Trevor Williams, Cristina Virto, Rosa Murillo, and Primitivo Caballero
31 Jan 2024
Schematic representation of baculovirus structure and infection cycle. (A) Nucleopolyhedrovirus occlusion bodies (OBs) are polyhedral proteinaceous bodies, mainly comprised of crystalline polyhedrin that surrounds occlusion derived virions (ODVs). The ODVs contain either a single nucleocapsid (single type) or between one and several nucleocapsids (multiple type) in each ODV. For granuloviruses the OB is granule-shaped and contains a single ODV with a single nucleocapsid surrounded by the crystalline protein granulin. In all cases each nucleocapsid contains a single viral genome. (B) Sequential steps of nucleopolyhedrovirus transmission and replication. During primary infection, (A) OBs are ingested during feeding on contaminated foliage. (B) OBs are solubilized in the insect midgut and release ODVs that pass through the peritrophic membrane (C) and fuse with the microvilli of midgut epithelial cells (D). Nucleocapsids travel to the nucleus where they release the viral genome to initiate replication. (E) Virus replication occurs in virogenic stroma. Progeny nucleocapsids assemble and bud through the basal membrane (F) during which they acquire an envelope containing GP64 or F fusion protein present in the virus-modified cell membrane. During the secondary phase of infection these budded virions (BVs) disperse in the hemolymph or along the cells of the insect traqueal system (traqueoblasts) to spread the infection to the cells of other tissues in the insect. (G) BVs enter cells by endocytosis and replicate in the nucleus. Newly assembled nucleocapsids (H) may bud out of the cell or may be enveloped to form ODVs that are occluded into OBs (I). At the end of the infectious cycle OBs accumulate in the nucleus (J). Upon death the larvae typically hang from the uppermost leaves of the host plant (K), the larval tegument ruptures and releases OBs that contaminate foliage for further cycles of horizontal transmission.[1]
Schematic representation of baculovirus structure and infection cycle. (A) Nucleopolyhedrovirus occlusion bodies (OBs) are polyhedral proteinaceous bodies, mainly comprised of crystalline polyhedrin that surrounds occlusion derived virions (ODVs). The ODVs contain either a single nucleocapsid (single type) or between one and several nucleocapsids (multiple type) in each ODV. For granuloviruses the OB is granule-shaped and contains a single ODV with a single nucleocapsid surrounded by the crystalline protein granulin. In all cases each nucleocapsid contains a single viral genome. (B) Sequential steps of nucleopolyhedrovirus transmission and replication. During primary infection, (A) OBs are ingested during feeding on contaminated foliage. (B) OBs are solubilized in the insect midgut and release ODVs that pass through the peritrophic membrane (C) and fuse with the microvilli of midgut epithelial cells (D). Nucleocapsids travel to the nucleus where they release the viral genome to initiate replication. (E) Virus replication occurs in virogenic stroma. Progeny nucleocapsids assemble and bud through the basal membrane (F) during which they acquire an envelope containing GP64 or F fusion protein present in the virus-modified cell membrane. During the secondary phase of infection these budded virions (BVs) disperse in the hemolymph or along the cells of the insect traqueal system (traqueoblasts) to spread the infection to the cells of other tissues in the insect. (G) BVs enter cells by endocytosis and replicate in the nucleus. Newly assembled nucleocapsids (H) may bud out of the cell or may be enveloped to form ODVs that are occluded into OBs (I). At the end of the infectious cycle OBs accumulate in the nucleus (J). Upon death the larvae typically hang from the uppermost leaves of the host plant (K), the larval tegument ruptures and releases OBs that contaminate foliage for further cycles of horizontal transmission.[1]
Trevor Williams, Cristina Virto, Rosa Murillo, and Primitivo Caballero
This highly-magnified, negative-stain transmission electron micrographic (TEM) image, reveals a M-type, or mulberry-type monkeypox virus particle, which was found in human vesicular fluid. The surface of M-type virions are covered with short, whorled filaments, while C-type, or capsular-type virions, are penetrated by stain, and therefore, will present as a sharply defined, dense core, surrounded by several laminated zones of differing densities.
This highly-magnified, negative-stain transmission electron micrographic (TEM) image, reveals a M-type, or mulberry-type monkeypox virus particle, which was found in human vesicular fluid. The surface of M-type virions are covered with short, whorled filaments, while C-type, or capsular-type virions, are penetrated by stain, and therefore, will present as a sharply defined, dense core, surrounded by several laminated zones of differing densities.
3D print of Norwalk virus, a type of norovirus. Noroviruses are the most common cause of acute gastroenteritis (infection of the stomach and intestines) in the United States.
3D print of Norwalk virus, a type of norovirus. Noroviruses are the most common cause of acute gastroenteritis (infection of the stomach and intestines) in the United States.
Cross section through measles virus. The virus is enveloped by a lipid membrane (light magenta) studded with many hemagglutinin and fusion proteins (outermost proteins in blue), which together bind to human cells and enter them. The viral genome is a strand of RNA (yellow) protected by nucleoproteins (green). RNA-dependent RNA polymerase (bright magenta) copies the RNA once the virus infects a cell, assisted by the largely-disordered phosphoprotein (purple strands connecting the polymerase to the nucleoprotein). Matrix protein (turquoise) helps the virus bud from infected cells. Several human proteins, such as actin and integrins, are also caught in the budding virus (shown in purple). This painting was created for the Molecule of the Month on Measles Virus Proteins.
Cross section through measles virus. The virus is enveloped by a lipid membrane (light magenta) studded with many hemagglutinin and fusion proteins (outermost proteins in blue), which together bind to human cells and enter them. The viral genome is a strand of RNA (yellow) protected by nucleoproteins (green). RNA-dependent RNA polymerase (bright magenta) copies the RNA once the virus infects a cell, assisted by the largely-disordered phosphoprotein (purple strands connecting the polymerase to the nucleoprotein). Matrix protein (turquoise) helps the virus bud from infected cells. Several human proteins, such as actin and integrins, are also caught in the budding virus (shown in purple). This painting was created for the Molecule of the Month on Measles Virus Proteins.
Myxomatosis virus is transmitted through vectors such as fleas, mosquitoes, and direct contact between infected and healthy rabbits. It causes swelling, lesions, and fluid-filled nodules on the skin, particularly around the head, face, and genital areas. Affected rabbits may also exhibit fever, lethargy, loss of appetite, and respiratory distress. In severe cases, myxomatosis can be fatal, with mortality rates reaching up to 99%.
Myxomatosis virus is transmitted through vectors such as fleas, mosquitoes, and direct contact between infected and healthy rabbits. It causes swelling, lesions, and fluid-filled nodules on the skin, particularly around the head, face, and genital areas. Affected rabbits may also exhibit fever, lethargy, loss of appetite, and respiratory distress. In severe cases, myxomatosis can be fatal, with mortality rates reaching up to 99%.
CDC/ C. Goldsmith, P. Feorino, E. L. Palmer, W. R. McManus, Public Health Image Library (PHIL)
08 Feb 2024
Scanning electron micrograph of human immunodeficiency virus-1 (HIV-1) budding from cultured lymphocyte. Multiple round bumps on cell surface represent sites of assembly and budding of virions.
Scanning electron micrograph of human immunodeficiency virus-1 (HIV-1) budding from cultured lymphocyte. Multiple round bumps on cell surface represent sites of assembly and budding of virions.
CDC/ C. Goldsmith, P. Feorino, E. L. Palmer, W. R. McManus, Public Health Image Library (PHIL)
Photograph of viral plaque formation to count viral titer (plaque assay). Vero cells, which grew confluently on the bottom of the 24-well plastic plate (1.5 cm diameter each), were infected with serially diluted solutions containing herpes simplex virus, and then cultured over night to make viral plaque. The number of plaques indicates the number of the infectious virus (= viral titer, as plaque forming unit). Photo: 4-fold dilution series from top-left to bottom-right. Living cells were stained with crystal violet. The viral plaques, each was from one virion, remained transparent.
Photograph of viral plaque formation to count viral titer (plaque assay). Vero cells, which grew confluently on the bottom of the 24-well plastic plate (1.5 cm diameter each), were infected with serially diluted solutions containing herpes simplex virus, and then cultured over night to make viral plaque. The number of plaques indicates the number of the infectious virus (= viral titer, as plaque forming unit). Photo: 4-fold dilution series from top-left to bottom-right. Living cells were stained with crystal violet. The viral plaques, each was from one virion, remained transparent.
Wikimedia Commons, Raj K. Singh, Kuldeep Dhama, Kumaragurubaran Karthik, Rekha Khandia, Ashok Munjal, Sandip K. Khurana, Sandip Chakraborty, Yashpal S. Malik, Nitin Virmani, Rajendra Singh, Bhupendra N. Tripathi, Muhammad Munir, and Johannes H. van der Ko
25 Jan 2024
Equine Influenza Virus (EIV) damages the upper and lower respiratory tract's ciliated epithelial cells thereby causes inability to clear foreign substances. Spike glycoprotein HA fastens to the receptors present on the respiratory epithelial cells and it enters the cells by endocytosis. After endocytosis, EIV undergoes fusion and uncoating. Opening of M2 channel leads to proton entry and subsequent release of viral RNA followed by synthesis of viral structures leading to assembly of EIV. EIV is released from the infected cells by the process of budding [1].
Equine Influenza Virus (EIV) damages the upper and lower respiratory tract's ciliated epithelial cells thereby causes inability to clear foreign substances. Spike glycoprotein HA fastens to the receptors present on the respiratory epithelial cells and it enters the cells by endocytosis. After endocytosis, EIV undergoes fusion and uncoating. Opening of M2 channel leads to proton entry and subsequent release of viral RNA followed by synthesis of viral structures leading to assembly of EIV. EIV is released from the infected cells by the process of budding [1].
Wikimedia Commons, Raj K. Singh, Kuldeep Dhama, Kumaragurubaran Karthik, Rekha Khandia, Ashok Munjal, Sandip K. Khurana, Sandip Chakraborty, Yashpal S. Malik, Nitin Virmani, Rajendra Singh, Bhupendra N. Tripathi, Muhammad Munir, and Johannes H. van der Ko
Wikimedia Commons, ViralZone, SIB Swiss Institute of Bioinformatics
01 Feb 2024
Coltivirus is a genus of viruses that belong to the family Reoviridae. Coltiviruses are non-enveloped arboviruses that have a double-stranded RNA genome and are transmitted by ticks or mosquitoes. They infect rodents and cause Colorado tick fever in humans.
Coltivirus is a genus of viruses that belong to the family Reoviridae. Coltiviruses are non-enveloped arboviruses that have a double-stranded RNA genome and are transmitted by ticks or mosquitoes. They infect rodents and cause Colorado tick fever in humans.
Wikimedia Commons, ViralZone, SIB Swiss Institute of Bioinformatics
ViralZone, SIB Swiss Institute of Bioinformatics, Wikimedia Commons
08 Feb 2024
Schematic drawings of Iridovirus virions. Polyhedral virions 185 nm in diameter. The capsid displays an icosahedral symmetry T=147, with an internal lipid membrane. Virions are either externally enveloped or not depending whether they budded from the cell membrane, or were arranged in paracrystaline array in the host cell cytoplasm and were released by lysis.
Schematic drawings of Iridovirus virions. Polyhedral virions 185 nm in diameter. The capsid displays an icosahedral symmetry T=147, with an internal lipid membrane. Virions are either externally enveloped or not depending whether they budded from the cell membrane, or were arranged in paracrystaline array in the host cell cytoplasm and were released by lysis.
ViralZone, SIB Swiss Institute of Bioinformatics, Wikimedia Commons
Parietaria mottle virus (PMoV) primarily infects species within the Parietaria genus, including Parietaria judaica, which is a common weed found in urban areas, along roadsides, and in disturbed habitats. This plant is characterized by its small, greenish flowers and lance-shaped leaves. Infected plants typically exhibit symptoms such as mottling or discoloration of the leaves, which appear as irregular patches of light and dark green. In addition to mottling, infected plants may also show stunting, leaf distortion, and reduced vigor, although symptoms can vary depending on factors such as the strain of the virus and environmental conditions.
Parietaria mottle virus (PMoV) primarily infects species within the Parietaria genus, including Parietaria judaica, which is a common weed found in urban areas, along roadsides, and in disturbed habitats. This plant is characterized by its small, greenish flowers and lance-shaped leaves. Infected plants typically exhibit symptoms such as mottling or discoloration of the leaves, which appear as irregular patches of light and dark green. In addition to mottling, infected plants may also show stunting, leaf distortion, and reduced vigor, although symptoms can vary depending on factors such as the strain of the virus and environmental conditions.
Classical strain improvement for antibiotic production in fungi. (a) The wild type (WT) strain is subjected to random mutagenesis at a sub-lethal level. Surviving clones carry random mutations, some of which may result in increased production of the targeted antibiotic. (b) The obtained clones are then screened (as a result of fermentation, plate tests or other methods) for the level of antibiotic production. (с) The level of antibiotic production in most of the clones obtained as a result of mutagenesis is less than or equal to that of the initial WT strain. However, clones are found in which antibiotic production is increased; they are selected. (d) The result is an improved strain that, after the first round of mutagenesis, with a higher yield than the WT strain. This strain is then used for a new round of random mutagenesis and selection [1].
Classical strain improvement for antibiotic production in fungi. (a) The wild type (WT) strain is subjected to random mutagenesis at a sub-lethal level. Surviving clones carry random mutations, some of which may result in increased production of the targeted antibiotic. (b) The obtained clones are then screened (as a result of fermentation, plate tests or other methods) for the level of antibiotic production. (с) The level of antibiotic production in most of the clones obtained as a result of mutagenesis is less than or equal to that of the initial WT strain. However, clones are found in which antibiotic production is increased; they are selected. (d) The result is an improved strain that, after the first round of mutagenesis, with a higher yield than the WT strain. This strain is then used for a new round of random mutagenesis and selection [1].
Psittacine beak and feather disease (PBFD), also referred to as psittacine circovirus (PCV) or Psittacine Circoviral Disease (PCD), stands as the prevalent and extremely contagious viral illness affecting parrots.
Psittacine beak and feather disease (PBFD), also referred to as psittacine circovirus (PCV) or Psittacine Circoviral Disease (PCD), stands as the prevalent and extremely contagious viral illness affecting parrots.
Created by CDC microbiologist Frederick A. Murphy, this colorized transmission electron micrograph (TEM) revealed some of the ultrastructural morphology displayed by an Ebola virus virion. See PHIL 1181 for a black and white version of this image. Ebola hemorrhagic fever (Ebola HF) is a severe, often-fatal disease in humans and nonhuman primates (monkeys, gorillas, and chimpanzees) that has appeared sporadically since its initial recognition in 1976. The disease is caused by infection with Ebola virus, named after a river in the Democratic Republic of the Congo (formerly Zaire) in Africa, where it was first recognized. The virus is one of two members of a family of RNA viruses called the Filoviridae. There are four identified subtypes of Ebola virus. Three of the four have caused disease in humans: Ebola-Zaire, Ebola-Sudan, and Ebola-Ivory Coast. The fourth, Ebola-Reston, has caused disease in nonhuman primates, but not in humans.
Created by CDC microbiologist Frederick A. Murphy, this colorized transmission electron micrograph (TEM) revealed some of the ultrastructural morphology displayed by an Ebola virus virion. See PHIL 1181 for a black and white version of this image. Ebola hemorrhagic fever (Ebola HF) is a severe, often-fatal disease in humans and nonhuman primates (monkeys, gorillas, and chimpanzees) that has appeared sporadically since its initial recognition in 1976. The disease is caused by infection with Ebola virus, named after a river in the Democratic Republic of the Congo (formerly Zaire) in Africa, where it was first recognized. The virus is one of two members of a family of RNA viruses called the Filoviridae. There are four identified subtypes of Ebola virus. Three of the four have caused disease in humans: Ebola-Zaire, Ebola-Sudan, and Ebola-Ivory Coast. The fourth, Ebola-Reston, has caused disease in nonhuman primates, but not in humans.