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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).

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. Lentiviruses are transmitted as single-stranded, positive-sense, enveloped RNA viruses. Upon entry of the target cell, the viral RNA genomeis converted to double-stranded DNAby a virally encoded reverse transcriptasethat is present in the virus particle. This viral DNA is then integrated into the cellular DNA by a virally encoded integraseso that the genome can be transcribed. Once the virus has infected the cell, two pathways are possible: either the virus becomes latentand the infected cell continues to function, or the virus becomes active and replicates, and a large number of virus particles are liberated that can then infect other cells.

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. Lentiviruses are transmitted as single-stranded, positive-sense, enveloped RNA viruses. Upon entry of the target cell, the viral RNA genomeis converted to double-stranded DNAby a virally encoded reverse transcriptasethat is present in the virus particle. This viral DNA is then integrated into the cellular DNA by a virally encoded integraseso that the genome can be transcribed. Once the virus has infected the cell, two pathways are possible: either the virus becomes latentand the infected cell continues to function, or the virus becomes active and replicates, and a large number of virus particles are liberated that can then infect other cells.

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.

Pregnancy Specific Beta-1-Glycoprotein 1 (PSG1) is a member of a subgroup of transcription factors which are phosphorylated upon binding to promoter sequences. PSGs belong to the carcinoembryonic antigen (CEA) family and function as early biochemical markers of syncytiotrophoblast formation. Furthermore, PSG1 is assumed to mediate placental vascular morphogenesis by enhancing VEGF-A production and endothelial tube formation. PSG1 is a major product of the syncytiotrophoblast, reaching concentrations of 100- 290 mg/l at term in the serum of pregnant women.

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.

NUDT1 is an enzyme that hydrolyzes oxidized purine nucleoside triphosphates, such as 8-oxo-dGTP, 8-oxo-dATP, 2-hydroxy-dATP, and 2-hydroxy rATP, to monophosphates, thereby preventing misincorporation of 8-oxo-dGTP into DNA thus preventing A:T to C:G transversions. NUDT1 is found mostly in the cytoplasm, with some in the mitochondria, suggesting that it is involved in the sanitization of nucleotide pools both for nuclear and mitochondrial genomes. Moreover, NUDT1 is expressed at much higher levels in proliferating cells than in resting cells. Misincorporation of oxidized nucleoside triphosphates into DNA/RNA during replication and transcription can cause mutations which may result in carcinogenesis or neurodegeneration.

Maltose Binding Protein (MBP) is a part of the maltose/maltodextrin system of Eschericia coli bacteria, which is responsible for the uptake and efficient catabolism of maltodextrins. It is a complex regulatory and transport system involving many proteins and protein complexes.
Maltose binding protein MalE,MBP, is part of the maltodextrin transport system in E. coli. The maltodextrins diffuse through the LamB pore located in the outer membrane into the periplasm. The sugar is bound to MalE which prevents it to diffuse back outside. MalE passes the sugar to a complex of MalF and MalG in the cytoplasmic membrane where active tranport is mediated by the ATPase MalK. MBP molecular weight is 40,622 dalton. There are two domains in the protein with similar secondary structure (central pleated sheets are surrounded by helices) . The domains are connected by three bridges, between the domains is a deep groove in which the sugar is bound. All hydroxyl groups of the sugar are fixed by sidechains of the protein by hydrogen bonds. Some water molecules are part of the hydrogen bridge network.

Chemokine (C-C motif) ligand 11 (CCL11) is a small cytokine belonging to the CC chemokine family that is also known as eotaxin. CCL11 selectively recruits eosinophilsby inducing their chemotaxis, and therefore, is implicated in allergic responses. The effects of CCL11 are mediated by its binding to a G-protein-linked receptor known as a chemokine receptor. Chemokine receptors for which CCL11 is a ligandinclude CCR2, CCR3and CCR5. The gene for human CCL11 (scya11) is encoded on three exons and is located on chromosome 17.

E-cadherin (uvomorulin, cell-CAM120/80) is a calcium dependent cell adhesion molecule expressed predominately in epithelial tissues. It plays an important role in the growth and development of cells via the mechanisms of control of tissue architecture and the maintenance of tissue integrity. Numerous studies have demonstrated that reduction and/or loss of Ecadherin expression in carcinomas correlates positively with the potential of these tumors for invasion and metastasis.

Borrelia belongs to a genus of bacteria of the spirochete phylum. Borrelia causes borreliosis, which is a zoonotic, vector-borne disease transmitted mainly by ticks and some by lice, depending on the species. Of the 36 known species of Borrelia, 12 are distinguished to cause Lyme disease or borreliosis and are transmitted by ticks. The main Borrelia species causing Lyme disease are Borrelia burgdorferi, Borrelia afzelii, and Borrelia garinii. The Borrelia genus members have a linear chromosome which is about 900 kbp in length as well as an excess of both linear and circular plasmids in the 5-220 kbp size range. The plasmids are atypical, as compared to most bacterial plasmids, since they contain many paralogous sequences, a large number of pseudogenes and, in some cases, essential genes. Moreover, a number of the plasmids have features suggesting that they are prophages.

Killer-cell immunoglobulin-like receptors (KIRs), are a family of cell surface glycoproteins found on Natural Killer (NK) Cells, which are important cells of the immune system. They control the killing function of these cells by interacting with MHC class I molecules, which are expressed on all cell types. This interaction allows them to identify virally infected cells or tumor cells that have a distinctive low level of Class I MHC on their surface. The majority of KIRs are inhibitory, which means that their recognition of MHC suppresses the cytotoxic activity of their NK cell. Only a limited number of KIRs have the capacity to activate cells.
The KIR genes are found in a cluster on chromosome 19q13.4 within the 1 Mb leukocyte receptor complex (LRC). KIR molecules are extremely polymorphic, meaning their gene sequences differ significantly between individuals, so that different individuals have different arrays/repertoires of KIR genes.
The KIR proteins are categorized by the number of extracellular immunoglobulin domains (2D or 3D) and by whether they have a long (L) or short (S) cytoplasmic domain. KIR proteins with the long cytoplasmic domain transduce inhibitory signals upon ligand binding via an immune tyrosine-based inhibitory motif (ITIM). Whereas KIR proteins with the short cytoplasmic domain lack the ITIM motif and instead associate with the TYRO protein tyrosine kinase binding protein to transduce activating signals.
KIR2DL3 is an inhibitory Killer Cell Ig-like Receptor (KIR, previously called p58 KIR, cl-6, NKAT2 or KIR-K7), which recognizes class I MHC molecules (HLA-Cw1, -Cw3, -Cw7, and Cw8). KIR2DL3 inhibits the activity of NK cells thus preventing cell lysis.

Aurora Kinase B (AURKB) belongs to a family of mitotic serine/threonine kinases. AURKB connects with chromosomes for the period of prophase prior to relocalizing to the spindle at anaphase. AURKB localizes to microtubules near kinetochores, specifically to the specialized microtubules called K-fibers. AURKB controls chromosome segregation through the control of microtubule-kinetochore attachment and cytokinesis. AURKB is required for kinetochore localization of BUB1 and SGOL1. AURKB expression during the G2/M phase transition is firmly coordinated with histone H3 phosphorylation, while overexpression is seen in many kinds of cancers. AURKB phosphorylates ''Ser-10'' and ''Ser-28'' of histone H3 during mitosis. AURKB is a component of the CPC (chromosomal passenger complex), which is a complex that acts as a key regulator of mitosis. High level expression of AURKB is seen in the thymus, which is also expressed in the spleen, lung, testis, colon, placenta and fetal liver. AURKB is expressed during S and G2/M phase and expression is up-regulated in cancer cells during M phase.

EXO2 is a 3'-to-5' exonuclease specific for small (primarily 5 nucleotides or less in length) single-stranded RNA and DNA oligomers. RNA Exonuclease 2 (REXO2) takes part in DNA repair, replication, and recombination, and in RNA processing and degradation. EXO2 is involved in resistance of human cells to UV-C-induced cell death via its part in the DNA repair process.

Interleukin-13 receptor subunit alpha-1 (IL13RA1) is a subunit of the interleukin 13 receptor. The IL13RA1 subunit forms a receptor complex with IL4 receptor alpha, which is a subunit shared by IL13 and IL4 receptors. IL13RA1 binds tyrosine kinase TYK2, and thus may mediate the signaling processes which leads to the activation of JAK1, STAT3 and STAT6 induced by IL13 and IL4. IL13RA1 is vital for allergen-induced airway hyperactivity and mucus hypersecretion.

AHA1 is a cochaperone that stimulates hsp90 ATPase activity. AHSA1 binds the middle domain of Hsp90 (amino acid 272-627) and functions as an ATPase-activating protein that competes with p23 and other co-chaperones for Hsp90 binding.
AHA1 affects a step in the endoplasmic reticulum to golgi trafficking.

PECI is an enzyme that localized to the peroxisomal matrix and encloses one ACB (acyl-CoA-binding) domain. PECI is expressed abundantly in liver, heart and skeletal muscle. PECI functions to catalyze the isomerization of both 3-cis and 3-trans double bonds into the 2-trans form in an array of enoyl-CoA species. PECI takes part in the beta-oxidation of unsaturated fatty acids.

Kruppel-Like Factor 7 (KLF7) is a part of the Kruppel-like transcriptional regulator family whose members regulate cell proliferation, differentiation and survival and contain 3 C2H2 zinc fingers at the C-terminus that mediate binding to GC-rich sites. KLF7 contributes to the progression of type 2 diabetes by inhibiting insulin expression and secretion in pancreatic beta-cells and also by deregulating adipocytokine secretion in adipocytes.

PPP1CA is one of the 3 catalytic subunits of protein phosphatase 1 (PP1). PP1 is a serine/threonine specific protein phosphatase which is involved in the regulation of a variety of cellular processes, such as cell division, glycogen metabolism, muscle contractility, protein synthesis, and HIV-1 viral transcription. Increased PP1 activity is detected in the end stage of heart failure. Studies in both human and mice suggest that PP1 is a significant regulator of cardiac function. Mouse studies also propose that PP1 functions as a suppressor of learning and memory.

C1QBP binds to the globular "heads" of c1q thus inhibiting c1 activation. C1QBP interacts with a wide range of ligands and is implicated in cell signaling. C1QBP associates with C1r and C1s in order to yield the first component of the serum complement system. C1QBP protein has been identified as the p32 subunit of pre-mRNA splicing factor SF2, as well as a hyaluronic acid-binding protein.
C1QBP is a new marker of tumor cells and tumor-associated macrophages/myeloid cells in hypoxic/metabolically deprived areas of tumors.
Mitochondrial C1QBP is a critical mediator of p14ARF-induced apoptosis.
C1QBP functions as a chemotactic factor for immature dendritic cells, and migration is mediated through ligation of both C1QBP and cC1qR/CR.
C1QBP overexpression successfully blocks mRNA accumulation from the adenovirus major late transcription unit (MLTU) and stimulates RNA polymerase II carboxy-terminal domain phosphorylation in virus-infected cells.
C1QBP binds with Hepacivirus core protein on CD8+ and CD4+ positive t-cells and inactivates lck and akt.

Trichomonas vaginalis, an anaerobic, flagellated protozoan parasite, is most dominant protozoan causing sexual transmitted disease. T. vaginalis induced vaginal tract infection occurs as multiple steps involving interactions between host macromolecules and protozoan virulent factor. Adhension protein P65 of T. vaginalis has a vital part in assisting the penetration into vaginal tract surface.

Pyridoxine-5'-phosphate oxidase (PNPO) is the rate-limiting enzyme in vitamin B6 synthesis. Vitamin B6 (Pyridoxal 5-prime-phosphate or PLP) is vital for normal cellular function, and some cancer cells have notable differences in vitamin B6 metabolism compared to their normal counterparts.Vitamin B6 is an essential co-factor for enzymes involved in both homocysteine metabolism and synthesis of neurotransmitters such as catecholamine. Mutations in the PNPO gene result in PNPO deficiency, a form of neonatal epileptic encephalopathy.

Glia Maturation Factor-Beta (GMF-Beta) is a 17 kDa protein nerve gorwth factor identified as a growth and differentiation factor in the vertebrate brain.

Glia Maturation Factor-Beta stimulates differentiation of normal neurons as well as glial cells. GMFB inhibits the proliferation of the N-18 neuroblastoma line and the C6 glioma line while promoting their phenotypic expression.
GMF-beta inhances the phenotypic expression of glia & neurons thus inhibits the proliferation of their respective tumors when added to cell culture. Although astrocytes produce GMF-b and stores it inside the cells, they don’t secrete the GMF-B into the cultured medium. Cell- surface GMFb acts on the target cells at close range when cells are in direct contact. GMF-Beta is produced by thymic epithelial cells and plays an important role in T cell development in favor of CD4+ T cells.
GMF-Beta is a brain-specific protein which belongs to the actin-binding proteins (ADF) family. GMF-beta appears to play a role in the differentiation, maintenance, and regeneration of the nervous system. It also supports the progression of certain auto-immune diseases, possibly through its ability to induce the production and secretion of various pro-inflammatory cytokines.