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Interleukin-8 (IL-8) is a chemokine produced by macrophages and other cell types such as epithelial cells. It is also synthesized by endothelial cells, which store IL-8 in their storage vesicles, the Weibel-Palade bodies. When first encountering an antigen, the primary cells to encounter it are the macrophages who phagocytose the particle. Upon processing, they release chemokines to signal other immune cells to come in to the site of inflammation. IL-8 is one such chemokine. It serves as a chemical signal that attracts neutrophils at the site of inflammation, and therefore is also known as Neutrophil Chemotactic Factor.

SARS Coronavirus is an enveloped virus containing three outer structural proteins, namely the membrane (M), envelope (E), and spike (S) proteins. Spike (S)-glycoprotein of the virus interacts with a cellular receptor and mediates membrane fusion to allow viral entry into susceptible target cells. Accordingly, S-protein plays an important role in virus infection cycle and is the primary target of neutralizing antibodies.
It has recently been shown that SARS (severe acute respiratory syndrome) is caused by a human coronavirus. Human coronaviruses are the major cause of upper respiratory tract illness, such as the common cold, in humans. Coronaviruses are positive-stranded RNA viruses, featuring the largest viral RNA genomes known to date (27-31 kb). The first step in coronavirus infection is binding of the viral spike protein, a 139-kDa protein, to certain receptors on host cells. The spike protein is the main surface antigen of the coronavirus. The glycosilated spike protein (as well as the nucleocapsid protein) can be detected in infected cell culture supernatants with antisera from SARS patients.

VSNL1 is a member of the visinin/recoverin subfamily of neuronal calcium sensor proteins. VILIP1 is strongly expressed in granule cells of the cerebellum where it associates with membranes in a calcium-dependent manner and modulates intracellular signaling pathways of the central nervous system by directly or indirectly regulating the activity of adenylyl cyclase. Changes in cellular expression of VSNL1 were found in hipppocampi of schizophrenics, since more interneurons showed immunoreactivity.
VILIP1 is expressed in pancreatic beta-cells. VILIP-1 interacts with cell membrane and actin-based cytoskeleton. VSNL1 modulates cAMP-accumulation in C6 glioma cells. HLP3 modulates cGMP-accumulation in transfected neural cells and cerebellar granule neurons.

Human immunodeficiency virus (HIV) is a retrovirusthat can lead to a condition in which the immune systembegins to fail, leading to opportunistic infections. HIV primarily infects vital cells in the humanimmune systemsuch as helper T cells(specifically CD4+ T cells), macrophagesand dendritic cells. HIV infection leads to low levels of CD4+ T cells through three main mechanisms: firstly, direct viral killing of infected cells; secondly, increased rates of apoptosisin infected cells; and thirdly, killing of infected CD4+ T cells by CD8 cytotoxic lymphocytesthat recognize infected cells. When CD4+ T cell numbers decline below a critical level, cell-mediated immunityis lost, and the body becomes progressively more susceptible to opportunistic infections. HIV was classified as a member of the genus Lentivirus, part of the family of Retroviridae. Lentiviruses have many common morphologies and biological properties. Many species are infected by lentiviruses, which are characteristically responsible for long-duration illnesses with a long incubation period.HIV-1 gp41 Subtype-c reacts to the specific antibody from HIV1 infection, in lateral flow assay, it is usually coated on the membrane to capture the specific antibody from HIV1 infection.

UFM1 is a ubiquitin-like protein which is conjugated to target proteins by E1-like activating enzyme UBA5 and E2-like conjugating enzyme UFC1 in a manner equivalent to ubiquitylation. UFM1 localizes principally to the nucleus, but is also present in diffuse amounts in the cytoplasm. UFM1 is expressed in a variety of tissues, including kidney, brain, heart, liver and lung.

IFN-gamma produced by lymphocytes activated by specific antigens or mitogens. IFN-gamma, in addition to having antiviral activity, has important immunoregulatory functions, it is a potent activator of macrophages, and has antiproliferative effects on transformed cells and it can potentiate the antiviral and antitumor effects of the type interferons.

Glucagon-like peptide-1 (GLP-1) is derived from the transcription product of the proglucagon gene. The major source of GLP-1 in the body is the intestinal L cell that secretes GLP-1 as a guthormone. The biologically active forms of GLP-1 are: GLP-1-(7-37) and GLP-1-(7-36)NH2.
GLP-1 secretion by L cells is dependent on the presence of nutrients in the lumen of the small intestine. The secretagogues (agents that causes or stimulates secretion) of this hormone include major nutrients like carbohydrate, proteinand lipid. Once in the circulation, GLP-1 has a half life of less than 2 minutes, due to rapid degradation by the enzyme dipeptidyl peptidase-4.
GLP-1 possesses several physiological properties that make it a subject of intensive investigation as a potential treatment of diabetes mellitus. The known physiological functions of GLP-1 include: Increases insulin secretion from the pancreas in a glucose-dependent manner, decreases glucagon secretion from the pancreas, increases beta cells mass and insulin gene expression, inhibits acid secretion and gastric emptying in the stomach, decreases food intake by increasing satiety.

DCUN1D4 holds 1 DCUN1 domain.

ULBP1 together with at least ULBP2 and ULBP3, is ligand for the NKG2D receptor. ULBPs stimulate various signaling pathways in primary NK cells, which result in cytokines and chemokines production. In CMV infected cells, ULBP1 cooperates with soluble CMV glycoprotein UL16 to inhibit the interaction with the NKG2D receptor providing a mechanism by which CMV infected cells escape the immune system. Additionally, UL16 retains ULBP1 to the ER and cis-Golgi apparatus to prevent it from reaching cell surface.

MCEE catalyzes the interconversion of D- and L-methylmalonyl-CoA throughout the degradation of branched chain amino acids, odd chain-length fatty acids, and other metabolites. MCEE protein deficiency is an autosomal recessive inborn error of amino acid metabolism, involving valine, threonine, isoleucine and methionine. This organic aciduria can appear in the neonatal period with life-threatening metabolic acidosis, hyperammonemia, feeding difficulties, pancytopenia and coma.

Chemokine (C-C motif) ligand 19 (CCL19) is a small cytokine belonging to the CC chemokine family that is also known as EBI1 ligand chemokine (ELC) and macrophage inflammatory protein-3-beta (MIP-3-beta). CCL19 is expressed abundantly in thymus and lymph nodes, with moderate levels in trachea and colon and low levels in stomach, small intestine, lung, kidney and spleen. The gene for CCL19 is located on human chromosome 9. This chemokine elicits its effects on its target cells by binding to the chemokine receptor chemokine receptor CCR7. It attracts certain cells of the immune system, including dendritic cells and antigen-engaged B cells.

IFN-tau is also known as TP-1 (trophoblast protein-1) is a new class of type I IFN that is secreted by the trophoblast and is the signal for maternal recognition of pregnancy in sheep. IFN- tau has potent immunosuppressive and antiviral activities similar to other type I IFN but is less cytotoxic than IFN-alpha and IFN-beta. The current investigation concerns the effect of recombinant ovine IFN- tau (rOIFN- tau) on the modulation of MHC class I and II expression on cloned mouse cerebrovascular endothelial (CVE) cells.
IFN-tau induced tyrosine phosphorylation of Stat1 and upregulated the expression of MHC class I on CVE. One proposed action by which type I IFN reduces the relapse rate in MS is via interference with IFN-?-induced MHC class II expression. IFN- tau was shown to downregulate IFN-?-induced MHC class II expression on CVE and, hence, may be of potential therapeutic value in downregulating inflammation in the central nervous system (CNS). IFN- tau did not upregulate the expression of MHC class II on CVE. IFN- tau also inhibited the replication of Theiler's virus in CVE.

MIA2 performs as a tumour suppressor in hepatocellular carcinoma. MIA2is a novel acute phase protein which its expression is found in the liver and reacts to liver damage in chronic liver diseases and is considerably higher in severe fibrosis patients . MIA2 is induced by IL6, TGF-B & and conditioned medium from activated hepatic stellate cells. MIA2 is is mainly expressed in hepatocytes.

Human IL-36a belongs to the IL-1 family which includes IL-1b, IL-1a, IL-1ra, IL-18, IL-36ra (IL1F5), IL-36b (IL1F8), IL-36g (IL1F9), IL-37 (IL1F7) and IL-38 (IL-1F10). The IL-1 family members display a 12 b-strand, b-trefoil configuration, and are thought to have ascended from a mutual ancestral gene. IL-36a is an 18-22kDa, 158aa intracellular and secreted protein which holds no signal sequence, no prosegment and no potential from N-linked glycosylation sites. IL-36a is released as a reaction to LPS and the cell ATP-induced activation of the P2X7 receptor.
Human IL-36a (aa 6-158) shares 57-68% aa sequence homology with mouse, rabbit, equine and bovine IL-36a and 27-57% aa sequence homology with other new IL-1 family members. IL-36a is mostly found in skin and lymphoid tissues, but also in fetal brain, trachea, stomach and intestine.

CoV HKU1 is 1 from 7 known coronaviruses to infect humans including CoV-229E, CoV-NL63, CoVHKU1, MERS-CoV, the original SARS-CoV1, and SARS-CoV-2 (Covid 19). CoV-229E, beta-coronavirus, NL63, CoV-HKU1 and OC43 are the viruses responsible for the common cold. Beta-coronaviruses has an additional shorter spike-like protein called hemagglutinin esterase. Human coronavirus HKU1 (CoV-HKU1) belongs to beta-coronavirus which are enveloped, positive-sense, single stranded RNA and enters its host celll by binding to the N-acetyl9-O-acetyl neuraminic acid receptor.

Interleukin-1b is produced by activated macrophages, IL-1B stimulates thymocyte proliferation by inducing il-2 release, b-cell maturation and proliferation, and fibroblast growth factor activity. IL1B proteins are involved in the inflammatory response, being identified as endogenous pyrogens, and are reported to stimulate the release of prostaglandin and collagenase from synovial cells.

Cystatin-A is the intracellular inhibitor of cysteine proteinase cathepsin B (CatB) and belongs to family 1 of the cystatin superfamily of inhibitor proteins. CSTA is a stefin that functions as a cysteine protease inhibitor, forming tight complexes with papain and the cathepsins B, H, and L. It has been proposed that extracellular CatB together with other classes of proteinases are all subjected to a cascade-like manner of activation. CatB and its inhibitor Cystatin-A are involved in degradation of extracellular matrix proteins during tissue remodeling. CSTA is one of the precursor proteins of cornified cell envelope in keratinocytes and plays a role in epidermal development and maintenance. Cystatin-A has been reported to be found in high concentrations in epithelial cells, polymorphonuclear leukocytes and lymphoid tissue. Stefins may be used as prognostic and diagnostic tools for cancer.

Glycolate oxidase (HAO1) belongs to the superfamily of the alpha hydroxy acid oxidases (HAO) enzymes. HAO1 catalyzes the FMN mediated oxidation of glycolate to glyoxylate and glyoxylate to oxalate with reduction of oxygen to hydrogen peroxide. HAO1 is most abundantly expressed in the liver and pancreas and is most active on twocarbon substrates such as glycolate. Lately, HAO1 has been identified as a key contributor to hyperoxaluria, a disorder in which large deposits of calcium oxalate form kidney stones.

SARS Coronavirus is an enveloped virus containing three outer structural proteins, namely the membrane (M), envelope (E), and spike (S) proteins. Spike (S)-glycoprotein of the virus interacts with a cellular receptor and mediates membrane fusion to allow viral entry into susceptible target cells. Accordingly, S-protein plays an important role in virus infection cycle and is the primary target of neutralizing antibodies.It has recently been shown that SARS is caused by a human coronavirus. Human coronaviruses are the major cause of upper respiratory tract illness in humans, such as the common cold. Coronaviruses are positive-stranded RNA viruses, featuring the largest viral RNA genomes known to date (27-31 kb). The first step in coronavirus infection is binding of the viral spike protein, a 139-kDa protein, to certain receptors on host cells. The spike protein is the main surface antigen of the coronavirus. The most prominent protein in the culture supernatants infected with SARS virus is a 46 kDa nucleocapsid protein. This suggests that the nucleocapsid protein is a major immunogen that may be useful for early diagnostics.

The cytokine Macrophage migration inhibitory factor (MIF) has been identified to be secreted by the pituitary gland and the monocyte/macrophage and to play an important role in endotoxic shock. MIF has the unique property of being released from macrophages and T cells in response to physiological concentrations of glucocorticoids. The secretion of MIF is tightly regulated and decreases at high, anti-inflammatory steroid concentration.

ASF1 Anti-Silencing Function 1 Homolog B (ASF1B) belongs to the H3/H4 family of histone chaperone proteins and is similar to the anti-silencing function-1 protein in yeast. ASF1B is the substrate of the tousled-like kinase family of cell cycle-regulated kinases, and may have a crucial role in modulating the nucleosome structure of chromatin by guaranteeing a regular supply of histones at sites of nucleosome assembly. ASF1B cooperates with CAF-1 (chromatin assembly factor 1) to stimulate replication-dependent chromatin assembly. ASF1B is highly expressed in the testis and at lower levels in colon, small intestine and thymus. ASF1B is necessary for spermatogenesis.

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.