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Human coronavirus NL63 also known as HCoV-NL63 is a type of coronavirus that was identified in 2004. Among the associated diseases are mild to moderate upper respiratory tract infections, bronchiolitis, severe lower respiratory tract infection and croup. Coronavirus NL63 appears mainly in young children, the elderly and immunocompromised patients with acute respiratory illness. Coronavirus NL63 has a seasonal association in temperate climates. Coronavirus NL63 is not an emerging virus, but rather one that continually circulates the human population. Transmission of HCoV-NL63 is likely through droplet expulsion from the respiratory tract, which may be cottages when close personal contact occurs. Coronavirus NL63 is able to endure for up to7 days in respiratory secretions and remains infective at room temperature. Once the virus has entered the host it binds to cellular receptors using spike proteins, similar to those found in HIV-1. Coronavirus NL63 is able to use Angiotensin-converting enzyme 2 (ACE2) as an entry receptor to target cells. Since coronavirus NL63 is a positive single-stranded RNA virus, the processes of replication via transcription and translation can be carried out in the cytoplasm of the infected 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.

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 HDV genome exists as a negative sense, single-stranded, closed circular RNA. Because of a nucleotide sequence that is 70% self-complementary, the HDV genome forms a partially double stranded RNA structure that is described as rod-like. With a genome of approximately 1700 nucleotides, It has been proposed that HDV may have originated from a class of plant viruses called viroids. Evidence in support of this hypothesis stems from the fact that both HDV and viroids exist as single-stranded, closed circular RNAs that have rod-like structures. Likewise, both HDV and viroids contain RNA sequences that can assume catalytically active structures called ribozymes.

H1N1 is a subtype specie of Influenza A virus. H1N1 Influenza Virus has mutated into various strains such as the Spanish Flu strain, mild human flu 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.

West Nile virus (WNV) is a virus of the family Flaviviridae part of the Japanese encephalitis (JE) antigenic complex of viruses. Image reconstructions and cryoelectron microscopyreveal a 45-50 nm virion covered with a relatively smooth proteinsurface. This structure is similar to virus; both belong to the genus flavivirus within the family Flaviviridae. WNV is a positive-sense, single strand of RNA, it is between 11,000 and 12,000 nucleotides long which encode seven non-structural proteins and three structural proteins. The RNA strand is held within a nucleocapsid formed from 12 kDaprotein blocks; the capsid is contained within a host-derived membrane altered by two viral glycoproteins.

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).

H3N2 is a subtype of the influenza A virus. Its name derives from the forms of the two kinds of proteinson 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 H2N2and H3N2 strains contained genesfrom avian influenzaviruses.

H3N2 is a subtype of the influenza A virus. Its name derives from the forms of the two kinds of proteinson 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 H2N2and H3N2 strains contained genesfrom avian influenzaviruses.

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.

H1N1 is a subtype specie of Influenza A virus. H1N1 Influenza Virus has mutated into various strains such as the Spanish Flu strain, mild human flu strains, endemic pig strains, 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.

CMV belongs to the Betaherpesvirinae subfamily of Herpesviridae which includes herpes simplex virustypes 1 and 2, varicella-zoster virus, and Epstein-Barrvirus. The herpesviruses share a characteristic ability to remain latentover long periods. CMV is a double-stranded linear DNA virus with 162 hexagonal protein capsomeres surrounded by a lipid membrane. CMV has the largest genome of the herpes viruses, ranging from 230-240 kilobase pairs. Human CMV is composed of unique and inverted repeats that include the existence of 4 genome isomers caused by inversion of L-S genome components (class E). Replication may be divided into immediate early, delayed early, and late gene expression based on time of synthesis after infection. The DNA is replicated by rolling circles. In vitro, CMV replicates in human fibroblasts.

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.

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

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.

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).
HTLV-1 p24 is usually used for clinical diagnosis and forms both monomer and dimer on
SDS-PAGE gel but the majority of protein is a dimer.

Human norovirus is classified into two groups, group 1& group 2. Norwalk virus is the species which belongs to group 1 and was discovered in 1968 at Ohio. Norovirus is a familiar virus which causes human gastroenteritis with the following symptoms vomiting, diarrhea and sickness. CDC report revealed that there are 19-21 million Americans infected by Nororvirus annually with 800 deaths, 1 in 15 people with infection. Around the world, this virus affects about 267 million people and causes over 200,000 deaths each year; these losses are mostly in less developed countries and in the very young, elderly and immuno-suppressed population, though, most cases are self-limited with a full recovery within just a few days.Norovirus is extremely contagious and can spread from human to human through infected food, water or contaminated surfaces. The outbreaks usually occur from November-April, while the peak is in January. Norovirus is a positive sense RNA virus with 7.5 kb nucleotides, encoding a major structural protein VP1 with 50-55kDa. The full length of VP1 capsid comprises the internal N-terminal, Hinge, shell (S) and protruding (P) domains. P domain from 225 to 520 forms P1- P2-P1 structure. Moreover, P domain has a receptor binding region which recognizes human histo-blood group antigens (HBGAs). P domain expressed in bacteria can spontaneously form a P dime as well as a P particle aggregated by 12 P dimmers. P particle displays an increased binding activity to HBGAs higher than virus-like particle (VLP) formed by the full-length capsid. For norovirus vaccine development, we consider P domain as a good candidate.

H3N2 is a subtype of the influenza A virus. Its name derives from the forms of the two kinds of proteinson 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 is a subtype of the influenza A virus. Its name derives from the forms of the two kinds of proteinson 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 H2N2by antigenic shift, in which genes from multiple subtypes re-assorted to form a new virus. Both the H2N2and H3N2 strains contained genesfrom avian influenzaviruses.

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.

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.