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TBE is caused by tick-borne encephalitis virus (TBEV), a member of the family Flaviviridae.
A closely related virus in Far Eastern Eurasia, Russian spring-summer encephalitis virus (RSSEV).
The family Flaviviridae includes other tick-borne viruses are closely related to TBEV and RSSEV, such as Omsk hemorrhagic fever virus & Kyasanur Forest virus.
Louping ill virus is also a member of this family.

Forty-two antigenic domains were identified across the hepatitis A virus (HAV) polyprotein by using a set of 237 overlapping 20-mer synthetic peptides spanning the entire HAV polyprotein. Nineteen antigenic domains were found within the structural proteins, and 22 were found within the nonstructural proteins, with 1 domain spanning the junction of VP1 and P2A proteins. Five of these domains were considered immunodominant, as judged by both the breadth and the strength of their immunoreactivity. One domain is located within the VP2 protein at position 57-90 aa. A second domain, located at position 767-842 aa, contains the C-terminal part of the VP1 protein and the entire P2A protein. A third domain, located at position 1403-1456 aa, comprises the C-terminal part of the P2C protein and the N-terminal half of the P3A protein. The fourth domain, located at position 1500-1519 aa, includes almost the entire P3B, and the last domain, located at position 1719-1764 aa, contains the C-terminal region of the P3C protein and the N-terminal region of the P3D protein. Four of the five most immunoreactive domains are derived from small HAV proteins and/or encompass protein cleavage sites separating different HAV proteins.

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.

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).

Hepatitis A virus cellular receptor 1 (HAVCR1) is a membrane receptor for both human hepatitis A virus (HHAV) and TIMD4. HAVCR1 is a type I trans-membrane structural glycoprotein located in the renal proximal tubule epithelial cells. HAVCR1 protein may be involved in the control of asthma and allergic diseases. The reference genome represents an allele which retains a MTTVP amino acid segment that presents defense against atopy in HHAV seropositive individuals.

Caused by one of four closely related virus serotypes of the genus Flavivirus, family Flaviviridae, each serotype is sufficiently different that there is no cross-protection and epidemics caused by multiple serotypes (hyperendemicity) can occur. In cell culture experiments and mice Morpholino antisense oligos have shown specific activity against Dengue virus.

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.

Caused by one of four closely related virus serotypes of the genus Flavivirus, family Flaviviridae, each serotype is sufficiently different that there is no cross-protection and epidemics caused by multiple serotypes (hyperendemicity) can occur. In cell culture experiments and mice Morpholino antisense oligos have shown specific activity against Dengue virus.

H1N1 is a subtype specie of Influenza A virus. H1N1 Influenza Virus has mutated into various strains such as the Spanish Flustrain, mild humanflu strains, endemic pigstrains, and various strains found in birds. The Influenza A Virus is a globular particle about 100nm in diameter, sheathed in a lipid bilayer derived from the plasma membrane of its host. Studded in the lipid bilayer are two integral membrane proteins some 500 molecules of hemagglutinin ("H") and some 100 molecules of neuraminidase ("N"). Within the lipid bilayer are 3000 molecules of matrix protein and 8 pieces of RNA. Each of the 8 RNA molecules is associated with many copies of a nucleoprotein, several molecules of the three subunits of its RNA polymerase some "non-structural" protein molecules of uncertain function.

H1N1 is a sub specie of the virus Influenza A. H1N1 Influenza Virus has evolved into many strains for example: the Spanish Flustrain, mild humanflu strains, endemic pigstrains & different strains found in birds.
The Virusis is a globular particle is sheathed in a lipid bilayer derived from the plasma membrane of its host and is about 100nm in diameter. In the lipid bilayer are two integral membrane antigens some 500 proteins of hemagglutinin ("H") and some 100 proteins of neuraminidase ("N").

Based on sequence similarity to VEGF-A, a gene encoding a VEGF homologue has recently been discovered in the genome of Orf virus (OV) (Lyttle et al., 1994). Different isolates of Orf virus show significant amino acid sequence similarity to VEGF-A and described as a viral virulence factor that appears to be derived from captured host genes. All eight cysteine residues of the central cysteine knot motif characteristic of members of the VEGF family are conserved among other residues in the VEGF-E proteins (Dehio et al., 1999; Wise et al., 1999). Alignment of all mammalian VEGF sequences indicated that VEGF-E is distinct from the previously described VEGFs but most closely related to VEGF-A. Like VEGF-A, VEGF-E was found to bind with high affinity to VEGF receptor-2 (KDR) resulting in receptor autophosphorylation, whilst in contrast to VEGF-A, VEGF-E can not bind to VEGF receptor-1 (Flt-1). Furthermore VEGF-E can also not bind to VEGF receptor-3 (FLT-4). Therefore VEGF-E is a potent angiog

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.

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.

H3N2 is a subtype of the influenza A virus. Its name derives from the forms of the two kinds of proteins on the surface of its coat, hemagglutinin (H) and neuraminidase (N). H3N2 exchanges genes for internal proteins with other influenza subtypes. H3N2 has tended to dominate in prevalence over H1N1, H1N2, and influenza B. H3N2 strain descended from H2N2 by antigenic shift, in which genes from multiple subtypes re-assorted to form a new virus. Both the H2N2 and H3N2 strains contained genes from avian influenza viruses.
H3N2 viruses are able to infect mammals and birds. In pigs, humans, and birds, the virus has mutated into many strains. Hemagglutinin(HA) binds to sialic acid-containing receptors on the cell surface, generating the attachment of the virus particle to the cell. HA has a vital part in the determination of host range restriction and virulence and is in charge of the diffusion of the virus into the cell cytoplasm by facilitating the fusion of the membrane of the endocytos

Dengue fever is affected by 1 of 4 closely linked virus serotypes of the genus Flavivirus, family Flaviviridae. One might have dengue fever infected by the different serotype virus after the primary infection. Detection of particular antibodies to dengue viruses is used for the diagnosis in clinic. Recently, lateral flow rapid test products have become a most suitable and known method in the clinical diagnosis. Though, there is difficulty for manufacturers to have the dengue antigens with a whole coverage for Dengue IgG & IgM recognition for all 4 serotype infections as well as with colloid gold binding ability. 8 dengue antigens have been established for the lateral flow products which are well defined for their coverage of dengue IgG & IgM recognition. The researcher can select the products below based on their own specific application.

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.

Lassa virus, which is a member of the Arenaviridae virus family, causes acute viral hemorrhagic fever. It was first reported in 1969 in the town of Lassa, in Borno State, Nigeria. Natal multimammate mouse is the primary reservoir of Lassa virus, found in sub-Saharan Africa. The virus is transmitted by contact with the feces or urine of animals, contributing to its high rate of incidence. Lassa fever occurs generally in West Africa. Lassa fever results in 300,000 to 500,000 cases annually and causes about 5,000 deaths each year. Outbreaks of this disease have been observed in Nigeria, Liberia, Sierra Leone, Guinea, and the Central African Republic. Protein structure: Lassa virus genome is comprised of two single-stranded RNA molecules defined as small (S) and large (L). Two genes on the S segment encode the nucleoprotein (NP) and two envelope glycoproteins (GP1 and GP2); while, the L segment encodes the viral polymerase (L protein) and RING finger Z matrix protein. GP1 subunit serves a putative role in receptor binding, while the structure of GP2 subunit is consistent with viral transmembrane fusion proteins. NP is a virion protein which binds and protects the viral RNA.

Hepatitis A virus cellular receptor 1 (HAVCR1) is a membrane receptor for both human hepatitis A virus (HHAV) and TIMD4. HAVCR1 is a type I trans-membrane structural glycoprotein located in the renal proximal tubule epithelial cells. HAVCR1 protein may be involved in the control of asthma and allergic diseases. The reference genome represents an allele which retains a MTTVP amino acid segment that presents defense against atopy in HHAV seropositive individuals.

TBE is caused by tick-borne encephalitis virus (TBEV), a member of the family Flaviviridae.
A closely related virus in Far Eastern Eurasia, Russian spring-summer encephalitis virus (RSSEV).
The family Flaviviridae includes other tick-borne viruses are closely related to TBEV and RSSEV, such as Omsk hemorrhagic fever virus & Kyasanur Forest virus.
Louping ill virus is also a member of this family.

The human cytomegalovirus UL99-encoded pp28 is a myristylated phosphoprotein that is a constituent of the virion. The pp28 protein is positioned within the tegument of the virus particle, a protein structure that resides between the capsid and envelope. In the infected cell, pp28 is found in a cytoplasmic compartment derived from the Golgi apparatus, where the virus buds into vesicles to acquire its final membrane.

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. It is commonly referred to as the Australian Antigen.

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.