Jason Kerkvliet, Ramakrishna Edukulla, Moses Rodriguez
25 Jan 2024
Genomic organization of picornaviruses with the covalently linked VPg peptide as it is packaged in the virion. The regions of the P1 (pink), P2 (blue), and P3 (brown) are shown along with the viral proteins encoded within each domain. P1 encodes capsid proteins and the P2 and P3 domains encode noncapsid proteins used for protein processing and replication. The plus-sense single stranded RNA genome is translated into a single polyprotein and then cleaved by cis and transacting viral proteases.[1]
Genomic organization of picornaviruses with the covalently linked VPg peptide as it is packaged in the virion. The regions of the P1 (pink), P2 (blue), and P3 (brown) are shown along with the viral proteins encoded within each domain. P1 encodes capsid proteins and the P2 and P3 domains encode noncapsid proteins used for protein processing and replication. The plus-sense single stranded RNA genome is translated into a single polyprotein and then cleaved by cis and transacting viral proteases.[1]
Jason Kerkvliet, Ramakrishna Edukulla, Moses Rodriguez
Two misshapen zucchini fruits and leaves from a plant infected with Zucchini yellow mosaic virus. The fruits are stunted as well as misshapen. Grown in Los Angeles, California.
Two misshapen zucchini fruits and leaves from a plant infected with Zucchini yellow mosaic virus. The fruits are stunted as well as misshapen. Grown in Los Angeles, California.
Electron Micrographs of viruses that cause gastroenteritis in humans. A = Rotavirus, B = Adenovirus, C = Norovirus and D = Astrovirus. They are shown at the same magnification of approximately x 200,000.
Electron Micrographs of viruses that cause gastroenteritis in humans. A = Rotavirus, B = Adenovirus, C = Norovirus and D = Astrovirus. They are shown at the same magnification of approximately x 200,000.
Wikimedia Commons, National Institute of Allergy and Infectious Diseases
24 Jan 2024
Colorized transmission electron micrograph of Ebola virus nucleocapsids (small orange circles) and virus particles (larger orange filamentous forms) within infected African green monkey kidney cells.
Colorized transmission electron micrograph of Ebola virus nucleocapsids (small orange circles) and virus particles (larger orange filamentous forms) within infected African green monkey kidney cells.
Wikimedia Commons, National Institute of Allergy and Infectious Diseases
This structural model has been constructed in UCSF Chimera software putting together all the structures that compose bacteriophage T5 using cryoEM reconstructions and pdb structures. [1]
This structural model has been constructed in UCSF Chimera software putting together all the structures that compose bacteriophage T5 using cryoEM reconstructions and pdb structures. [1]
Satellite tobacco mosaic virus (STMV) rendering produced by VMD and Tachyon. The capsid is colored using a radial color scale. The VMD axes are left in the image to show rendering of text and other non-molecular geometry in Tachyon. Ambient occlusion lighting improves perception of shape.
Satellite tobacco mosaic virus (STMV) rendering produced by VMD and Tachyon. The capsid is colored using a radial color scale. The VMD axes are left in the image to show rendering of text and other non-molecular geometry in Tachyon. Ambient occlusion lighting improves perception of shape.
Public Health Image Library, Fred Murphy, Sylvia Whitfield
24 Jan 2024
This colorized transmission electron micrograph (TEM) depicts a salivary gland that had been extracted from a mosquito, which was infected by the eastern equine encephalitis (EEE) virus, which has been colorized red; magnified 83,900x.
This colorized transmission electron micrograph (TEM) depicts a salivary gland that had been extracted from a mosquito, which was infected by the eastern equine encephalitis (EEE) virus, which has been colorized red; magnified 83,900x.
Public Health Image Library, Fred Murphy, Sylvia Whitfield
Colorized transmission electron micrograph of monkeypox particles (red) found within an infected cell (blue), cultured in the laboratory. Image captured and color-enhanced at the NIAID Integrated Research Facility (IRF) in Fort Detrick, Maryland.
Colorized transmission electron micrograph of monkeypox particles (red) found within an infected cell (blue), cultured in the laboratory. Image captured and color-enhanced at the NIAID Integrated Research Facility (IRF) in Fort Detrick, Maryland.
Dr. Yazami Rachid, a distinguished scientist and innovator, is celebrated for his groundbreaking contributions to lithium-ion battery technology. A Moroccan National Treasure, his pioneering research has revolutionized energy storage, paving the way for advancements in portable electronics, electric vehicles, and renewable energy systems. Despite his remarkable achievements, including being widely considered for the Nobel Prize, Dr. Yazami's recognition in this prestigious arena remains elusive. Nevertheless, his numerous patents and accolades attest to his profound impact on technology and sustainability, inspiring ongoing innovation in the field of energy solutions.
Dr. Yazami Rachid, a distinguished scientist and innovator, is celebrated for his groundbreaking contributions to lithium-ion battery technology. A Moroccan National Treasure, his pioneering research has revolutionized energy storage, paving the way for advancements in portable electronics, electric vehicles, and renewable energy systems. Despite his remarkable achievements, including being widely considered for the Nobel Prize, Dr. Yazami's recognition in this prestigious arena remains elusive. Nevertheless, his numerous patents and accolades attest to his profound impact on technology and sustainability, inspiring ongoing innovation in the field of energy solutions.
In the hepatocellular carcinoma (HCC) microenvironment, various overexpressed miRNAs favor the tumor progression: in particular, miR-221 [targeting TIMP1/PTEN (AkT), and DDIT4 (mTOR) pathways] [1], miR-302d (targeting TGFBR2) [2], miR-96 (targeting Caspase-9) [3], miR-25 targeting TRAIL) [4], and miR-92a (targeting FBXW7) [5] impact on cancer cells’ proliferation and survival mechanisms, whereas miR-130 (targeting HOXA5)[46] and miR-210 (targeting FGFRL1)[47] are principally involved in promoting angiogenesis. The overexpression of miR-574 (targeting BMP2) [6], miR-214 (targeting WASL) [7], miR-424 (targeting SRF – STAT1/2 pathway) [8], and miR-135 (targeting FOXO1) [9] facilitates invasion, migration, and metastatisation. Moreover, miR-18a (targeting Bcl2l10) [10], miR-550a (targeting GNE – b-catenin/Wnt pathway) [11], and miR-512 (targeting various MRPS) [12] have been reported to influence both proliferation/apoptosis and invasion/migration/metastatisation processes, as well as miR-21 (targeting KLF5-PI3K-Akt pathway) [13], miR-155 (targeting PTEN) [14], and miR-873 (targeting TSLC1, among others) [15], whose pleiotropical involvement in various crucial cancer-progression mechanism (proliferation, angiogenesis, invasion, and metastasis) has been widely reported. In HCC cells, the down-regulation of miR-195 (targeting CDC42 and other proteins regulating the cell cycle) [16], miR-15b (targeting Bcl2) [17], miR-26a (targeting ULK1) [18], miR-766 and miR-148 (influencing b-catenin/Wnt pathway) [19][20] represents dramatic events for the loss of control of proliferation/survival mechanisms. Moreover, miR-126 (targeting VEGF) [21], miR-451 (targeting IL6R) [22], and miR-338-3p (targeting VEGF and MACC1) [23] are pivotally involved in HCC angiogenesis. The down-regulation of miR-539 (targeting FSCN1) [24], miR-101 (targeting ROCK) [25], miR-497 (targeting Rictor) [25], miR-345 (targeting INF1) [26], and miR-200a (targeting GAB1)[27] favour invasion, migration, and metastatisation, consistently with the following miRNAs which regulate also HCC-related proliferation/apoptosis processes: miR-31-5p (targeting SP1) [28], miR-33b (targeting SALL4) [29], and miR-29a (targeting CLDN1) [30]. About this last, some evidence supports miR-29 (targeting, among several others, BCL2, IGF2BP1, VEGF) [31][32][33] involvement in each of the crucial cancer-progression mechanism as well as for miR-122 (targeting, among others, p53 and MDM2) [34] and miR-1301 (targeting, among others, BCL9, VEGF, and b-catenin pathway) [35]. TIMP1: TIMP metallopeptidase inhibitor 1; PTEN: Phosphatase and TENsin homolog; DDIT4: DNA damage-inducible transcript 4; mTOR: mammalian target of rapamycin; TGFBR2; transforming growth factor beta receptor 2; TRAIL: Tumor necrosis factor-related apoptosis-inducing ligand; HOX: Homeobox; FGFRL1: Fibroblast growth factor receptor-like 1; BCL: B-cell lymphoma; GNE: UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase; WASL: WASP like actin nucleation promoting factor; MRPs: Mitochondrial ribosomal proteins; KLF5: Krüppel-like factor 5; TSLC1: tumor suppressor of lung cancer 1; ULK1: Unc-51 Like Autophagy Activating Kinase 1; MACC1: Metastasis-associated in colon cancer 1; SALL4: Sal-like protein 4; Insulin-like growth factor 2 mRNA-binding protein 1.
In the hepatocellular carcinoma (HCC) microenvironment, various overexpressed miRNAs favor the tumor progression: in particular, miR-221 [targeting TIMP1/PTEN (AkT), and DDIT4 (mTOR) pathways] [1], miR-302d (targeting TGFBR2) [2], miR-96 (targeting Caspase-9) [3], miR-25 targeting TRAIL) [4], and miR-92a (targeting FBXW7) [5] impact on cancer cells’ proliferation and survival mechanisms, whereas miR-130 (targeting HOXA5)[46] and miR-210 (targeting FGFRL1)[47] are principally involved in promoting angiogenesis. The overexpression of miR-574 (targeting BMP2) [6], miR-214 (targeting WASL) [7], miR-424 (targeting SRF – STAT1/2 pathway) [8], and miR-135 (targeting FOXO1) [9] facilitates invasion, migration, and metastatisation. Moreover, miR-18a (targeting Bcl2l10) [10], miR-550a (targeting GNE – b-catenin/Wnt pathway) [11], and miR-512 (targeting various MRPS) [12] have been reported to influence both proliferation/apoptosis and invasion/migration/metastatisation processes, as well as miR-21 (targeting KLF5-PI3K-Akt pathway) [13], miR-155 (targeting PTEN) [14], and miR-873 (targeting TSLC1, among others) [15], whose pleiotropical involvement in various crucial cancer-progression mechanism (proliferation, angiogenesis, invasion, and metastasis) has been widely reported. In HCC cells, the down-regulation of miR-195 (targeting CDC42 and other proteins regulating the cell cycle) [16], miR-15b (targeting Bcl2) [17], miR-26a (targeting ULK1) [18], miR-766 and miR-148 (influencing b-catenin/Wnt pathway) [19][20] represents dramatic events for the loss of control of proliferation/survival mechanisms. Moreover, miR-126 (targeting VEGF) [21], miR-451 (targeting IL6R) [22], and miR-338-3p (targeting VEGF and MACC1) [23] are pivotally involved in HCC angiogenesis. The down-regulation of miR-539 (targeting FSCN1) [24], miR-101 (targeting ROCK) [25], miR-497 (targeting Rictor) [25], miR-345 (targeting INF1) [26], and miR-200a (targeting GAB1)[27] favour invasion, migration, and metastatisation, consistently with the following miRNAs which regulate also HCC-related proliferation/apoptosis processes: miR-31-5p (targeting SP1) [28], miR-33b (targeting SALL4) [29], and miR-29a (targeting CLDN1) [30]. About this last, some evidence supports miR-29 (targeting, among several others, BCL2, IGF2BP1, VEGF) [31][32][33] involvement in each of the crucial cancer-progression mechanism as well as for miR-122 (targeting, among others, p53 and MDM2) [34] and miR-1301 (targeting, among others, BCL9, VEGF, and b-catenin pathway) [35]. TIMP1: TIMP metallopeptidase inhibitor 1; PTEN: Phosphatase and TENsin homolog; DDIT4: DNA damage-inducible transcript 4; mTOR: mammalian target of rapamycin; TGFBR2; transforming growth factor beta receptor 2; TRAIL: Tumor necrosis factor-related apoptosis-inducing ligand; HOX: Homeobox; FGFRL1: Fibroblast growth factor receptor-like 1; BCL: B-cell lymphoma; GNE: UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase; WASL: WASP like actin nucleation promoting factor; MRPs: Mitochondrial ribosomal proteins; KLF5: Krüppel-like factor 5; TSLC1: tumor suppressor of lung cancer 1; ULK1: Unc-51 Like Autophagy Activating Kinase 1; MACC1: Metastasis-associated in colon cancer 1; SALL4: Sal-like protein 4; Insulin-like growth factor 2 mRNA-binding protein 1.
Adenovirus D26 structural model at atomic resolution. This structural model has been constructed in UCSF Chimera software putting together all the structures that compose Adenovirus D26 using cryoEM reconstructions and pdb structures. [1]
Adenovirus D26 structural model at atomic resolution. This structural model has been constructed in UCSF Chimera software putting together all the structures that compose Adenovirus D26 using cryoEM reconstructions and pdb structures. [1]
ViralZone, SIB Swiss Institute of Bioinformatics, Wikimedia Commons
22 Feb 2024
Schematic drawing of a rhabdoviridae virion. Enveloped, bullet shaped. 180 nm long and 75 nm wide. Certain plant rhabdoviruses are bacilliform in shape and almost twice the length.
Schematic drawing of a rhabdoviridae virion. Enveloped, bullet shaped. 180 nm long and 75 nm wide. Certain plant rhabdoviruses are bacilliform in shape and almost twice the length.
ViralZone, SIB Swiss Institute of Bioinformatics, Wikimedia Commons