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Herpes simplex virus 1 and 2 (HSV-1 and HSV-2) are two strains of the Herpes virus family, Herpesviridae, which cause infections in humans. After an initial, or primary, infection, HSV establishes latency, during which the virus is present in the cell bodies of nerves which innervate the area of original outbreak.
Herpes infections are marked by painful, watery blisters in the skin or mucous membranes (such as the mouth or lips) or on the genitals. HSV is generally transmitted by direct contact of lips or genitals when the sores are present, or just before they appear (known as shedding).
Entry and replication of the HSV involves interactions of several viral glycoproteins with cell surface receptors or particles. Once bound to the HVEM, glycoprotein D changes its conformation and interacts with glycoproteins H and L, which form a complex. The packaging of the viral particles, which include the genome, core and the capsid, occur in the nucleus.
About Me“The master in the art of living makes little distinction between his work and his play, his labor and his leisure, his mind and his body, his information and his recreation, his love and his religion. Diagram illustrating the shapes and sizes of viruses of families that include animal, zoonotic and human pathogens. This is an ultra-thin section of the brain of a mouse infected with Bunyamwera virus (family Bunyaviridae, genus Bunyavirus) at six days post-infection when the mouse was moribund. Thin section and negative contrast electron microscopy of mouse tissue and purified virus. Thin section electron microscopy of infected cell culture and negative contrast electron microscopy of virus from cell culture. Ebola virus (image 1), diagnostic specimen from the first passage in Vero cells of a specimen from a human patienta€”this image is from the first isolation and visualization of Ebola virus, 1976. Ebola virus (image 1 colorized 1), diagnostic specimen from the first passage in Vero cells of a specimen from a human patienta€”this image is from the first isolation and visualization of Ebola virus, 1976. Ebola virus (image 1 colorized 2), diagnostic specimen from the first passage in Vero cells of a specimen from a human patienta€”this image is from the first isolation and visualization of Ebola virus, 1976. Ebola virions (image 2), diagnostic specimen from the first passage in Vero cells of a specimen from a human patient a€” this image is from the first isolation and visualization of Ebola virus, 1976.
Ebola virions (image 2 colorized 1), diagnostic specimen from the first passage in Vero cells of a specimen from a human patient a€” this image is from the first isolation and visualization of Ebola virus, 1976.
Ebola virions (image 2 colorized 2), diagnostic specimen from the first passage in Vero cells of a specimen from a human patient a€” this image is from the first isolation and visualization of Ebola virus, 1976. Ebola virus infected Vero cell, with virions budding from the plasma membrane at 2 days post infection. Ebola virus infected Vero cell, with viral nucleocapsid inclusion bodies in massed array in its cytoplasm at 2 days post infection. Thin section electron microscopy of infected mouse brain and negative contrast electron microscopy of purified virus.
During reactivation, virus is produced in the cell and transported outwardly via the nerve cell’s axon to the skin. The blisters resemble those seen in Chickenpox — an infection caused by a third member of the alpha-Herpesviridae subfamily, Varicella Zoster Virus (VZV), also known as Human Herpes Virus 3 (HHV-3).
In addition, herpes may be transmitted during childbirth, which can be fatal to the infant. The virus particle contains an envelope which, when bound to specific receptors on the cell surface, will fuse with the cell membrane.


Glycoprotein B interaction with the glycoprotein H and L complex allows the virus to enter into the cell. In the nucleus, cleavage of genome concatemers occurs and these are placed into pre-formed capsids.
This tab also contains the file for my 565 page eBook, with the same title, Foundations of Virology.
This tab also contains .pdf files of several of my old papers that are not available on the Internet. The virions are drawn to scale, but artistic license has been used in representing their structure.
Virions have accumulated in the normally narrow spaces between neurons as a result of budding from the intracytoplasmic (Golgi) membranes and exocytosis via membrane fusion. This is an ultra-thin section of the salivary gland of an Aedes triseriatus (Say) mosquito, 21 days after infection, showing large numbers of virions within the lumen of an upstream divereticulum of the salivary space. This image has been "borrowed" so often for various public uses that many people think that all Ebola virions look just like thisa€”indeed, in the film Outbreak every virion seen looked just like this. In this case, some of the filamentous virions are fused together, end-to-end, giving the appearance of a "bowl of spaghetti." Negatively stained virions. These inclusions may be dramatic in scale, beautiful in appearance, but this is "a terrible beauty" (Yeats). This is the same ultra-thin section of an infected cell in a cell culture as above, only colorized.
Negatively stained virions showing surface projections which contain the receptors by which the virus attaches to host respiratory tract epithelial cells. This is an ultra-thin section of the brain of a mouse infected with La Crosse virus (family Bunyaviridae, genus Bunyavirus) at six days post-infection when the mouse was moribund. Virions have been penetrated by the negative contrast stain; the fine surface projections and envelope (derived from Golgi membrane of the infected cell) that are characteristic of viruses like this (family Bunyaviridae, genus Bunyavirus) are clear, but viral nucleocapsids, which are very fine strands, are not. The ability of Herpes virus to establish latency leads to the chronic nature of Herpes infection; after the initial infection subsides, Herpes symptoms may periodically recur in the form of outbreaks of herpetic sores near the site of original infection. The immature immune system of the child is unable to defend against the virus and even if treated, infection can result in brain damage. The viral particle migrates to the nucleus, where the genome is replicated using enzymes from the host cell. The viral envelope is acquired from the nuclear envelope, more specifically the inner lamellae of the membrane. He simply pursues his vision of excellence at whatever he does, leaving others to decide whether he is working or playing. This is a 180Mb .pdf file, which takes about 2 minutes to download on my home computer, but it is the lowest resolution (smallest file) possible.
In some, the cross-sectional structure of capsid and envelope are shown, with a representation of the genome; with the very small virions, only their size and symmetry are depicted. Virions have accumulated in the space between cells as a result of budding from the surface membrane of infected cells.
In this infection large numbers of the 60 nm (nanometer) spherical virions crowd the salivary space, ready to be transmitted to the next vertebrate host when the mosquito seeks a blood meal. In fact, Ebola virions are extremely varied in appearance -- they are flexible filaments with a consistent diameter of 80 nm (nanometers), but they vary greatly in length (although their genome length is constant) and degree of twisting.
In fact, Ebola virions are extremely varied in appearance a€” they are flexible filaments with a consistent diameter of 80 nm (nanometers), but they vary greatly in length (although their genome length is constant) and degree of twisting.


Here, virion budding is occurring "perpendicular" to the plane of the plasma membrane -- in other instances budding has been seen to occur in "parallel" fashion, with the entire virion nucleocapsid first lying in contact with the inner face of the plasma membrane and budding occurring along its entire length.
Herpes simplex virus infection becomes latent, that is it becomes invisible after a fever blister episode, but the virus persists, in ganglia at the floor of the brain; when conditions are right the virus can re-emerge. Adenoviruses replicate in the nucleus of cells and as seen here they may reach extraordinary concentrations.
Rotaviruses replicate in the cytoplasm of cells, usually in association with granular inclusions ("virus factories") as shown here. Virions (100nm in diameter) are accumulating within intracytoplasmic (Golgi) vesicles as a result of budding. Transmission occurs while passing through the birth canal and the risk of infection is minimal if there are no symptoms or exposed blisters during delivery. Initially, glycoprotein C, on the surface of the viral envelope, targets and binds to a cell surface particle, heparan sulfate. Upon entering the cell, an ?-TIF protein also joins the viral particle and aids in immediate early Transcription.
The highest resolution file, suitable for printing, is also available, but I would have to send it via Dropbox. Classical negative contrast images of coronaviruses are really not the way they look when in their native state. In this infection very large numbers of the 60 nm (nanometer) spherical virions are produced quickly and as quickly the cells are destroyed.
When isometric particles are crowded together they form six-fold, three-dimensional arraysa€”when such arrays are sectioned one sees various planes of section because the pseudocrystalline array is not perfect. This is particularly likely during an outbreak, although individuals may shed virus between outbreaks. The first outbreak after exposure to HSV is commonly more severe than future outbreaks, as the body has not had a chance to produce antibodies; this first outbreak also carries the risk of developing meningitis. Although no cure is yet available, treatments exist which reduce the likelihood of viral shedding. Two major glycoproteins, glycoprotein B and glycoprotein D, also associate with the cell membrane. This enzyme shuts off protein synthesis in the host, degrades host mRNA, helps in viral replication, and regulates gene expression of viral proteins.
Here, the top micrograph represents the classical image and the bottom micrograph the way coronaviruses look in their native state. Native virions are actually so heavily covered with peoplmers that virions might not be recognized if only the classical images are in mind. Glycoprotein D binds specifically to the herpesvirus entry mediator receptor (HVEM), thus providing a strong, fixed attachment to the host cell.
While the viral genome immediately travels to the nucleus, the VHF protein remains in the cytoplasm. This is an ultra -- thin section of the small intestine of an infant mouse at two days post-infection when the mouse was moribund. Virions have accumulated upon the plasma membrane of this intestinal epithelial cell as a result of transport from sites of virion production in the endoplasmic reticulum and exocytosis via membrane fusion -- the virions then stick to the outer surface of the cell.



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