290 likes | 303 Views
This text discusses the characteristics of viruses, including their structure, classification, and multiplication methods. It also explores the challenges in targeting viruses and the process of virus identification. Additionally, it covers topics such as viral infections, lysogeny, animal virus infection, viruses and cancer, and prions.
E N D
Living • Nonliving
Contain a single type of nucleic acid (DNA or RNA), protein coat, sometimes an envelope. • Are obligatory intracellular parasites. Multiply by using host cell’s synthesizing machinery to cause the production of specialized elements that can transfer the nucleic acid to other cells.
Multiply inside living cells by using the synthesizing machinery of the cell. • Why does this make targeting viruses difficult?
Host Range • The spectrum of host cells in which a virus can multiply. • Mot viruses infect only specific types of cells in one host species. • The host is determined by the specific attachment site on the host cell’s surface and the availability of host cellular factors.
Virus Size Figure 13.1
Taxonomy of viruses • Currently based on type of nucleic acid, strategy for replication and morphology. • Virus family names end in –viridae; genus names end in –virus • A viral species is a group of viruses sharing the same genetic information and ecological niche
Viral Taxonomy • Herpesviridae • Herpesvirus • Human herpes virus 1, HHV 2, HHV 3 • Flue H1N1 • Retroviridae • Lentivirus • Human Immunodeficiency Virus 1, HIV 2
Isolation, growth and identification • Must be grown on living cells. • Easiest to grow are bacteriophage, because bacteria are easy to grow.
Growth results. • Plaques for bacteriophage. • Cytopathic effects on cell culture.
Growing Viruses • Viruses must be grown in living cells. • Bacteriophages form plaques on a lawn of bacteria. Figure 13.6
Growing Viruses • Animal viruses may be grown in living animals or in embryonated eggs. Figure 13.7
Growing Viruses • Animal and plants viruses may be grown in cell culture. • Continuous cell lines may be maintained indefinitely. Figure 13.8
Identification. • Serological tests (Antibodies) • RFLP and PCR • (Discussion)
Typical viral infection • Attachment • Penetration • Biosynthesis • Maturation • Release • Burst size and burst time
Bacterial cell wall Bacterial chromosome Capsid DNA Capsid Sheath Tail fiber Tail 1 Attachment:Phage attaches to host cell. Base plate Pin Cell wall Plasma membrane 2 Penetration:Phage pnetrates host cell and injects its DNA. Sheath contracted Tail core 3 Merozoites released into bloodsteam from liver may infect new red blood cells Figure 13.10.1
Tail DNA 4 Maturation:Viral components are assembled into virions. Capsid 5 Release:Host cell lyses and new virions are released. Tail fibers Figure 13.10.2
One-step Growth Curve Figure 13.11
The Lysogenic Cycle Figure 13.12
Animal virus infection • Attachment • Penetration (endocytosis) • Uncoating • Biosynthesis
Attachment, Penetration, and Uncoating Figure 13.14
Release of an enveloped virus by budding Figure 13.20
Multiplication of DNA Virus Papovavirus 1 Virion attaches to host cell 7 Virions are released Host cell DNA Capsid 2 DNA Virion penetrates cell and its DNA is uncoated Cytoplasm 6 Virions mature Capsid proteins mRNA 5 Late translation; capsid proteins are synthesized 3 Early transcription and translation; enzymes are synthesized 4 Late transcription; DNA is replicated Figure 13.15
Viruses and Cancer. • Viruses incorporated in to the host genome can cause mistakes and errors resulting in unchecked growth of the cell. • It this accidental or are these sites targeted?
Latent Viral Infections • Virus remains in asymptomatic host cell for long periods • Cold sores, shingles • Persistent Viral Infections • Disease processes occurs over a long period, generally fatal • Subacute sclerosing panencephalitis (measles virus)
Prions • Infectious proteins • Inherited and transmissible by ingestion, transplant, & surgical instruments • Spongiform encephalopathies: Sheep scrapie, Creutzfeldt-Jakob disease, Gerstmann-Sträussler-Scheinker syndrome, fatal familial insomnia, mad cow disease • PrPC, normal cellular prion protein, on cell surface • PrPSc, scrapie protein, accumulate in brain cells forming plaques
Prions PrPSc PrPc 2 3 4 1 Lysosome Endosome 5 6 7 8 Figure 13.21
Topics on the flue • http://content.nejm.org/cgi/content/full/NEJMe0903995 • NEJM N1H1 site http://h1n1.nejm.org/ • An Old presentation http://www.strongnet.org/171520529114210850/lib/171520529114210850/Influenza_presentation.pdf