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Clase terica 14

estructura de los virus

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Preserial high-

resolution electronmicroscope (1938)

from Siemens and

Halske. In 1939 first

EM micrograph of a

virus: TMV byRuska et al.

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Bats are the reservoir host for viral pathogens, including Nipah,SARS, Ebola,

Hendra, Rabies.

MICROBE 2 (9): 418-419, 2007

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Viruses in the sea

Curtis A. Suttle. Department of Chemistry, University of

California, Berkeley and the Molecular Foundry, Lawrence

Berkeley National Laboratory, Berkeley, California 94720, USA.

Viruses exist wherever life is found. They are a major cause of

mortality, a driver of global geochemical cyclesand a reservoir

of the greatest genetic diversity on Earth.In the oceans, virusesprobably infect all living things, from bacteria to whales. They

affect the form of available nutrients and the termination of algal

blooms. Viruses can move between marine and terrestrial

reservoirs, raising the specter of emerging pathogens.Ourunderstanding of the effect of viruses on global systems and

processes continues to unfold, overthrowing the idea that viruses

and virus-mediated processes are sidebars to global processes.

Nature437, 356-361 (15 September 2005)

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PROPIEDADES DE LOS VIRUS USADAS PARA CONSTRUCCIONES TAXONOMICAS

A. PROPIEDADES DE LOS VIRIONES.1. Tamao del virin2. Forma del virin3. Presencia o ausencia de envoltura y peplmeros4. Simetra de los capsmeros y estructura.

B. PROPIEDADES DEL GENOMA

1. Tipo de cido nucleico - DNA o RNA2. Cadena simple o doble.3. Linear o Circular.4. Cadena positiva o negativa5. Nmero de segmentos.6. Tamao del genoma.

C. PROPIEDADES DE LAS PROTEINAS1. Nmero de las proteinas2. Tamao de las proteinas.3. Actividades funcionales de las proteinas(Especialmente

transcriptasa, transcriptasa reversa, hemaglutinina,neuraminidasa y proteina de fusin)

D. SINTESIS DE MACROMOLECULAS1. Estrategia de replicacin del cido nucleico.2. Caractersticas de la transcripcin.3. Caractersticas de la traduccin y procesamiento deprotenas

4. Lugar de acumulacin de las protenas virales, lugar deensamblaje, lugar de maduracin y liberacin.

5. Citopatologa, formacin de cuerpos de inclusin.

E. PROPIEDADES FISICAS1. Estabilidad trmica y pH2. Estabilidad en solventes, detergentes.3. Estabilidad a la radiacin.

F. PROPIEDADES BIOLOGICAS1. Serologa2. Rango de huespedes.3. Patogenicidad.4. Tropismo tisular.5. Transmisin y vectores.6. Distribucin geogrfica.

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ADENOVIRUS 80 nm D

INFLUENZA VIRUS (200 nm D)HERPESVIRUS (100 nm D)

PAPILLOMAVIRUS 55 nm D POLIOVIRUS (30 nm D)

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Journal of Virology 74: 9646-9654, 2000

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Journal of Virology 74: 9646-9654, 2000

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11/33FUNDAMENTAL VIROLOGY, FIELDS.

PEPLOMEROS

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ESQUEMA PARCIAL DEL VIRUS INFLUENZA.

THE BIOLOGY OF ANIMAL VIRUSES, FENNER.

PEPLOMEROS

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FUNDAMENTAL VIROLOGY, FIELDS

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CICLO DE MULTIPLICACION

1. ADSORCION.

- ES ESPECIFICA (RECEPTORES EN LA SUPERFICIE DE LA CELULA).

2. PENETRACION.

- VARIA DE ACUERDO AL VIRUS

3. DECAPSIDACION.

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Figure 1. Steps in the Endocytic Entry Program of a

Typical Animal Virus

Many viruses depend on the host cell's endocytic

pathways for entry. In this example, the virus

proceeds to deliver its uncoated genome into the

nucleoplasm. The interaction between the virus and

the host cell starts with virus binding to attachmentfactors and receptors on the cell surface, followed

by lateral movement of the virus-receptor complexes

and the induction of signals that result in the

endocytic internalization of the virus particle. After

vesicular trafficking and delivery into the lumen of

endosomes, caveosomes, or the ER, a change in thevirus conformation is induced by cellular cues. This

alteration results in the penetration of the virus or its

capsids through the vacuole membrane into the

cytosolic compartment. Enveloped viruses use

membrane fusion for penetration, whereas

nonenveloped viruses induce lysis or pore

formation. After targeting and transport alongmicrotubules, the virus or the capsid binds, as in this

example, to the nuclear pore complex, undergoes a

final conversion, and releases the viral genome into

the nucleus. The details in the entry program vary

for different viruses and cell types, but many of the

key steps shown here are general.

CELL 124(4): 729-740, 2006

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CELL 124(4): 729-740, 2006

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Figure 2. Endocytic Pathways Used by VirusesIn mammalian cells, many different mechanisms are available for the endocytic

internalization of virus particles. Some of these mechanisms, such as clathrin-

mediated endocytosis, are ongoing, whereas others, such as caveolae, are ligand

and cargo induced. Currently, there is evidence for six pathways.(A) Macropinocytosis is involved in the entry of adenoviruses.

(B) A clathrin-independent pathway from the plasma membrane has been shown to

exist for influenza virus and arenaviruses.

(C) The clathrin-mediated pathway is the most commonly observed uptake

pathway for viruses. The viruses are transported via early endosomes to lateendosomes and eventually to lysosomes.

(D) The caveolar pathway is one of several closely related, cholesterol-dependent

pathways that bring viruses including SV40, coxsackie B, mouse polyoma, and

Echo 1 to caveosomes, from which many of them continue, by a second vesicle

transport step, to the ER.(E) A cholesterol-dependent endocytic pathway devoid of clathrin and caveolin-1,

used by polyomavirus and SV40.

(F) A pathway similar to (D) except dependent on dynamin-2. It is used by Echo

virus 1.

CELL 124(4): 729-740, 2006

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PRIMEROS ESTADIOS DE INFECCION POR SEMLINKI FORESSST VIRUS,

MICROBIOLOGY, DAVIS.

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CELL 124(4): 729-740, 2006

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Figure 3. Electron Micrographs Showing Virus Internalization by Clathrin- or

Caveolar/Raft-Mediated Endocytosis

(A and B) Semliki Forest virus, a 70 nm diameter enveloped alphavirus, is

internalized by clathrin-coated pits (A) and vesicles (B) for endocytosis and

infection. Here, the virus is interacting with a BHK-21 cell.

(C and D) Simian virus 40, a small 50 nm diameter nonenveloped DNA virus, binds

to gangliosides in the plasma membrane of CV-1 cells and enters via caveolae (C)

and tight-fitting small vesicles. The viruses are transported through caveosomes tothe ER, where many accumulate in smooth membrane domains (D).

Scale bar in (A) and (C) = 100 nm, (B) = 200 nm, and (D) = 250 nm.

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CLATRINA-VACUOLAS

http://localhost/var/www/apps/My%20Documents/ZZYPRESENTACIONES%2030-07-10/VIDEOS/VIDEOS%201/Tommy/ClathrinFinal.mov

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JOURNAL OF VIROLOGY 74:1342-1354, 2000

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MECANISMO PROBABLE DE TRANSFERENCIA DEL RNA DEL

POLIOVIRUS A TRAVES DE LA MEMBRANA CELULAR(PROTEINAS

VIRALES: VP1; VP2; VP3; VP4).

Journal of Virology 74: 1342-1354, 2000

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CICLO DE MULTIPLICACION

3. SINTESIS DE MACROMOLECULAS VIRALES

- TRANSCRIPCION:

mRNA TEMPRANO: SINTESIS DE PROTEINAS PARA REPLICACION

mRNA TARDIO: SINTESIS DE PROTEINAS ESTRUCTURALES.

- TRADUCCION

- REPLICACION

4. ENSAMBLAJE Y LIBERACION

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MICROBIOLOGY, DAVIS.

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MULTIPLICACION DE UN RETROVIRUS

http://localhost/var/www/apps/conversion/tmp/scratch_6/LIFE-RETRO.MOV

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Cell 138: 31-50, 2009 Figure 1. The Course of Viral Infection

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Figure 1. The Course of Viral Infection

When a virus enters the host, there is an initial nonequilibrium

phase of acute infection. During this phase, viral and immunestrategies compete for dominance.

Assuming the host survives, a decision point is reached at which

the infection is either cleared or becomes chronic. This decisionpoint may be reached very early in infection for viruses that can

establish a latent infection, in which case the infection is

permanent regardless of the course of acute infection.

If recovery occurs, the immune system must reset by clearing theantigen and re-establishing immune homeostasis. If the balance

shifts toward chronic infection, a new set of viral and host

strategies interact to define a metastable equilibrium in which

viral replication is held in check, but the virus is not cleared.

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Cell 138: 31-50, 2009

Figure 2. Chronic Viral Infections in Humans

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Figure 2. Chronic Viral Infections in Humans

The number of humans infected with different chronic viruses is

estimated from the percentage of humans carrying a given virus,

(estimated by the prevalence of antiviral antibodies in serum)

and assuming that the world population is 6.75 billion.

For adenovirus, the situation is unclear and the prevalence of

chronic infection is arbitrarily set at 1%. For some viruses, theprevalence of infection is not sufficiently well defined for

inclusion in the graph. These include xenotropic murine

leukemia virus-related virus (XMLV), human T cell leukemia

virus (HTLV II, III, IV), and polyomaviruses MC, KI, and WU.The estimates in the graph are approximate as they apply data

on prevalence in the limited populations studied to date to the

global human population.