School of Veterinary Medicine
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Diagram illustrating the shapes and sizes of viruses of families that include animal, zoonotic and human pathogens. The virions are drawn to scale, but artistic license has been used in representing their structure. 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. From F. A. Murphy, School of Veterinary Medicine, University of California, Davis.
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Bunyamwera virus infection in mouse brain. 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. 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. Some virions are still located within the lumen of Golgi vesicles. Magnification approximately x40,000. Micrograph from F. A. Murphy, School of Veterinary Medicine, University of California, Davis. |
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Coronavirus. Mouse hepatitis virus, strain MHV-S/CDC. This virus, formerly called "lethal intestinal virus of infant mice" (LIVIM), is the etiologic agent of a lethal enteritis, the most important disease of infant laboratory mice [see Hierholzer JC, Broderson JR, Murphy FA. New strain of mouse hepatitis virus as the cause of lethal enteritis in infant mice. Infect Immun. 1979 May;24(2):508-22.]. 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. Magnification approximately x40,000. Micrograph from F. A. Murphy, School of Veterinary Medicine, University of California, Davis. |
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Coronavirus. Top, human coronavirus 229E; bottom, mouse hepatitis virus, strain MHV-S/CDC. Negative contrast electron microscopy. Classical negative contrast images of coronaviruses are really not the way they look when in their native state. The peplomers (spikes) fall off so easily that most images seen in atlases and textbooks are really partly "bald." Native virions are actually so heavily covered with peoplmers that virions might not be recognized if only the classical images are in mind. Here, the top micrograph represents the classical image and the bottom micrograph the way coronaviruses look in their native state. Magnification approximately x60,000. Micrograph from F. A. Murphy, School of Veterinary Medicine, University of California, Davis. |
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Eastern equine encephalitis virus. This is an ultra-thin section of a Vero cell culture infected for 24 hours. Virions have accumulated in the space between cells as a result of budding from the surface membrane of infected cells. In this infection very large numbers of the 60 nm (nanometer) spherical virions are produced quickly and as quickly the cells are destroyed. Magnification approximately x70,000. Micrograph from F. A. Murphy, School of Veterinary Medicine, University of California, Davis. |
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Ebola virus (image 1), diagnostic specimen from the first passage in Vero cells of a specimen from a human patient—this image is from the first isolation and visualization of Ebola virus, 1976. This image has been "borrowed" so often for various public uses that many people think that all Ebola virions look just like this—indeed, in the film Outbreak every virion seen looked just like this. 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. Negatively stained virions. Magnification: approximately x60,000. Micrograph from F. A. Murphy, School of Veterinary Medicine, University of California, Davis. |
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Ebola virions (image 2), diagnostic specimen from the first passage in Vero cells of a specimen from a human patient — this image is from the first isolation and visualization of Ebola virus, 1976. 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. Magnification: approximately x40,000. Micrograph from F. A. Murphy, School of Veterinary Medicine, University of California, Davis. |
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Herpes simplex virus, the causative agent of fever blisters. Thin section of virions as they leave the nucleus of an infected cell. 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. Magnification approximately x40,000. Micrograph from F. A. Murphy, School of Veterinary Medicine, University of California, Davis. |
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Human adenovirus 5. This is an ultra-thin section of an infected cell in a culture. Adenoviruses replicate in the nucleus of cells and as seen here they may reach extraordinary concentrations. When isometric particles are crowded together they form six-fold, three-dimensional arrays—when such arrays are sectioned one sees various planes of section because the pseudocrystalline array is not perfect. Magnification: approximately x80,000. Micrograph from F. A. Murphy, School of Veterinary Medicine, University of California, Davis. |
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Influenza virus, A/Hong Kong/1/68, the causative agent of the 1968 global epidemic. Negatively stained virions showing surface projections which contain the receptors by which the virus attaches to host respiratory tract epithelial cells. Magnification: approximately x70,000. Micrograph from F. A. Murphy, School of Veterinary Medicine, University of California, Davis. |
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LaCrosse virus infection in mouse brain. 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 (100nm in diameter) are accumulating within intracytoplasmic (Golgi) vesicles as a result of budding. Magnification approximately x40,000 (composite). Micrograph from F. A. Murphy, School of Veterinary Medicine, University of California, Davis. |
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La Crosse virus, purified from an infected Vero cell culture. 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. Magnification: approximately x80,000. Micrograph from F. A. Murphy, School of Veterinary Medicine, University of California, Davis. |
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Lassa virus, the causative agent of Lassa fever, an important hemorrhagic disease of West Africa. Thin section of virions in a space between cells—Lassa virus buds from the surface membrane of cells where it is then free to invade other nearby cells and is free to enter the bloodstream. Magnification approximately x55,000. Micrograph from F. A. Murphy, School of Veterinary Medicine, University of California, Davis. |
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Marburg virus in the liver of an experimentally infected monkey. Virions bud off the surface membrane of liver cells and accumulate in the narrow spaces between cells. This infection is extremely destructive—shortly after this phase of infection the liver cells are destroyed. The uniformly cylindrical virions are sectioned in various planes—some are seen in longitudinal-section, some in cross-section, some in between. Magnification approximately x40,000. Micrograph from F. A. Murphy, School of Veterinary Medicine, University of California, Davis. |
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Poliovirus 1. Poliovirus was purified and prepared for negative contrast electron microscopy. This image shows uniform 29 nm (nanometer) virions arranged in pseudocrystalline array. It is just that isometric particles often fit together in six-fold, two-dimensional array, as had occurred here on the background support film. Their array is like the arrangement that peas take when shaken in a pan. Magnification approximately x200,000. Micrograph from J. Esposito, Centers for Disease Control and Prevention, Atlanta, Georgia, and F. A. Murphy, School of Veterinary Medicine, University of California, Davis. |
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Rabies infection in the brain. This micrograph covers just part of the cytoplasm of an infected neuron. Two hallmarks of rabies virus infection are seen — there is minimal damage seen to the structure of infected neurons even though the extent of the infection is dramatic, and large numbers of bullet-shaped virions accumulate as a result of budding upon the endoplasmic reticulum membranes of these cells. Magnification approximately x25,000. Micrograph from F. A. Murphy, School of Veterinary Medicine, University of California, Davis. |
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Rabies virus in the salivary gland of a rabid fox. In this image there are salivary gland cells (cells that make mucous saliva) on both edges. The salivary space in the center, which leads downstream to the salivary duct, is filled with bullet-shaped virions. The virions are sectioned in various planes so they do not all look like bullets. Magnification: approximately x40,000. Micrograph from F. A. Murphy, School of Veterinary Medicine, University of California, Davis. |
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Rabies virus, purified from an infected cell culture. Negatively stained virions: note their characteristic "bullet shape." Magnification approximately x70,000. Micrograph from F. A. Murphy, School of Veterinary Medicine, University of California, Davis. |
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Rift Valley fever virus. In this micrograph virions are seen budding into membrane vesicles (Golgi vesicles) in the cytoplasm of a liver cell (hepatocyte) of an infected rat. The 100 nm (nanometer) virions then make their way to the cell surface and are released. This virus replicates to very high concentrations very quickly and causes very rapid damage to the liver and other organs. The virus is mosquito-borne and in nature affects sheep, cattle, wild mammals and humans. The virus was the cause of one of the most explosive epidemics ever seen when it appeared in 1977 in Egypt. A recent epidemic in Saudi Arabia and Yemen represents the first time that the virus has appeared outside Africa. This virus, because it can infect many different vertebrates and many different mosquitoes, presents perhaps the greatest potential threat posed by any virus. Magnification approximately x30,000. Micrograph from T. W. Geisbert, U. S. Army Medical Research Institute of Infectious Diseases, Ft. Detrick, Maryland. |
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Scrapie: Lesions in the gray matter of the brain of a sheep with scrapie: (A) typical spongiform change in neurons; (B) spongiform change and astrocytic hypertrophy and hyperplasia. A, hematoxylin and eosin stain; B, glial fibrillar acid protein (GFAP) stain. Magnification x500. [Courtesy of Dr. R. Higgins, School of Veterinary Medicine, University of California, Davis] |
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Sin Nombre virus, the cause of Hantavirus pulmonary syndrome in southwestern US. This virus was discovered in 1993 when there was a cluster of cases in one place at one time. Magnification approximately. x45,000. Micrograph from C. Goldsmith, Division of Viral and Rickettsial Diseases, Centers for Disease Control and Prevention. |
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Smallpox virus, growing in the cytoplasm of an infected cell. Thin section of infected chick embryo cell. Mature virions are brick-shaped, but here immature forms are also visible. Smallpox virus was globally eradicated in 1977 by an international vaccination campaign, one of the greatest achievements in history. Magnification approximately x25,000. Micrograph from F. A. Murphy, School of Veterinary Medicine, University of California, Davis. |
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Smallpox virus, single virion, as seen by negative stain electron microscopy. The brick-shaped virion is covered with what looks like filaments (although in reality this outer layer is not really like a ball of string). This virion is from a human skin lesion, from a diagnostic specimen that came to the Centers for Disease Control in 1966 as part of the WHO Global Smallpox Eradication Program. Magnification about x150,000. Micrograph from F. A. Murphy, School of Veterinary Medicine, University of California, Davis. |
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St. Louis encephalitis virus in the salivary gland of a Culex pipiens mosquito 26 days after infection. Massive amounts of virus, some in paracrystalline array, may be seen within the salivary space - transmission to the next vertebrate host occurs when the mosquito injects its saliva (which contains anticoagulants) when taking a blood meal. Magnification approximately x30,000. Micrograph from F. A. Murphy, School of Veterinary Medicine, University of California, Davis. |
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Vesicular stomatitis virus, purified from an infected cell culture. This is an important pathogenic virus of cattle, causing fever and vesicles in the mouth and on the feet. Negatively stained virions: note that they are clearly "bullet shaped" just like rabies virus. Magnification approximately x40,000. Micrograph from F. A. Murphy, School of Veterinary Medicine, University of California, Davis. |
