSEV, such as Omsk hemorrhagic fever virus & Kyasanur Forest virus.
Louping ill virus is also a member of this family.

T-cell surface glycoprotein CD3 zeta chain (CD247) is a member of the CD3Z/FCER1G family. CD247 is T-cell receptor zeta, which along with T-cell receptor alpha/beta and gamma/delta heterodimers, and also with CD3-gamma, -delta and -epsilon, creates the T-cell receptor-CD3 complex. The zeta chain has a central role in coupling antigen recognition to several intracellular signal-transduction pathways. Low expression of the CD247 antigen causes impaired immune response.

C-Type Lectin Domain Family 10, Member A (CLEC10A) is a part of the C-type lectin superfamily. CLEC10A is expressed in immature myeloid dendritic cells and alternatively activated macrophages. CLEC10A takes part in regulating adaptive and innate immune responses and also binds in a calcium dependent way to terminal galactose and N-acetylgalactosamine, linked to serine or threonine.

IFN-alpha is produced by macrophages, IFN-alpha has antiviral activities and stimulates the production of two enzymes: a protein kinase and an oligoadenylate synthetase.

CCL3L1 is a small cytokine that belongs to the CC chemokines. The CCL3L1 gene is one of several cytokine genes clustered on the q-arm of chromosome 17. CCL3L1 is involved in immunoregulatory and inflammatory processes. CCL3L1 binds to several chemokine receptors including CCBP2 and CCR5. CCR5 is a co-receptor for HIV, and binding of the CCL3L1 protein to CCR5 inhibits HIV entry.

HCV is a small 50nm, enveloped, single-stranded, positive sense RNAvirus in the family Flaviviridae.
HCV has a high rate of replication with approximately one trillion particles produced each day in an infected individual. Due to lack of proofreading by the HCV RNA polymerase, the HCV has an exceptionally high mutation rate, a factor that may help it elude the host's immune response. Hepatitis C virus is classified into six genotypes(1-6) with several subtypes within each genotype. The preponderance and distribution of HCV genotypes varies globally. Genotype is clinically important in determining potential response to interferon-based therapy and the required duration of such therapy. Genotypes 1 and 4 are less responsive to interferon-based treatment than are the other genotypes (2, 3, 5 and 6).

The SARS Nucleocaspid is a protein that has a crucial structural importance, by making the virions associates with the RNA genome and therefore create a nucleocapsid that has the specific helical form. There has been found 3 different domain structures to the nucleocapsid antigen. This protein contains 3 outer structural proteins, the membrane (M), envelope (E), and spike (S) proteins.

MHC Class I is a membrane spanning molecule consisting of 2 proteins. MHC Class I is just about 350 amino acids in length, with roughly 75 amino acids at the carboxylic end comprising the transmembrane and cytoplasmic portions. The remaining 270 amino acids, are divided into three globular domains labeled Alpha-1, Alpha-2 and Alpha-3 prime, with Alpha-1 being closest to the amino terminus and Alpha-3 closest to the membrane. The second portion of the molecule is a small globular protein called Beta-2 Microglobulin. It links primarily with the Alpha-3 prime domain and is essential for MHC stability.
The MHC ability to show a vast range of antigenic peptides for T cell recognition needs a compromise between broad specificity and high affinity. Both MHC class I and MHC class II show an exceptional structure while the peptide main chain is tightly bound and peptide side chains show less restrictive interactions. It is primarily the peptide side-chain contacts and conformational variability that ensures that the peptide-MHC complex presents an antigenically unique surface to T cell receptors.

Fc Fragment Of IgA Receptor, also known as FCAR, is part of the multichain immune recognition receptor family which is the most abundant immunoglobulin in mucosal areas however it is only the second most common antibody isotype in serum. FCAR participates in both pro-and anti-inflammatory responses depending on the state of IgA bound. FCAR is also a vital Fc receptor for neutrophil killing of tumor cells. Once FCAR expressing neutrophils interact with IgA-opsonized tumor cells, the neutrophils not only show antibody-dependent cell-mediated cytotoxicity, but also release the cytokines TNF-α and IL-1β which cause increased neutrophil migration to the site.

Thymine-DNA glycosylase (TDG) is a member of the TDG/mug DNA glycosylase family.
TDG is a nuclear protein that fixes G/T mismatches to G/C pairs by hydrolyzing the carbon-nitrogen bond between the sugar-phosphate backbone of the DNA and the mispaired thymin. In addition, TDG removes uracil and 5-bromouracil from mispairings with guanine. The TDG enzyme has an essential role in cellular defense against genetic mutation triggered by the spontaneous deamination of 5-methylcytosine and cytosine.

ACAA1 is part of the thiolase family of enzymes and is takes part in lipid metabolism. ACAA1 enzyme is localized to the peroxisome and catalyzes the conversion of acyl-CoA and acetyl-CoA to 3-oxoacyl-CoA in the fatty acid oxidation pathway. ACAA1 shows high enzymatic activity in liver, kidney, intestine and white adipose tissue in rats. ACAA1 deficiency causes pseudo-Zellweger syndrome.

ACAT2 enzyme participates in lipid metabolism. ACAT2 takes part in lipoprotein assembly, catalyzing cholesterol esterification in mammalian cells. ACAT2 is an integral membrane protein that localizes to the endoplasmic reticulum of human intestinal cells. ACAT2 deficiency contributes to severe mental retardation and hypotonus.

AK3L1 is an affiliate of the adenylate kinase family of enzymes. AK3L1 enzyme is restricted to the mitochondrial matrix. Adenylate kinases-3 regulates the adenine and guanine nucleotide compositions within a cell by means of catalyzing the reversible transfer of phosphate group among these nucleotides. 5 different isozymes of adenylate kinase have been identified in vertebrates. The enzyme expression of various adenylate kinase isozymes is growth regulated and tissue-specific.

EPM2A is a dual-specificity phosphatase which associates with polyribosomes. The EPM2A protein may be involved in the regulation of glycogen metabolism. Mutations in the EPM2A gene have been linked to myoclonic epilepsy of Lafora.

Immunoglobulin Lambda-Like Polypeptide 1 (IGLL1) is one of the substitute light chain subunits and is a part of the immunoglobulin gene superfamily which does not undergo rearrangement. Two transcript variants encoding diverse isoforms have been found for IGLL1. Mutations in IGLL1 can bring about B cell deficiency and agammaglobulinemia, an autosomal recessive disease in which few or no gamma globulins or antibodies are made.

Plasminogen activator inhibitor-1 is the principal inhibitor of tissue plasminogen activator(tPA) and urokinase(uPA), the activators of plasminogenand hence fibrinolysis(the physiological breakdown of blood clots). It is a serine protease inhibitor(serpin) protein (SERPINE1). The other PAI, plasminogen activator inhibitor-2(PAI-2) is secreted by the placentaand only present in significant amounts during pregnancy. In addition, protease nexinacts as an inhibitor of tPA and urokinase. PAI-1, however, is the main inhibitor of the plasminogen activators.

TBE is caused by tick-borne encephalitis virus (TBEV), a member of the family Flaviviridae.
A closely related virus in Far Eastern Eurasia, Russian spring-summer encephalitis virus (RSSEV).
The family Flaviviridae includes other tick-borne viruses are closely related to TBEV and RSSEV, such as Omsk hemorrhagic fever virus & Kyasanur Forest virus.
Louping ill virus is also a member of this family.

HCV is a small 50nm, enveloped, single-stranded, positive sense RNAvirus in the family Flaviviridae.
HCV has a high rate of replication with approximately one trillion particles produced each day in an infected individual. Due to lack of proofreading by the HCV RNA polymerase, the HCV has an exceptionally high mutation rate, a factor that may help it elude the host's immune response. Hepatitis C virus is classified into six genotypes(1-6) with several subtypes within each genotype. The preponderance and distribution of HCV genotypes varies globally. Genotype is clinically important in determining potential response to interferon-based therapy and the required duration of such therapy. Genotypes 1 and 4 are less responsive to interferon-based treatment than are the other genotypes (2, 3, 5 and 6).