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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.

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.

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.

Src-Like-Adaptor 2, also known as SLA2, is a part of the SLAP family of adapter proteins. SLA2 acts as a significant receptor-proximal in downregulating T and B cell-mediated responses and inhibits antigen receptor-induced calcium mobilization. SLA2 interacts with Cas-Br-M (murine) ecotropic retroviral transforming sequence c.

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.

The bone morphogenetic protein (BMP) receptors are a family of transmembrane serine/threonine kinases that include the type I receptors BMPR1A and BMPR1B and the type II receptor BMPR2. These receptors are also closely related to the activin receptors, ACVR1 and ACVR2. The ligands of these receptors are members of the TGF-beta superfamily. TGF-betas and activins transduce their signals through the formation of heteromeric complexes with 2 different types of serine (threonine) kinase receptors: type I receptors of about 50-55 kD and type II receptors of about 70-80 kD. Type II receptors bind ligands in the absence of type I receptors, but they require their respective type I receptors for signaling, whereas type I receptors require their respective type II receptors for ligand binding.

Salmonella Typhi is a pathogen causing typhoid fever, affecting over 17 million people with approximately 600,000 deaths annually worldwide. If untreated, typhoid fever cases result in mortality rates ranging from 12-30%.

The OmpA protein is one of the main outer-membrane proteins of a large array of Gram-negative bacteria such as A.salmonicida, Shigella dysenteriae and E.coli.OmpA’s major physiological functions include maintenance of the structural integrity and morphology of the cells and porin activity, as well as a role in conjugation and bacteriophage binding.Achromogenic atypical Aeromonas salmonicida is the causative agent of goldfish ulcer disease.Virulence of this bacterium is associated with the production of a paracrystalline outer membrane A-layer protein.The species specific structural gene for the monomeric form of A-protein was cloned into a pET-3d plasmid in order to express and produce a recombinant form of the protein in E.coli BL21(DE3). The induced protein was isolated from inclusion bodies by a simple solubilization-renaturation procedure and purified by ion exchange chromatography on Q-Sepharose to over 95% pure monomeric protein.Recombinant A-protein was compared by biochemical, immunological and molecular methods with the A-protein isolated from atypical A.salmonicida bacterial cells by the glycine and the membrane extraction methods.

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.

Human immunodeficiency virus (HIV) is a retrovirus that can lead to a condition in which the immune system begins to fail, leading to opportunistic infections. HIV primarily infects vital cells in the human immune system such as helper T cells (specifically CD4+ T cells), macrophages and 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 apoptosis in infected cells; and thirdly, killing of infected CD4+ T cells by CD8 cytotoxic lymphocytes that recognize infected cells. When CD4+ T cell numbers decline below a critical level, cell-mediated immunity is 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 genome is converted to double-stranded DNA by a virally encoded reverse transcriptase that is present in the virus particle. This viral DNA is then integrated into the cellular DNA by a virally encoded integrase so that the genome can be transcribed. Once the virus has infected the cell, two pathways are possible: either the virus becomes latent and 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.

The Epstein-Barr virus (EBV), also called Human herpes virus 4 (HHV-4), is a virusof the herpes family (which includes Herpes simplex virusand Cytomegalo virus. On infecting the B-lymphocyte, the linear virus genome circularizes and the virus subsequently persists within the cell as an episome. The virus can execute several distinct programs of gene expressionwhich can be broadly categorized as being lytic cycle or latent cycle. The lytic cycleor productive infection results in staged expression of a host of viral proteinswith the ultimate objective of producing infectious virions. Formally, this phase of infection does not inevitably lead to lysis of the host cellas EBV virions are produced by budding from the infected cell. The latent cycle(lysogenic) programs are those that do not result in production of virions. A very limited, distinct set of viral proteins are produced during latent cycle infection. These include Epstein-Barr nuclear antigen(EBNA)-1, EBNA-2, EBNA-3A, EBNA-3B, EBNA-3C, EBNA-leader protein (EBNA-LP) and latent membrane proteins(LMP)-1, LMP-2A and LMP-2B and the Epstein-Barr encoded RNAs(EBERs).

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). HCV NS3 Genotype-3a contains 2 domains which are serine protinase and helicase.

Glycophorin C, also known as GYPC, is an integral membrane glycoprotein. GYPC is a minor species which is carried by human erythrocytes, however plays an important role in regulating the mechanical stability of red cells. Numeral glycophorin C mutations have been described. The Gerbich and Yus phenotypes are due to deletion of exon 3 & 2, respectively. The Webb & Duch antigens, also identified as glycophorin D, result from single point mutations of the glycophorin C gene. The glycophorin C protein has very slight homology with glycophorins A & B.

CD33 is putative adhesion molecule of myelomonocytic-derived cells which mediates sialic-acid dependent binding to cells. CD33 prefers to bind to alpha-2,6-linked sialic acid. The sialic acid recognition site is masked by cis interactions with sialic acids on the same cell surface. In the immune response, CD33 perform as an inhibitory receptor upon ligand induced tyrosine phosphorylation by recruiting cytoplasmic phosphatases through their SH2 domains which block signal transduction through dephosphorylation of signaling molecules. In addition, CD33 induces apoptosis in acute myeloid leukemia.

SARS Coronavirus is an enveloped virus containing 3 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 takes part in virus infection cycle and is the primary target of neutralizing antibodies.

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.

Glutamate Decarboxylase 2 (GAD2) is one of several forms of glutamic acid decarboxylase, identified as a main autoantigen in type II diabetes. The GAD2 enzyme is responsible for catalyzing the production of gamma-aminobutyric acid from L-glutamic acid. A pathogenic role for the GAD2 enzyme has been characterized in the human pancreas since it has been identified as an autoantibody and an autoreactive T cell target in type II diabetes. GAD2 gene may also have a role in the stiff man syndrome. In addition, GAD2 catalyzes the production of GABA.

HIV-1 Nef is a 27kDa protein highly produced after a very short time after virus infection. HIV-1 Nef is an essential factor for efficient viral replication and phatogenesis.
HIV-1 Nef facilitates virus replication and improves virions infectivity. HIV-1 Nef exerts pleiotropic effect. HIV-1 Nef down-modulates surface MHC-I molecules, decreases cell surface CD4 antigen by interacting with the Src family kinase LCK thereby inducing LCK-CD4 dissociation and by increasing clathrindependent endocytosis of this antigen to target it to lysosomial degradation. HIV-1 Nef guards the infected cell from apoptosis in order to keep it alive until the next virus generation is ready to strike. HIV-1 Nef protein bypasses host Tcell signaling by inducing a transcriptional program nearly identical to that of anti-CD3 cell activation.

Treponema pallidum is a gram-negative spirochaete bacterium and is considered to be metabolically crippled. There are at least four known subspecies: T. pallidum pallidum, T. pallidum pertenue, T. pallidum carateum and T. pallidum endemicum. The helical structure of T. pallidum pallidum allows it to move in a corkscrew motion through viscous mediums such as mucus. Treponema pallidum sub sp. pallidum has one of the smallest bacterial genomes at 1.14 million base pairs (Mb) and has limited metabolic capabilities, reflecting its adaptation through genome reduction to the rich environment of mammalian tissue.

CD68 encodes a 110-kD transmembrane glycoprotein that is highly expressed by human monocytes and tissue macrophages. It is a member of the lysosomal/endosomal-associated membrane glycoprotein (LAMP) family. The protein primarily localizes to lysosomes and endosomes with a smaller fraction circulating to the cell surface. It is a type I integral membrane protein with a heavily glycosylated extracellular domain and binds to tissue- and organ-specific lectins or selectins. The protein is also a member of the scavenger receptor family. Scavenger receptors typically function to clear cellular debris, promote phagocytosis, and mediate the recruitment and activation of macrophages. Alternative splicing results in multiple transcripts encoding different isoforms.

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.

Helicobacter pylori, a Gram-negative, microaerophilic bacterium that populates in the stomach, predominantly at the antrum. Helicobacter pylori causes a chronic inflammation of the mucoid lining of stomach and is highly related to the growth of duodenal and gastric ulcers and stomach cancer. Over 50% of the world's population harbor H. pylori in their upper gastrointestinal tract, infection is more prevalent in developing countries. Thus far, no ideal target H. pylori antigen has been developed for the diagnostic purpose. 23 kDa H. pylori outer membrane protein was identified with a good sensitivity and coverage in the diagnosis of H. pylori infection.

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).