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Hepatitis E virus (HEV), the major etiologic agent of enterically transmitted non-A, non-B hepatitis worldwide, is a spherical, non-enveloped, single stranded RNA virus that is approximately 32 to 34 nm in diameter. HEV belongs to a genus of HEV-like viruses (unassigned genus). HEV has a single-stranded polyadenylated RNA genome of approximately 8 kb. Based on its physicochemical properties it is presumed to be a calici-like virus.

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.

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.

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.

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

A main factor of pathogenic Yersinia enterocolitica strains is a plasmid-encoded type 3 secretion system, through which Yersinia outer proteins (Yops) are injected into the host cell. Yop E is a GTPase activation protein which controls pore formation by activating small Rho GTPase, causing inhibition of actin polymerization.

Insulin decreases blood glucose concentration. it increases cell permeability to monosaccharides, amino acids and fatty acids. it accelerates glycolysis, the pentose phosphate cycle, and glycogen synthesis in liver.

Anaplasma p44 which belongs to the outer membrane antigen superfamily (OMP1/Msp2/p44), is a serodiagnostic antigen for HGA. Anaplasma p44 allows the bacterium to adhere to the host cell and prevents host immune surveillance.

Hepatitis B is one of a few known non-retroviralviruses which employ reverse transcriptionas a part of its replication process. (HIV, a completely unrelated virus, also uses reverse transcription, but it is a retrovirus.) HBV invades the cell by binding to surface receptor and become internalized. The viral core particles then migrate to the hepatocyte nucleus and the partially double-stranded, relaxed circular genomes (RC-DNA) are repaired to form a covalently closed circular DNA (cccDNA), which is the template for viral genomic and sub-genomic RNAs by cellular RNA polymerase II. Of these, the pregenomic RNA (pgRNA is selectively packaged into progeny capsids and is then reverse-transcribed into new RC-DNA. The core can either bud into the endoplasmic reticulum to be enveloped or exported from the cell or recycled back into the genome for conversion to cccDNA.

EPH Receptor B2 (EPHB2) is a part of the transmembrane Eph receptor tyrosine kinase family (RTKs) which binds proteins of the Ephrin family on adjacent cells. The interaction leads to contact-dependent bidirectional signaling into neighboring cells. Hippocampal neurons can release vesicles containing full length EPHB2, and these are taken up by neighboring glial cells. EPHB2 takes part in the guidance of commissural axons through the embryonic midline and regulates dendritic spines development and maturation and stimulates the formation of excitatory synapses.

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.

HBsAg is the surface antigen of the Hepatitis-B-Virus (HBV). The capsid of a virus has different surface proteins from the rest of the virus. The antigen is a protein that binds specifically on one of these surface proteins and is commonly referred to as the Australian Antigen. HBsAg is an essential parameter to diagnose hepatitis B disease in the clinic and to monitor antiviral treatment.

Ras-related protein Ral-A (RALA) is a member of the small GTPase superfamily, Ras family of proteins. RALA mediates a distinct downstream signaling pathway from Ras which facilitates cellular transformation. Furthermore, RALA is thought to be involved in various signaling cascades, including regulation of the cytoskeleton, vesicle trafficking, and endocytosis.

Influenza-B virus is a genus in the virusfamily Orthomyxoviridae. The only species in this genus is called "Influenza B virus". Influenza B virus only infects humansand seals. This limited host range is apparently in contrast with those caused by the similar Influenza virus Aas 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 capsidis enveloped while its virionconsists of a matrix protein + envelope + nucleoprotein complex + nucleocapsid, and a polymerasecomplex. 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 nucleotideslong 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.

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 probably 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.

Hepatitis E virus (HEV), the major etiologic agent of enterically transmitted non-A, non-B hepatitis worldwide, is a spherical, non-enveloped, single stranded RNA virus that is approximately 32 to 34 nm in diameter. HEV belongs to a genus of HEV-like viruses (unassigned genus). HEV has a single-stranded polyadenylated RNA genome of approximately 8 kb. Based on its physicochemical properties it is presumed to be a calici-like virus.

Shiga-like toxin (verotoxin) is a toxin produced by some strains of Escherichia coli. Shiga-like toxin is named for its similarity to the AB5-type Shiga toxin produced by the bacteria Shigella dysenteriae. There are two known types-SLT1 and SLT2. The Shiga-like toxin is linked with hemolytic-uremic syndrome. Shiga-like toxin requires highly specific receptors on the cells' surface in order to attach and enter the cell. Species such as cattle, swine, and deer which do not carry these receptors may harbor toxigenic bacteria without any ill effect, dropping them in their feces, from where they may be distributed to humans. Shiga Like Toxin-1 Subunit B has nontoxic action, it is the functional region which binds to the receptor. The Shiga Like Toxin-1 Subunit B can be useful in vaccine study, antibody test and other functional research.

Entry of HSV into the host cell involves interactions of several viral glycoproteins with cell surface receptors. The virus particle is covered by an envelope which, when bound to specific receptors on the cell surface, will fuse with the cell membrane and create an opening, or pore, through which the virus enters the host cell. The sequential stages of HSV entry are analagous to those of other viruses. At first, complementary receptors on the virus and cell surface bring the two membranes into proximity. In an intermediate state, the two membranes begin to merge, forming a hemifusion state. Finally, a stable entry pore is formed through which the viral envelope contents are introduced to the host cell.

Entry of HSV into the host cell involves interactions of several viral glycoproteins with cell surface receptors. The virus particle is covered by an envelope which, when bound to specific receptors on the cell surface, will fuse with the cell membrane and create an opening, or pore, through which the virus enters the host cell. The sequential stages of HSV entry are analagous to those of other viruses. At first, complementary receptors on the virus and cell surface bring the two membranes into proximity. In an intermediate state, the two membranes begin to merge, forming a hemifusion state. Finally, a stable entry pore is formed through which the viral envelope contents are introduced to the host cell.

Plasmodium falciparum is a protozoan parasite, one of the species of Plasmodium that cause malaria. Malaria parasites are members of the Apicomplexa. Apicomplexa are characterized by a set of organelles found in some stages of the parasite's life cycle. These organelles, collectively known as apical organelles because of their localization at one end of the parasite, are involved in interactions between the parasite and host. In particular, the apical organelles have been implicated in the process of host cell invasion. In the case of Plasmodium, three distinct invasive forms have been identified: sporozoite, merozoite, and ookinete.

Receptors across the cell membrane interact with some viral glycoproteins therefor enabling HSV to enter the host cell. The HSV enter through pores created by the binding of particular receptors across the cell membrane with the virus's coating envelope, following by a fusion of the HSV and the host cell. HSV enters the host cell through the same mechanism and stages as other viruses do. Initially, matching receptors across the virus's envelope and host cell's membrane interacts and bring the two together. During the transitional stage, begins fusion between the host cell and virus (hemifusion state). The closing stage happens when a steady pore was made; through these pores the virus's particles enter the cell.

Darbepoetin is a mutant recombinant human EPO-Alpha protein re-engineered, containing 5 amino acid changes at N30, T32, V87, N88, T90. Darbepoetin exhibits longer half-life stimulating red blood cell production than Erythropoietin. Darbepoetin maintains hemoglobin more effectively compared to EPO-Alpha.