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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.

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.

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.

Simian immunodeficiency virus, SIV, is a retrovirusthat is found in strains, having the HIV-1and HIV-2specific strains that infect humans. SIV strains may cause an AIDS-like immune deficiency known as SAIDS (simian acquired immunodeficiency syndrome) if they cross species boundaries. HIV-2 is more similar to SIV strains than to HIV-1, suggesting for the first time the simian origin of HIV. HIV-2 is derived from the SIV strain found in sooty mangabeys whereas HIV-1, the predominant virus found in humans, is derived from SIV strains infecting chimpanzees.

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.

Zika virus (ZIKV) belongs to the family Flaviviridae and the genus Flavivirus, it is transmitted by daytime-active Aedes mosquitoes, such as A. aegypti and A. albopictus. The Zika virus is related to the dengue, yellow fever, Japanese encephalitis, and West Nile viruses. Much like the other flaviviruses, Zika virus is enveloped and icosahedral and has a nonsegmented, single-stranded, positive-sense RNA genome. Zika fever is an infection, which often causes no symptoms or only mild ones, like a mild form of dengue fever, and it is treated by rest. As of February 2016, there has been mounting evidence that Zika fever in pregnant women can cause abnormal brain development in their fetuses by mother-to-child transmission, which may result in miscarriage or microcephaly, however it is not yet known whether Zika virus causes microcephaly. Furthermore, a connection has been established with neurologic conditions in infected adults, including Guillain–Barre syndrome. Since the 1950s, Zika virus has been detected only within a narrow equatorial belt from Africa to Asia. Between the years 2013 and 2014, Zika virus has spread eastward across the Pacific Ocean to French Polynesia, New Caledonia, the Cook Islands, and Easter Island, and in 2015 to Mexico, Central America, the Caribbean, and South America, where the Zika outbreak has reached pandemic levels.

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.

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.

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.

Hepatitis C is one type of viral hepatitis - a liver disease - caused by the hepatitis C virus (HCV) which is usually passed through contact with infected blood but can also pass through sex with an infected person and from mother to baby during childbirth.
HCV core protein, NS3, NS4, and NS5 proteins of hepatitis C virus are all essential for detection of antibodies against HCV.

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.

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.

The SARS CoV-2 3CL protease (C30 Endopeptidase) derived from human SARS-CoV-2 is a C30-type cysteine protease situated in the NS3 segment. SARS CoV-2 3CL protease biological functionality is needed to process viral polyproteins to functional complete units. SARS CoV-2 3CL protease (main protease) is the core protease protein in CoV and corresponds to non-structural protein 5. SARS CoV-2 3CL cleaves the CoV polyprotein at 11 locations. SARS CoV-2 3CL protease has a cysteine-histidine catalytic dyad at its active site and cleaves a Gln–(Ser/Ala/Gly) peptide bond. SARS CoV-2 3CL protease at position P1 cleaves the bond between the glutamine and serine/alanine/glycine. SARS CoV-2 3CL protease is necessary in the processing of the CoV replicase polyprotein.

Chlamydia is a common term for infection with any bacterium belonging to the phylum Chlamydiae. This term derives from the name of the bacterial genus Chlamydiain the family Chlamydiaceae, order Chlamydiales, class and phylum Chlamydiae. There are two genera in Chlamydiaceae: Chlamydia and Chlamydophila. The genus Chlamydia includes three species: C. trachomatis, C. muridarum, and C. suis.

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.

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.

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.

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.

Rubella virus is an enveloped positive-strand RNA virus of the family TOGAVIRIDAE: Virions are composed of three structural proteins: a capsid and two membrane-spanning glycoproteins, E2 and E1. During virus assembly, the capsid interacts with genomic RNA to form nucleocapsids. The rubella virus (RV) structural proteins: capsid, E2, and E1 are synthesized as a polyprotein precursor. The signal peptide that initiates translocation of E2 into the lumen of the endoplasmic reticulum remains attached to the carboxy terminus of the capsid protein after cleavage by signal peptidase.

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.

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.

HCV is a small 50nm, enveloped, single-stranded, positive sense RNA virus 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).