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Influenza-B virus is a genus in the virus family Orthomyxoviridae. The only species in this genus is called "Influenza B virus". Influenza B virus only infects humans and seals. This limited host range is apparently in contrast with those caused by the similar Influenza virus A as both mutate by both genetic drift and reassortment. Influenza-B virus evolves slower than A viruses and faster than C viruses. Influenza-B virus mutates at a rate 2-3 times lower than type A. However, influenza B mutates enough that lasting immunity is not possible. The Influenza B virus capsid is enveloped while its virion consists of a matrix protein + envelope + nucleoprotein complex + nucleocapsid, and a polymerase complex. Influenza B is sometimes spherical and sometimes filamentous. Its 500 or so surface projections are made of hemagglutinin and neuraminidase.
The Influenza B virus is 14648 nucleotides long and consists of eight segments of linear negative-sense, single-stranded RNA. The multipartite genome is encapsidated, each segment in a separate nucleocapsid, and the nucleocapsids are surrounded by one envelope.

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.

Macrophage Inflammatory Proteins (MIP) belong to the family of chemotactic cytokines known as chemokines. In humans, there are two major forms, MIP-1? and MIP-1? that are now officially named CCL3 and CCL4 respectively. Both are major factors produced by macrophages after they are stimulated with bacterial endotoxins. They activate human granulocytes (neutrophils, eosinophils and basophils) which can lead to acute neutrophilic inflammation. They also induce the synthesis and release of other pro-inflammatory cytokines such as interleukin 1 (IL-1), IL-6 and TNF-? from fibroblasts and macrophages. The genes for CCL3 and CCL4 are both located on human chromosome 17.

The type II transmembrane protein FASLG is a member of the tumor necrosis factor (TNF) superfamily. A fas ligand/receptor interaction has a significant part in the regulation of the immune system and the advancement of cancer. FASLG is expressed on the activated T cell surface as a nondisulfidelinked homotrimer. FASLG binding to Fas/CD95/TNFRSF6 on a nearby cell prompts apoptosis in the Fas expressing cell. FASLG is released from the cell surface by metalloproteinases as a soluble molecule that stays trimeric and is able to bind with Fas, but its capability to activate apoptosis is radically reduced. In addition, FASLG binds to DcR3 - a soluble trap receptor with no signal transduction capabilities. Flawed Fas-mediated apoptosis causes oncogenesis in addition to drug resistance in existing tumors. Constitutive expression of FASLG in a variety of tumors enables their immune evasion. Both mouse and human FASLG are active on mouse and human cells.

Calnexin (CANX) belongs to the calnexin family of molecular chaperones. Calnexin is a calcium-binding, ER-associated protein that interacts briefly with newly synthesized N-linked glycoproteins, facilitating protein folding and assembly. Calnexin may also have a key role in the quality control of protein folding by retaining incorrectly folded protein subunits within the ER for degradation. Calnexin grants long-term protection of wild-type Shaker protein from ER-associated degradation. Polypeptide substrate recognition by Calnexin requires specific conformations of the Calnexin protein. Calnexin dwindles with aging and might contribute to a cytoprotection in an array of human age-related diseases.

Thymic Stromal Lymphopoietin Receptor (TSLPR) is a member of the type I cytokine receptor family. TSLPR alongside the interleukin 7 receptor (IL7R) activate STAT3, STAT5, and JAK2 pathways, which is regulated processes such as cell proliferation and development of the hematopoietic system. Two transcript variants encoding dissimilar isoforms have been found for this gene. TSLPR is expressed in heart, skeletal muscle, kidney and adult and fetal liver.

4-1BBL is a transmembrane cytokine that is part of the tumor necrosis factor (TNF) ligand family. 4-1BBL is a bidirectional signal transducer that performs as a ligand for TNFRSF9, which is a costimulatory receptor molecule in T lymphocytes. TNFSF9 and its TNFRSF9 take part in the antigen presentation development and in the generation of cytotoxic T cells. 4-1BBR is absent from resting T lymphocytes but rapidly expressed upon antigenic stimulation. TNFSF9 reactivates anergic T lymphocytes as well as promoting T lymphocyte proliferation. 4-1BB Ligand is needed for the optimal CD8 responses in CD8 T cells. 4-1BBL is expressed in carcinoma cell lines, and is thought to be involved in T cell-tumor cell interaction. 4-1BBL is expressed by activated B cells, macrophages, dendritic cells, activated T cells, neurons and astrocytes. The interaction of 4-1BB with TNFRSF9 strongly regulates immunity and has been proposed to preferentially control T cell responses based on studies in various murin

Sjogren syndrome/scleroderma autoantigen 1, SSSCA1 is involved in mitosis. SSSCA1 is a centromere-associated protein which can induce anti-centromere antibodies. In addition SSSCA1 is recognized by a subset of anti-centromere antibodies from patients with sclerodermaand Sjogren's syndrome.

HIV-1 and HIV-2 appear to package their RNA differently. HIV-1 binds to any appropriate RNA whereas HIV-2 preferentially binds to mRNA which creates the Gag protein itself. This means that HIV-1 is better able to mutate. HIV-2 is transmitted in the same ways as HIV-1: Through exposure to bodily fluids such as blood, semen, tears and vaginal fluids.
Immunodeficiency develops more slowly with HIV-2.
HIV-2 is less infectious in the early stages of the virus than with HIV-1.
The infectiousness of HIV-2 increases as the virus progresses.
Major differences include reduced pathogenicity of HIV-2 relative to HIV-1, enhanced immune control of HIV-2 infection and often some degree of CD4-independence. Despite considerable sequence and phenotypic differences between HIV-1 and 2 envelopes, structurally they are quite similar. Both membrane-anchored proteins eventually form the 6-helix bundles from the N-terminal and C-terminal regions of the ectodomain, which is common to many viral and cellular fusion proteins and which seems to drive fusion.
HIV-1 gp41 helical regions can form more stable 6-helix bundles than HIV-2 gp41 helical regions however HIV-2 fusion occurs at a lower threshold temperature (25°C), does not require Ca2+ in the medium, is insensitive to treatment of target cells with cytochalasin B, and is not affected by target membrane glycosphingolipid composition.

Human papillomaviruses (HPVs) are a group family with more than 150 related viruses. HP 6 and 11 considered as low-risk HPVs can be sexually transmitted, causing warts to emerge on or around the genitals or anus, known as condylomata acuminate. HPV 11 major/large capsid antigen is used in clinical diagnosis to test the specific antibody to this virus induced by the virus infection, the positive reaction of this antibody is deemed as a marker for present and past infection. Furthermore, HPV 11 large capsid is used as a potential candiadate for vaccine development.

Chikungunya is an infection caused by the chikungunya virus which is passed to humans by two species of mosquito of the genus Aedes: A. albopictus and A. aegypti. Animal reservoirs of the virus include monkeys, birds, cattle, and rodents. The features of the disease are a sudden onset of fever 2-4 days after exposure. The fever typically lasts 2-7 days, while the associated joint pains usually last weeks or months but sometimes years. The mortality rate is a little less than 1 in 1,000. The disease has occurred in outbreaks in Asia, Europe and the Americas since 2004. CHIKV is a single-stranded positive-sense RNA genome, 11,800 nts long which encodes 2 open reading frames. The nucleocapsid is tightly enveloped by a host-derived lipid bilayer (envelope) supporting the virus-encoded envelope proteins. 80 glycoprotein spikes are C- terminally anchored within the viral envelope. The structural polyprotein is translated from a viral sub genomic mRNA, while as the 5 structural proteins (capsid, E3, E2, 6K, E1) are translated as a single polyprotein, from which capsid (C) is cleaved off to encapsidate. The envelope polyprotein precursor E3-E2-6K-E1 is translocated to the endoplasmatic reticulum. Polyprotein is processed by host signalases, resulting in E3, E2 & E1 forming viral hetero-trimeric spikes. The viral spikes majorly contains E2 and E1 facilitate cell receptor recognition, cell entry thru pH-dependent endocytosis and support viral budding.

Cyclosporin A is a noncytotoxic, natural, 11 amino acid cyclic peptide used clinically as an immunosuppressant for the treatment of autoimmune and inflammatory disorders and to prevent organ rejection after transplantation. Cyclosporin acts chiefly by inhibiting T lymphocyte function, which is vital for the propagation of inflammation. Cyclosporin A does not suppress the activity of other hematopoietic cells, does not cause bone marrow suppression and has a rapid onset of action as opposed to other immunosuppressive agents. Nevertheless, Cyclosporin A -induced nephrotoxicity remains an important clinical problem, and oxidative stress has been implicated as a potential responsible mechanism.

A human infecting coronavirus (viral pneumonia) called 2019 novel coronavirus, 2019-nCoV was found in the fish market at the city of Wuhan, Hubei province of China on December 2019.

The 2019-nCoV shares an 87% identity to the 2 bat-derived severe acute respiratory syndrome 2018 SARS-CoV-2 located in Zhoushan of eastern China. 2019-nCoV has an analogous receptor-BD-structure to that of 2018 SARS-CoV, even though there is a.a. diversity so thus the 2019-nCoV might bind to ACE2 receptor protein (angiotensin-converting enzyme 2) in humans.

While bats are possibly the host of 2019-nCoV, researchers suspect that animal from the ocean sold at the seafood market was an intermediate host. RSCU analysis proposes that the 2019-nCoV is a recombinant within the viral spike glycoprotein between the bat coronavirus and an unknown coronavirus.

Antigen 85A is a member of the antigen 85 complex (Antigen 85A, B, C). The enzymes of the antigen 85 complex have mycolyltransferase activity and catalyze the synthesis of the very rich glycolipid of the mycobacterial cell wall, the cord factor (trehalose 6,6'-dimycolate, TDM). The cord factor is vital for the integrity of the mycobacterial cell wall and pathogenesis of the bacillus. TDM is synthesized from two molecules of trehalose-6'-monomycolate (TMM) by Antigen 85A.

Alpha 1-microglobulin (A1M) is a lipocalin superfamily member (kernal lipocalins). A1M is a low molecular weight protein component of plasma. A1M is distributed in plasma and extravascular compartments of all organs. Alpha-1 Microglobulin is found in mammals, birds, amphibians and fish. The primary sites of A1M synthesis are the liver and the kidney. Around the opening of the lipocalin pocket three lysyl residues are situated; those residues carry yellow-brown modification derived from the binding and degradation of heme and kynurenin (a tryptophan metabolite). A1-Microglobulin’s reductase and dehydrogenase have broad biological substrate specificity properties due to its’ free cysteine side-chain which is located in a flexible loop. Alpha-1-microglobulin is glycosylated by three separate carbohydrate chains: two complex carbohydrates which are N-linked to asparagines at residues 17 and 96, and the other simple carbohydrate which is O-linked to threonine at position 5. The carbohydrates comprise 22% of the total molecular mass of the protein. The glycosylation varies between species.
A1M exists in two forms- a free form and complexed to other macromolecules: in humans- complexed to immunoglobulin A (IgA), in rat- complexed to alpha-1-inhibitor-3. Free A1M is exceptionally heterogeneous in charge (therefore also known as protein HC), and is found tightly linked to a chromophore. The free Alpha-1-microglobulin is a monomeric protein composed of one 188 residue polypeptide and contains three cysteines, two of which (residues 75 and 173) form a conserved intra-molecular disulphide link. The chromophoric group is covalently bound to the free cysteine residue at position 34. A1M binds retinol as a major ligand, but this is probably distinct from its covalent chromophore.
Half of all human plasma A1M (approximately 0.03mg/ml) forms a 1:1 complex with about 5% of plasma immunoglobulin A. The resulting macromolecular complexes’ molecular weight is 200000, and a plasma concentration of 0.3mg/ml. The complex can exhibit both antibody activity and affect many of the biological actions of free Alpha-1-microglobulin.
Alpha-1-microglobulin was first discovered in pathological human urine.
It was suggested that A1M might be involved in tissue defense against reactive oxygen species, oxidation by heme and kynurenin. Evidence also suggests that A1M functions in the regulation of the immune system. Other functions include inhibition of stimulation of cultured lymphocytes by protein antigens; induction of cell division of lymphocytes, a mitogenic effect that can either be enhanced or inhibited by the action of other plasma components; inhibition of neutrophil granulocyte migration in vitro; and inhibition of chemotaxis.

Tumor necrosis factor is a cytokine involved in systemic inflammation and is a member of a group of cytokines that all stimulate the acute phase reaction. TNF is mainly secreted by macrophages.
TNF causes apoptotic cell death, cellular proliferation, differentiation, inflammation, tumorigenesis and viral replication, TNF is also involved in lipid metabolism, and coagulation. TNF's primary role is in the regulation of immune cells.
Dysregulation and, in particular, overproduction of TNF have been implicated in a variety of human diseases- autoimmune diseases, insulin resistance, and cancer.

General Transcription Factor IIA, 1 (GTF2A1) in a complex along with TBP mediates transcriptional activity. GTF2A1 is a part of the transcription machinery of RNA polymerase II and is also participates in transcriptional activation.

Human Adiponectin is a secreted protein expressed exclusively in differentiated adipocyte (adipokine). Adiponectin contains a modular structure comprising an N-terminal collagenous domain followed by a C-terminal globular domain. APM-1 plays a role in various physiological processes such as energy homeostasis and obesity. Plasma levels of adiponectin are reduced in obese humans, and decreased levels are associated with insulin resistance and hyperinsulinemia.

MHC Class II is consists of 2 membrane spanning proteins. Each of these proteins is roughly 30 kDa, and has of two Globular domains, Alpha-1, Alpha-2, Beta-1 and Beta-2. The two regions farthest away from the membrane are alpha-1 and beta-1. The two proteins link without Covalent Bonds. The MHC Class II protein mainly presents peptides, which have been digested from external sources. MHC Class II is normally only expressed by Antigen Presenting Cells (APC) which digest foreign protein. Within the RER the alpha and beta proteins of the molecule, associate with each other, while a third protein called the "invariant chain," is necessary for stabilizing the complex, without it, they will not associate. The MHC-invariant complex is then passed from the RER, into and out of, the Golgi body. It fuses with an Endocytic compartment, where an external protein has been sampled and degraded.

Eotaxin-2, also called MPIF2 & Ckb6, is a novel CC chemokine produced by activated monocytes and T lymphocytes. Eotaxin-2 selectively chemoattracts cells expressing CCR3 including eosinophils, basophils, Th2 T cells, mast cells, and certain subsets of dendritic cells. Furthermore, Eotaxin-2 inhibits the proliferation of multipotential hematopoietic progenitor cells. The mature protein, which includes C-terminal truncation, contains 78 amino acids (92 amino acids for the mouse homolog, without C-terminal truncation).
CCL24 functions as a chemotactic chemokine for resting t-lymphocytes, and eosinophils. CCL24 has lower chemotactic activity for neutrophils but none for monocytes and activated lymphocytes. CCL24 is a strong suppressor of colony formation by a multipotential hematopoietic progenitor cell line and binds to CCR3.

Listeria monocytogenes is a pathogenic bacteria that manufactures flagella.At 37 °C inside humans, it causes MogR to repress the expression of flagellar proteins, thus stopping the manufacturing of flagella. Though, in the low-temperatures externally of the host, the GmaR inactivates MogR, enabling flagellar formation.

Lymphotoxin alpha, a member of the tumor necrosis factor family, is a cytokine produced by lymphocytes. LTA is highly inducible, secreted, and exists as homotrimeric molecule. LTA forms heterotrimers with lymphotoxin-beta which anchors lymphotoxin-alpha to the cell surface. LTA mediates a large variety of inflammatory, immunostimulatory, and antiviral responses. LTA is also involved in the formation of secondary lymphoid organs during development and plays a role in apoptosis.

TNFRSF6B is a member of the Tumor necrosis factor receptor superfamily. TNFRSF6B performs as a decoy receptor which races against death receptors for ligand binding. TNFRSF6B has a regulatory role in suppressing FasL- and LIGHT-mediated cell death and T cell activation in addition to inducing angiogenesis via neutralization of TL1A.